Se volete porto degli esempi di Epigenetica e obesita. Di flora intestinale ed obesita e di Leaky Gut e codice genetico.

Io sono interessato! posta pure. Grazie!:)

Come promesso un po di informazioni.

Epigenetica ed evoluzione umana: il fattore Leaky Gut
sito di Jack Kruse, per chi volesse leggerlo per intero ed avere piu notizie.

Cosa ci distingue dagli altri primati, che secondo una teoria evoluzionistica sarebbero i nostri ancestori?
Non e’certo il codice genetico. Dopo il completo sequenziamento del genoma umano si e’visto che il nostro genoma e’all’98,5 % simile a quello di altri primati. Sara’ quel che mangiamo, non ne esistono prove certe ne tanto meno ne sono convinto.
Nel nostro genoma ci sono molte sequenze uniche che non appartengono a quelle dei primati ma a quelle Virali. L’8% del nostro genoma e’ costituito da sequenze virali, human endogenous retrovirus, HERV che hanno apportato mutazioni incredibili.
Di virus c’e’ne sono molti in giro, molto piu dei batteri. E non parlo dei virus tipo Herpes o influenza, ma di enterovirus, retrovirus. Milioni di particelle virali sono presenti nelle acque marine, di fiume, nell’aria. In una goccia di acqua di mare sono stati trovati milioni di particelle virali. Sono il principio della vita anche se non sono certo vivi, hanno bisogno di cellule vive per potersi moltiplicare.

There is radical changes in the X and Y chromosomes of humans. The Y chromosome genes code for few new things yet have a massive expansion of retroposons on it, and there is one in particular, that made the primate clade more susceptible to latent or persistent infections that were innocuous to our immune systems. This was called the HERV K virus. The acronym HERV, stands for human endogenous retrovirus. Make sure you really look at those highlighted links just posted. It maybe the most important links in this entire series. You might be asking, what do HERV do for us?
J R Soc Med. 2004 December; 97(12): 560–565.
PMCID: PMC1079666
Human endogenous retroviruses in health and disease: a symbiotic perspective
Frank P Ryan, FRCP FLS
Questo articolo ci dimostra come la presenza del virus HERV-K113 e del HERV-H/RGH-2 e’indispensabile per la vita umana. Le sequenze integrate di questi virus esplicano azioni ORMONALI nell’uomo.
In that same year Hughes and Coffin used phylogenetic and sequence analysis to suggest that human endogenous retroviruses may have induced large-scale deletions, duplications and chromosome reshuffling in human genomic evolution.17 In the opinion of the geneticist Eugene Sverdlov, these viruses played a significant role in the evolution and divergence of the hominids.18
Addirittura ci sarebbero prove/teorie che il virus proteggerebbe i feti umani:

This line of discovery gained momentum in the 1980s when virologists, among them Erik Larsson at the University of Uppsala, suggested that HERVs may help protect the fetus. Certain viruses have the capacity to fuse mammalian cells into confluent multinucleated sheets of tissue. Multinucleated giant cells are a pathological feature of AIDS. Fusion of cells is also a characteristic feature of the mammalian placenta, where a microscopically thin and confluent tissue layer known as the syncytium forms the physiological barrier between maternal and fetal circulations. All nutrients from the mother and waste from the fetus must pass through this syncytial layer. The syncytium also serves to prevent maternal immune rejection of the fetus, which inherits half of its antigens from the father. There is growing evidence that endogenous retroviruses contribute importantly to the structure and function of the syncytium.
Ancora nello stesso articolo:
Over the succeeding years, continuing investigation by the McCoy and Mallet groups, and several others, confirmed and extended this finding, and today there is general acceptance that this HERV-W and its translated product syncytin have important functions in human placental physiology.26 Other researchers raised the possibility that HERVs might help protect their hosts, including the fetuses of HIV infected mothers, by blocking infection by exogenous retroviruses. In 2003, Ponferrada and colleagues reported confirmation that the envelope glycoprotein of HERV-W protected a human tissue cell line from infection with the exogenous retrovirus known as spleen necrosis virus.27 An exciting line of investigation by Stoye and colleagues at Mill Hill suggested that a retroviral capsid protein, Fv1, might reduce the infectivity of HIV-1 in monkeys but Sodroski, of Harvard, then showed the protective agent to be a protein coded by the Trim5 gene.28
Il virus codifica per una proteina la SYNCYTIN che e’ indispensabile per la produzione dell’ormone Gonadotropina..:
Recently, Rote and colleagues have overviewed the functional roles of all three endogenous retroviruses, ERV-3, HERV-W and HERV-FRD, to construct a testable model of villous cytotrophoblast differentiation. Refuting any fusogenic role for ERV-3 env, they propose that its main action is hormonal, initiating the production of human gonadotropic hormone. If true, this is yet another example of a key HERV role in human physiology, suggesting that the three envelope proteins, syncytin, syncytin 2 and ERV-3 env, have differing but essentially complementary functions in the multistep process of placentation.30
Da altri studi sembra che l’intestino umano sia “fatto”su misura per far passare informazioni virali/virus nel nostro genoma...insomma il Leaky Gut sembrerebbe non patologico ma potrebbe essere un meccanismo di evoluzione.

A persisting genetic parasite like a retroposon, must superimpose onto its host a new molecular genetic identity that compels persistence and precludes competition and displacement. How did we do this? I believe we did it by first transforming the endogenous gut bacteria genomes and then assimilating the non infectious genomic elements into our own DNA using our own gut immune system. This is why we have evolved a leaky gut and primates do not. I believe, developing this strategy is simply a molecular stroke of genius of precisely how a leaky gut and retrovirus work in human DNA today

Ritorniamo un attimo ai virus:
Il premio Nobel McClintock disse che : una volta integrati, i DNA virali, agiscono come gene saltanti, jumping genes, che sanno esattamente dove andare a porsi. Questo jumping e’legato alla adattabilita ambientale. Sotto particolare pressione alcuni geni cominciano a “saltellare”dando luogo a variazioni che nel corto periodo potrebbero sembrare non sempre positive...ma che nel lungo periodo salvano la specie. Una sequenza genetica non codifica solo una determinato numero di proteine o una sola proteina. Nella drosofila..il moscerino della frutta, un solo gene puo esprimere 40.000 diverse proteine.

Mi seguite. I geni come si sapeva si modificano per effetto ambientale..ma non solo nel lungo periodo. L’epigenetica agisce intragenerazionale.
Non sono i geni “BASE”ad essere importanti, quelli che per intenderci che ci posizionano in un certo albero genealogico...mammiferi, a poterci distinguere da altri mammiferi.
Sono quei “jumping gene” i fattori dell’evoluzione.
Queste sequenze virali le abbiamo acquisiste principalmente attraverso l’ingestione di molluschi marini infetti quando ci siamo evoluti nella zona costiera Africana. Consequenza delle continue mutazioni ambientali il nostro intestino e’per cosi dire diventato “Leaky Gut”assimilando una moltitudine di virus che hanno fatto scattare una sorta di “circo genetico”.

Ora saltiamo dal Leaky Gut, dalla epigenetica alla dieta per cosi dire Paleo, prima che vi addormentiate leggendo sto papelo lunghissimo.

Lo sapevate che il nostro cervello non si e’evoluto ma che si e’rimpicciolito dal paleolitico ad oggi. Gli ominidi tipo Cro-Magnon avevano circa 130 grammi di cervello in piu.

In seguito a drastici cambiamenti ambientali, la dieta degli ominidi/uomo e’mutata. Il freddo cambio drasticamente la diffusione delle prede preferite dall’uomo che “si adatto mangiando vegetali e graminacee ed in seguito coltivandoli. Questo come descrive Cordain ha dato all’uomo la possibilita di controllare l’ambiente in cui viveva. Ma non senza conseguenze.

Abbiamo detto e letto come ogni cambiamento ambientale provoca una serie di “salti genetici”variazioni epigenetiche. La roulet russa gira finche non trova un adattamento..il migliore dei peggiori.
Qui arriviamo alle diete e alle paleodiete.
Quando Weston Price ando’ a cercare ed ad analizzare le varie tribu e gruppi di popolazioni che non avevano mutato le loro condizioni alimentari e stile di vita in millenni si accorse che tutte avevano trovato un optimus. Sia che consumassero formaggi e pan di segale, villaggi svizzeri, sia che consumassero latte, sangue e mais, Himba e Masai, sia che si nutrissero di vegetali e pochi prodotti animali, in India, etc. Quando membri di queste societa’ si trasferivano in un altro ambiente, citta moderne, assumendo un altro stile di vita e cambiando alimentazione, lui riscontro che “IN UNA SOLA GENERAZIONE LA SALUTE FISICA E DENTALE “PEGGIORAVA. Mi seguite ancora..non in generazioni ma in una sola.
Perche...
L’epigenetica
La Weston Price dieta e’una estrapolazione dei risultati delle ricerche di Weston. L’errore e’stato generalizzarla.
Non e’il latte ad essere non “naturale per l’uomo”, non le graminacee, non la carne, i saturi o i polyinsaturi. E’il personale adattamento.
Quindi come puo’una Paleodieta essere uguale per tutti. Da quel che ho descritto la Paleodieta degli Himba e’”Latte , mais etc”. Quella degli eschimo e’carne di balena, foca etc.
La mia non puo essere quella degli Himba con 2 litri di latte, che poi non e’lo stesso latte e‘ un altro discorso. Ma quale e’? Non lo sappiamo piu perche le variazioni culturali sono state cosi intense che ci siamo persi tutto.

Bisogna trovarsela da soli. Ma attenti quel che fate ora si ripercuote sulla prole. E si perche l’epigenetica e’ sempre attiva. Ritornare ad una paleo, con cibi base non raffinati, attiva/riattiva/spege geni saltellanti, se i vostri figli continuano la stessa dieta, allora questi geni si fissano altrimenti continuano a saltellare.
Ecco perche tutte le diete che implicano una dieta fatta di cibi base, il meno possibile indistrializzati, con un buon apporto di grassi, proteine etc, e’una dieta che porta benefici. Si avvicina alla dieta ottimale.

Grazie Roberto,

leggendo la parte dei virus mi è venuto in mente, come un flash, che un certo Arnold Ehret (ho un certo disagio nel nominarlo) sosteneva che i virus in se non sono pericolosi e che in un organismo sano transitano indisturbati svolgendo dentro di noi svariate utili funzioni. Questi virus vengono paragonati a dei topi che nutrendosi della spazzatura ripuliscono il territorio (i virus il nostro organismo). Se la spazzatura e poca tutto va bene ma se tanta allora le tossine che scaturiscono da questo processo di pulizia non vengono espulse causando la malattia. Credo che Ehret si riferisse a Bechamp, infatti lui ha scoperto che i germi non sono la causa della malattia ma si occupano solo di decomporre i tessuti in degrado e sono prodotti dall'organismo; di fatto sono gli spazzini dell'organismo. Quindi quando noi, con i farmaci, uccidiamo i virus è come se uccidessimo i topi lasciando che la montagna di spazzatura continui a crescere. Così dopo che l'effetto del farmaco svanisce e i virus ritornano, si troveranno una super montagna di spazzatura da metabolizzare con un effetto ancora più drammatico per il nostro organismo. Lo stesso Pasteur in punto di morte disse ad un suo assistente: "Claude Bernard aveva ragione, il terreno è tutto, il microbo è nulla".
Anche un certo dr. Hamer disse: Se fossero i germi o i virus le cause delle malattie noi saremmo già morti perché ne abbiamo in gran quantità nel nostro organismo.

Grazie Roberto,

leggendo la parte dei virus mi è venuto in mente, come un flash, che un certo Arnold Ehret (ho un certo disagio nel nominarlo) sosteneva che i virus in se non sono pericolosi e che in un organismo sano transitano indisturbati svolgendo dentro di noi svariate utili funzioni. Questi virus vengono paragonati a dei topi che nutrendosi della spazzatura ripuliscono il territorio (i virus il nostro organismo). Se la spazzatura e poca tutto va bene ma se tanta allora le tossine che scaturiscono da questo processo di pulizia non vengono espulse causando la malattia. Credo che Ehret si riferisse a Bechamp, infatti lui ha scoperto che i germi non sono la causa della malattia ma si occupano solo di decomporre i tessuti in degrado e sono prodotti dall'organismo; di fatto sono gli spazzini dell'organismo. Quindi quando noi, con i farmaci, uccidiamo i virus è come se uccidessimo i topi lasciando che la montagna di spazzatura continui a crescere. Così dopo che l'effetto del farmaco svanisce e i virus ritornano, si troveranno una super montagna di spazzatura da metabolizzare con un effetto ancora più drammatico per il nostro organismo. Lo stesso Pasteur in punto di morte disse ad un suo assistente: "Claude Bernard aveva ragione, il terreno è tutto, il microbo è nulla".
Anche un certo dr. Hamer disse: Se fossero i germi o i virus le cause delle malattie noi saremmo già morti perché ne abbiamo in gran quantità nel nostro organismo.

Si e no.
hai ragione nel dire che i virus non hanno per cosi dire lo scopo di distruggere l´ospite. se lo facessero si autodistruggerebbero. la interazione ospite/patogeno e molto complessa. ci sono una miriade, per cosi dire , di domande/risposte tra i due organismi e solo se tutte concordano il virus entra nella cellula...ma se non tutte concordano ti ammali. I farmaci antivirali sono acqua fresca. e lo dico da virologo. servono a bloccare la replicazione virale, a rallentare la replicazione del loro RNA dando alle cellule il tempo di ripristinare il sistema cellulare. L´Ebola uccide perche l´ospite non e´ quello giusto.
ciao

Il modo di alimentarsi ha qualche implicazione/interferenza su questa "simbiosi" virale? Questa intuizione/scoperta come si potrebbe manipolare a nostro vantaggio?
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L´Ebola uccide perché l´ospite non e´ quello giusto.

Come i virus dell'aviaria, della suina, etc. per i quali l'uomo non è "l'ospite giusto"?
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Tu, Roberto, che sei un virologo, alla luce dell'epigenetica, come le vedi le vaccinazioni di profilassi?
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P.S. Mi viene in mente, anche se è un batterio e non un virus, che Escherichia coli, normalmente non pericolosa per l'uomo, diventa un problema per via della "mutazione" causata, si presume, da un alimentazione sbagliata del ruminante e farmaci usati negli allevamenti.

Il modo di alimentarsi ha qualche implicazione/interferenza su questa "simbiosi" virale? Questa intuizione/scoperta come si potrebbe manipolare a nostro vantaggio?
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L´Ebola uccide perché l´ospite non e´ quello giusto.

Come i virus dell'aviaria, della suina, etc. per i quali l'uomo non è "l'ospite giusto"?
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Tu, Roberto, che sei un virologo, alla luce dell'epigenetica, come le vedi le vaccinazioni di profilassi?
----------------------
P.S. Mi viene in mente, anche se è un batterio e non un virus, che Escherichia coli, normalmente non pericolosa per l'uomo, diventa un problema per via della "mutazione" causata, si presume, da un alimentazione sbagliata del ruminante e farmaci usati negli allevamenti.

Ciao, scusa per non aver risposto prima...impegni con i figli.
Allora andiamo per domanda

vaccinazioni...sono inutili e pericolose. e non e'certo una mia idea. molti illustri virologi e ricercatori la pensano come me. pericolosa per il contenuto di eccipienti che poi servono a creare uno stato infiammatorio/reazione al vaccino. Molti di questi contengono squalene e mercurio che sono neurotossici. Io stesso preparo isolati virali da iniettare in conigli per ottenere vaccini. Ebbene se non utilizzi un eccipiente come il Frued adiuvante, un carcinogenico, non ottieni un buon vaccino. Perche'? ..perche il corpo regisce al virus/epitopo virale e scatena la reazione immunologica che normalmente dopo 1-2 giorni va scemando.
Inoltre i vaccini non proteggono dal'infezione ma rendono il corpo pronto ad una reazione...ma non ti proteggono dall'infezione virale. Ci sono casi in cui soggetti deboli o con non ottimale reazione immunitaria, si sono ammalati di epatite etc dopo essersi fatta vaccinare. inoltre i virus mutano continuamente. Ricordo che 2 - 3 anni fa con l'aviaria..allora mandai un articolo sul Corriere della sera dicendo che era una burla, un modo di far fare soldi alle ditte farmaceutiche. Ricordo che ebbi una fruttuosa corrispondenza con la Rita Levi Moltalcini che la pensava come me.
Non ti puoi vaccinare contro l'influenza ...stagionale...ma che dicono? ti vaccini contro un virus che isoli, fai il vaccino e lo inietti e poi preghi che non muti. La mutazione avviene sia prima che durante l'infezione in corso.
Alla luce della epigenetica non tutti reagiscono allo stesso modo. Una volta si diceva prendi un po di vitamina C che fa bene. ma quanta? un grammo e stai bene dice tizio, caio dice 2 grammi etc. questo perche siamo diversi. e questa e'"il challenge"del futuro. La nutrigenomica,cosi come la terapia genomica mira a vedere il giusto dosaggio di medicinali e non, vitamine etc, per ogn'uno di noi.
Il modo di alimentarsi influenza sia il nostro corredo genetico, epigenetica, sia il nostro corredo batterico intestinale, che svolge molteplici attivita immunitarie. ritornero su questo con un nuovo post sulla epigenetica/flora batterica e cervello.
La storia che i batteri siano muati, E coli, in seguito all'uso stupido degli antibiotici e'non provata. io personalmente non ne sono convinto. Alcuni anni fa ricercatori russi, se non sbaglio, trovarono in mammut estratti dal permafrost, batteri resistenti a molti antibiotici.
Virus e batteri mutano molto di piu perche noi viviamo in modo diverso rispetto al paleolitico, e non perche ci alimentiamo diversamente, ma perche viviamo in "gruppi"che non sono piu di poche centinaia, dove l'incrocio e'anche molto alto, ma in citta di milioni di persono. Anche se non ti ammali il virus/batterio salta tra milioni di persone mutando. Poi con la facilita di spostamento, aerei, il gioco e'fatto.
Cerchero l'articolo che fu pubblicato su american scientific. Altri ricercatori hanno trovato giant virus resistenti ai batteri nelle alghe marine di milioni di anni fa. insomma i batteri mutano da soli...ma se li si forza, uso indiscriminato di antibiotici, mutano piu velocemente.
Pochi mesi fa c'e'stato un altro caso di cibi infettati dall'e coli in Olanda, salmone, prodotto su larga scala in Grecia. Io penso sia la produzione di massa che stimola i batteri. Se fai crescere colonie batteriche su una piasta con del media, e diventano molte i batteri muatno per "eliminare la conpetizione"e sopravvivere.
DISEASE IN HUMAN EVOLUTION: THE RE-EMERGENCE OF INFECTIOUS DISEASE IN
THE THIRD EPIDEMIOLOGICAL TRANSITION
by George J. Armelagos, Kathleen C. Barnes, and James Lin
For millions of years, humans and their ancestors suffered from diseases -- both the kind caused by
infectious pathogens (e.g., bacteria, viruses, parasites) and the kind caused by our own bodies as they age
and degenerate. Over this long period, humans constantly created new ways of living and eating, and
actual physical or genetic changes evolved to minimize the effects of these diseases. From the point of
view of a bacteria or virus, however, any shift in the physical makeup or behavior of its human host
represents not only an obstacle but also a challenge to be overcome. As a result, new diseases emerged
with each major change in the human way of life.
For nearly four million years, humans lived in widely dispersed, nomadic, small populations that
minimized the effect of infectious diseases. With the agricultural revolution about 10,000 years ago,
increasing sedentism and larger population groupings resulted in the first epidemiological transition in
which infectious and nutritional diseases increased. Within the last century, with the advent of public
health measures, improved nutrition and medicine, some populations in developed nations underwent a
second epidemiological transition. During this transition, infectious diseases declined and non-infectious,
chronic diseases, and degenerative conditions increased. Today, with the increasing use of antibiotics, we
are facing a third epidemiological transition, a reemergence of infectious disease, with pathogens that are
antibiotic-resistant and have the potential to be transmitted on a global scale. Populations that experienced
and those that never experienced the second epidemiological transition are both increasingly exposed to
antibiotic-resistant pathogens.
"Emerging" pathogens are seen as new diseases, discovered when they have an impact on our adaptation
or survival. Even when we take a more holistic ecological perspective, it is often limited to a position that
considers emerging disease as the result of environmental changes that are only relevant to the present
situation as it affects humans here and now. This article argues that the emergence of new diseases has
been the human pattern since the origin of the hominids and accelerated with the shift to agriculture
10,000 years ago.
Paleolithic Baseline
For most of their 4,000,000 years of evolutionary history, human populations lived in small, sparsely
settled groups. Population size and density remained low throughout the Paleolithic. Fertility and
mortality rates in small gathering-hunting populations would have to have been balanced for the
population size to remain small.
Demographic factors creating this stability are still a matter of discussion. Some demographers argue that
gatherer-hunters were at their maximum natural fertility, balanced by high mortality. Armelagos,
Goodman and Jacobs (1991) argue, however, that gatherer-hunters maintained a stable population with
controlled moderate fertility balanced by moderate mortality.
The demographic changes following the Neolithic may provide insights into the case for population
stability controlled by moderate fertility and mortality during the Paleolithic. Following the Neolithic
revolution, a dramatic increase in population size and density occurred. It was thought that the Neolithic
economy generated food surpluses that led to a better nourished and healthier population with a reduced
rate of mortality. Since populations were at their natural maximum fertility, there would have been a rapid
increase in population size.
The empirical evidence suggests an alternative scenario in the shift from gathering and hunting to
agriculture. The picture suggests a much bleaker picture of health. Instead of experiencing improved
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health, there is evidence of a substantial increase in infectious and nutritional disease (Cohen and
Armelagos 1984). A paradox emerges if the traditionally accepted models of Paleolithic fertility and
mortality are correct. How can a population experiencing maximum fertility during the Paleolithic
respond with exponential growth in population when their health is deteriorating?
A consideration of the disease ecology of contemporary gatherer-hunters provides insights into the types
of disease that probably affected our gatherer-hunter ancestors. Polgar (1964) suggests that gathererhunters
had two types of disease to contend with in their adaptation to their environment. One class of
disease would be those organisms that had adapted to prehominid ancestors and persisted with them as
they evolved into hominids. Head and body lice (Pediculus humanus), pinworms, yaws, and possibly
malaria would be included in this group. Cockburn (1967) adds to this list most of the internal protozoa
found in modern humans and such bacteria as salmonella, typhi, and staphylococci.
The second class of diseases are the zoonotic, which have non-human animals as their primary host and
only incidentally infect humans. Humans can be infected by zoonoses through insect bites, by preparation
and consumption of contaminated flesh, and from wounds inflicted by animals. Sleeping sickness,
tetanus, scrub typhus, relapsing fever, trichinosis, tularemia, avian or ichthyic tuberculosis, leptospirosis,
and schistosomiasis are among the zoonotic diseases that could have afflicted earlier gatherer-hunters
(Cockburn 1971).
Although early human populations were too small to support endemic (constantly present) pathogens,
they maintained some kind of relationships with the vectors that would later serve to perpetuate such
human host-specific diseases as yellow fever and louse-borne relapsing fever. Certain lice were
ectoparasites as early as the Oligocene, and the prehumans of the early Pliocene probably suffered from
malaria, since the Anopheles (mosquito) necessary for transmission of the disease evolved by the
Miocene era. Frank Livingstone, an anthropological epidemiologist, dismisses, however, the potential of
malaria in early hominids except in isolated incidences because of the small population size and an
adaptation to the savanna, an environment that would not have included the mosquitoes that carry the
malaria plasmodium.
The range of the earliest hominids was probably restricted to the tropical savanna. This would have
limited the pathogens that were potential disease agents. During the course of human evolution, the
habitat expanded gradually into the temperate and eventually the tundra zones. Hominids, according to
epidemiologist Frank Lambrecht, would have avoided large areas of the African landscape because of
tsetse flies and thus avoided the trypanosomes they carried. He also argues that the evolution of the
human species and its expansion into new ecological niches would have led to a change in the pattern of
trypanosome infection. While this list of diseases that may have plagued our gathering-hunting ancestors
is informative, those diseases that would have been absent are also of interest. The contagious community
diseases such as influenza, measles, mumps, and smallpox would have been missing. There probably
would have been few viruses infecting these early hominids, although Cockburn (1967) disagrees and
suggests that the viral diseases found in non-human primates would have been easily transmitted to
hominids.
The First Epidemiological Transition:
Disease in Agricultural Populations
The reliance on primary food production (agriculture) increased the incidence and the impact of disease.
Sedentism, an important feature of agricultural adaptation, conceivably increased parasitic disease spread
by contact with human waste. In gathering-hunting groups, the frequent movement of the base camp and
frequent forays away from the base camp by men and women would decrease their contact with human
wastes. In sedentary populations, the proximity of habitation area and waste deposit sites to the water
- 3 -
supply is a source of contamination. While sedentarism did occur prior to the Neolithic period in those
areas with abundant resources, once there was the shift to agriculture, sedentary living was necessary.
The domestication of animals provided a steady supply of vectors and greater exposure to zoonotic
diseases. The zoonotic infections most likely increased because of domesticated animals, such as goats,
sheep, cattle, pigs, and fowl, as well as the unwanted domestic animals such as rodents and sparrows,
which developed (Polgar 1964) permanent habitats in and around human dwellings. Products of
domesticated animals such as milk, hair, and skin, as well as the dust raised by the animals, could
transmit anthrax, Q fever, brucellosis, and tuberculosis. Breaking the sod during cultivation exposed
workers to insect bites and diseases such as scrub typhus. Frank Livingstone showed that slash-and-burn
agriculture in west Africa exposed populations to Anopheles gambiae, a mosquito which is the vector for
Plasmodium falciparum, which causes malaria. Agricultural practices also create pools of water,
expanding the potential breeding sites for mosquitos. The combination of disruptive environmental
farming practices and the presence of domestic animals also increased human contact with arthropod
(insect) vectors carrying yellow fever, trypanosomiasis, and filariasis, which then developed a preference
for human blood. Some disease vectors developed dependent relationships with human habitats, the best
example of which is Aedes aegypti (vector for yellow fever and dengue), which breeds in stagnant pools
of water in open containers. Various agricultural practices increased contact with non-vector parasites.
Irrigation brought contact with schistosomal cercariae, and the use of feces as fertilizer caused infection
from intestinal flukes (Cockburn 1971).
The shift to agriculture led to a change in ecology; this resulted in diseases not frequently encountered by
forager populations. The shift from a varied, well-balanced diet to one which contained fewer types of
food sometimes resulted in dietary deficiencies. Food was stored in large quantities and widely
distributed, probably resulting in outbreaks of food poisoning. Intensive agricultural practices among the
prehistoric Nubians resulted in iron deficiency anemia as did the reliance on cereal grain, weaning
practices, and parasitic infestation. The combination of a complex society, increasing divisions of class,
epidemic disease, and dietary insufficiencies no doubt added mental stress to the list of illnesses.
Disease in Urban Populations
The development of urban centers is a recent development in human history. In the Near East, cities as
large as 50,000 people were established by 3000 BC. In the New World, large urban settlements were in
existence by AD 600. Settlements of this size increase the already difficult problem of removing human
wastes and delivering uncontaminated water to the people. Cholera, which is transmitted by contaminated
water, was a potential problem. Diseases such as typhus (carried by lice) and the plague bacillus
(transmitted by fleas or by the respiratory route) could be spread from person to person. Viral diseases
such as measles, mumps, chicken pox, and smallpox could be spread in a similar fashion. Due to
urbanization, populations for the first time were large enough to maintain disease in an endemic form.
Aidan Cockburn, a paleopathologist, estimated that populations of one million would be necessary to
maintain measles as an endemic disease. What was an endemic disease in one population could be the
source of a serious epidemic (affecting a large number of people at the same time) disease in another
group. Cross-continental trade and travel resulted in intense epidemics (McNeill 1976). The Black Death,
resulting from a new pathogen, took its toll in Europe in the 1300s; this epidemic eliminated at least a
quarter of the European population (approximately 25 million people).
The period of urban development can also be characterized by the exploration and expansion of
populations into new areas that resulted in the introduction of novel diseases to groups that had little
resistance to them (McNeill 1976). For example, the exploration of the New World may have been the
source of the treponemal infection (syphilis) that was transmitted to the Old World. This New World
infection was endemic and not sexually transmitted. When it was introduced into the Old World, a
different mode of disease transmission occurred. The sexual transmission of the treponeme created a
different environment for the pathogen, and it resulted in a more severe and acute infection. Furthermore,
- 4 -
crowding in the urban centers, changes in sexual practices, such as prostitution, and an increase in sexual
promiscuity may have been factors in the venereal transmission of the pathogen.
The process of industrialization, which began a little over 200 years ago, led to an even greater
environmental and social transformation. City dwellers were forced to contend with industrial wastes and
polluted water and air. Slums that arose in industrial cities became focal points for poverty and the spread
of disease. Epidemics of smallpox, typhus, typhoid, diphtheria, measles, and yellow fever in urban
settings were well documented. Tuberculosis and respiratory diseases such as pneumonia and bronchitis
were even more serious problems, with harsh working situations and crowded living conditions. Urban
population centers, with their extremely high mortality, were not able to maintain their population bases
by the reproductive capacity of those living in the city. Mortality outstripped fertility, requiring
immigration to maintain the size of the population.
The Second Epidemiological Transition: The Rise of Chronic and Degenerative Disease
The second epidemiological transition refers to the shift from acute infectious diseases to chronic noninfectious,
degenerative diseases. The increasing prevalence of these chronic diseases is related to an
increase in longevity. Cultural advances results in a larger percentage of individuals reaching the oldest
age segment of the population. In addition, the technological advances that characterize the second
epidemiological transition resulted in an increase in environmental degradation. An interesting
characteristic of many of the chronic diseases is their particular prevalence and 'epidemic'-like occurrence
in transitional societies, or in those populations undergoing the shift from developing to developed modes
of production. In developing countries, many of the chronic diseases associated with the epidemiological
transition appear first in members of the upper socioeconomic strata, because of their access to Western
products and practices.
With increasing developments in technology, medicine, and science, the germ theory of disease causation
developed. While there is some controversy about the role that medicine has played in the decline of some
of the infectious diseases, a better understanding of the source of infectious disease exists, and this
admittedly has resulted in increasing control over many infectious diseases. The development of
immunization resulted in the control of many infections and recently was the primary factor in the
eradication of smallpox. In the developed nations, a number of other communicable diseases have
diminished in importance. The decrease in infectious disease and the subsequent reduction in infant
mortality has resulted in greater life expectancy at birth. In addition, there has been an increase in
longevity for adults and this has resulted in an increase in chronic and degenerative diseases.
Many of the diseases of the second epidemiological transition share common etiological factors related to
human adaptation, including diet, activity level, mental stress, behavioral practices, and environmental
pollution. For example, the industrialization and commercialization of food often results in malnutrition,
especially for those societies in "transition" from subsistence forms of food provision to agribusiness. The
economic capacity to purchase food that meets nutritional requirements is often not possible. Obesity and
high intakes of refined carbohydrates are related to the increasing incidence of heart disease and diabetes.
Obesity is considered to be a common form of malnutrition in developed countries and is a direct result of
an increasingly sedentary lifestyle in conjunction with steady or increasing caloric intakes.
A unique characteristic of the chronic diseases is their relatively recent appearance in human history as a
major cause of morbidity. This is indicative of a strong environmental factor in disease etiology. While
biological factors such as genetics are no doubt important in determining who is most likely to succumb
to which disease, genetics alone cannot explain the rapid increase in chronic disease. While some of our
current chronic diseases such as osteoarthritis were prevalent in early human populations, other more
serious degenerative conditions such as cardiovascular disease and carcinoma were much rarer.
- 5 -
The Third Epidemiological Transition
Today, human populations are moving into the third epidemiological transition. There is a reemergence of
infectious diseases with multiple antibiotic resistance. Furthermore, this emergence of diseases has a
potential for global impact. In a sense, the contemporary transition does not eliminate the possible coexistence
of infectious diseases typical of the first epidemiological transition (some 10,000 years ago) in
our own time; the World Health Organization (WHO) reports that of the 50,000,000 deaths each year,
17,500,000 are the result of infectious and parasitic disease. WHO reports that 1.7 million have
tuberculosis and 30 million people are infected with HIV.
The emergence of infectious disease has been one of the most interesting evolutionary stories of the last
decade, and has captured the interest of scientists and the public. The popular media, with the publication
of books such as The Hot Zone and movies such as Outbreak, has captured the public's fascination with
emerging diseases as threats to human survival. There is genuine scientific concern about the problem.
David Satcher (Director of the Centers for Disease Control in Atlanta, GA) lists 22 diseases that have
emerged in the last 22 years, including Rotovirus, Ebola virus, Legionella pneumophila (Legionnaire s
Disease), Hantaan Virus (Korean hemorrhagic fever), HTLV I, Staphylococcus toxin, Escherichia coli
0157:h7, HTLV II, HIV, Human Herpes Virus 6, Hepatitis C, and Hantavirus isolates.
The emergence of disease is the result of an interaction of social, demographic, and environmental
changes in a global ecology and in the adaptation and genetics of the microbe, influenced by international
commerce and travel, technological change, breakdown of public health measures, and microbial
adaptation. Ecological changes such as agricultural development projects, dams, deforestation, floods,
droughts and climatic changes have resulted in the emergence of diseases such as Argentine hemorrhagic
fever, Korean hemorrhagic fever (Hantaan) and Hantavirus pulmonary syndrome. Human demographic
behavior has been a factor in the spread of dengue fever, and the source for the introduction and spread of
HIV and other sexually transmitted diseases.
The engine that is driving the reemergence of many of the diseases is ecological change that brings
humans into contact with pathogens. Except for the Brazilian pururic fever, which may represent a new
strain of Haemophilus influenzae, biotype aegyptius, most of the emerging diseases are of cultural origin.
The development of antibiotic resistance in any pathogen is the result of medical and agricultural
practices. The indiscriminate and inappropriate use of antibiotics in medicine has resulted in hospitals that
are the source of multi-drug resistant strains of bacteria that infect a large number of patients. Agricultural
use in which animal feed is supplemented with sub-therapeutic doses of antibiotics has risen dramatically
in the last half century. In 1954, 500,000 pounds of antibiotics were produced in the United States; today,
40,000,000 pounds are produced annually.
Conclusion
Recently, much attention has focused on the detrimental effects of industrialization on the international
environment, including water, land, and atmosphere. Massive industrial production of commodities has
caused pollution. Increasingly there is concern over the health implications of contaminated water
supplies, over-use of pesticides in commercialized agriculture, atmospheric chemicals, and the future
effects of a depleted ozone layer on human health and food production. At no other time in human history
have the changes in the environment been more rapid or so extreme. Increasing incidence of cancer
among young people and the increase in respiratory disease has been implicated in these environmental
changes.
Anthropogenic impact from technology has been the pattern since Neolithic times. Within the last 300
years, transportation has played a major role in disease patterns by bringing larger segments of humans
into contact with the pathogens at an accelerated rate. The emergence of disease in the New World upon
contact with Europeans was a consequence of large sailing ships that became a major mode of
- 6 -
transportation. Now it is possible for a pathogen to move between continents within a matter of hours. We
live in a time where there exists a virtual viral superhighway, bringing people into contact with pathogens
that affect our adaptation. The present pattern reflects an evolutionary trend that can be traced to the
beginning of primary food production. The scale has changed. The rates of emerging disease and their
impact can now affect large segments of the world population at an ever increasing rate, and we need to
be increasingly aware of the implications for today s human populations around the globe.
For further reading
Armelagos, G. J. Human evolution and the evolution of human disease. Ethnicity and Disease 1(1): 21-
26, 1991.
Armelagos, G. J., A. H. Goodman, et al. The origins of agriculture: Population growth during a period of
declining health. Population and Environment 13(1): 9-22, 1991.
Cockburn, T. A. The evolution of human infectious diseases. In Infectious Diseases: Their Evolution and
Eradication, T. A. Cockburn, ed. Springfield, IL: Charles C. Thomas, 1967.
Cockburn, T. A. Infectious disease in ancient populations. Current Anthropology 12(1): 45-62, 1971.
Cohen, M. N. and G. J. Armelagos, eds. Paleopathology at the Origin of Agriculure. Orlando: Academic
Press, 1984.
Ewald, P. W. Evolution of Infectious Disease. New York: Oxford University Press, 1994.
McNeill, W. H. Plagues and People. Garden City: Anchor/Doubleday, 1976.
Polgar, S. Evolution and the ills of mankind. In Horizons of Anthropology, Sol Tax, ed. Chicago: Aldine,
1964.

Questo anche interessante

Wild sharks, redfish harbor antibiotic-resistant bacteria
Published: Wednesday, June 16, 2010 - 15:04 in Biology & Nature
Related images
(click to enlarge)

Photo by L. Brian Stauffer, U. of I. News Bureau.
Graphic produced by Diana Yates. Photo credits: Bull shark (NSW Department of Primary Industries); Lemon shark (drawing by Robbie Cada); Nurse shark (modified from photo by Joseph Thomas); Spinner shark (image by Dieno); Blacktip shark (modified from photo by Albert Kok); Smooth dogfish (image from U.S. Fish & Wildlife Service).Scientists have found antibiotic-resistant bacteria in seven species of sharks and redfish captured in waters off Belize, Florida, Louisiana and Massachusetts. Most of these wild, free-swimming fish harbored several drug-resistant bacterial strains. The study, published in the Journal of Zoo and Wildlife Medicine, found antibiotic-resistant bacteria in every fish species sampled.

The researchers also found multidrug-resistant bacteria in fish at nearly all of the study sites, said Mark Mitchell, a professor of veterinary clinical medicine at the University of Illinois and a senior author of the paper.

"Ultimately the idea of this study was to see if there were organisms out there that had exposures or resistance patterns to antibiotics that we might not expect," Mitchell said. "We found that there was resistance to antibiotics that these fish shouldn't be exposed to."

Among the animals sampled, nurse sharks in Belize and in the Florida Keys had the highest occurrence of antibiotic-resistant bacteria. These sharks feed on crustaceans, small fish and other animals living in shallow waters close to shore.

Random mutations may account for drug-resistant bacteria in marine environments, Mitchell said, but there is a lot of evidence for a human origin.

"The shark population in Belize, for example, is a big tourist area, so there are people in the water right there," he said. "The sampling site is not far from a sewage plant, and so all those exposures we think are playing a role."

Sewage also is a problem in the Atlantic coastal waters of the United States, he said. Previous studies have shown that sewage outflows can leak antibiotic-resistant bacteria into the environment.

In the new study, the researchers looked for and found bacterial resistance to 13 antibacterial drugs in the fish. Patterns of resistance varied among the sites.

Bacteria from sharks off Martha's Vineyard in Massachusetts and in offshore Louisiana were resistant to the fewest number of antibiotics, while sharks in the Florida Keys and Belize harbored bacteria that were resistant to amikacin, ceftazidime, chloramphenicol, ciprofloxacin, doxycycline, penicillin, piperacillin, sulfamethoxazole and ticarcillin.

Redfish in the Louisiana offshore site hosted more varieties of drug-resistance than sharks in the same waters. This may reflect differences in their age (the redfish were more mature than the sharks), feeding or migratory habits, Mitchell said.

While the presence of antibiotic-resistant bacteria in sharks and other fish does not necessarily harm them, Mitchell said, the findings point to a growing problem for human health.

"There are estimates of over 100,000 deaths from infections in hospitals per year, many of them from antibiotic-resistant organisms," Mitchell said. "And we're creating even more of these organisms out in the environment. … Unfortunately, as these things collect, there's probably a threshold at some point where there's going to be a spillover and it will start to affect us as a species."

People do eat sharks and redfish, Mitchell said, and now these fish represent a potential new route of exposure to drug-resistant bacteria. Sharks and redfish also are predators, and so may function as sentinels for human health.

"Some people might say, well, a bull shark in offshore Louisiana doesn't really have an influence on my health," Mitchell said. "But these fish eat what we eat. We're sharing the same food sources. There should be a concern for us as well."

Ancora uno

Antibiotic resistance in the environment: a link to the clinic?
Gerard D Wright
M.G. DeGroote Institute for Infectious Disease Research, Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada L8N 3Z5
Available online 16 September 2010
http://dx.doi.org/10.1016/j.mib.2010.08.005, How to Cite or Link Using DOI
View full textPurchase $41.95Introduction: antibiotic resistance is a global phenomenonThe environmental antibiotic resistomeAntibiotic resistance in animalsConclusions: the clinical impact of environmental resistanceReferences and recommended readingAcknowledgmentsReferences

--------------------------------------------------------------------------------

The emergence of resistance to all classes of antibiotics in previously susceptible bacterial pathogens is a major challenge to infectious disease medicine. The origin of the genes associated with resistance has long been a mystery. There is a growing body of evidence that is demonstrating that environmental microbes are highly drug resistant. The genes that make up this environmental resistome have the potential to be transferred to pathogens and indeed there is some evidence that at least some clinically relevant resistance genes have originated in environmental microbes. Understanding the extent of the environmental resistome and its mobilization into pathogenic bacteria is essential for the management and discovery of antibiotics

e qui

There is evidence that naturally occurring antibiotic resistance is common.[17] The genes that confer this resistance are known as the environmental resistome.[17] These genes may be transferred from non-disease-causing bacteria to those that do cause disease, leading to clinically significant antibiotic resistance.[17]

In 1952 an experiment conducted by Joshua and Esther Lederberg showed that penicillin-resistant bacteria existed before penicillin treatment.[18] While experimenting at the University of Wisconsin-Madison, Joshua Lederberg and his graduate student Norton Zinder also demonstrated preexistent bacterial resistance to streptomycin.[19] In 1962, the presence of penicillinase was detected in dormant Bacillus licheniformis endospores, revived from dried soil on the roots of plants, preserved since 1689 in the British Museum.[20][21][22] Six strains of Clostridium, found in the bowels of William Braine and John Hartnell (members of Franklin Expedition) showed resistance to cefoxitin and clindamycin.[23] It was suggested that penicillinase may have emerged as a defense mechanism for the bacteria in their habitats, as in the case of penicillinase-rich Staphylococcus aureus, living with penicillin-producing Trichophyton. This, however, was deemed circumstantial.[22] Search for a penicillinase ancestor has focused on the class of proteins that must be a priori capable of specific combination with penicillin.[24] The resistance to cefoxitin and clindamycin in turn was speculatively attributed to Braine's and Hartnell's contact with microorganisms that naturally produce them or to random mutation in the chromosomes of Clostridium strains.[23] Nonetheless there is an evidence that heavy metals and some pollutants may select for antibiotic-resistant bacteria, generating a constant source of them in small numbers.[25]

facciamo il punto..
io vivo in una comunita molto densa quindi molti virus e batteri hanno molti ospiti. Vivo male in rapporto al mio corredo genetico, mi nutro male/non corretto rispetto al mio codice genetico, la mia flora batterica muta. mi becco un batterio che interaggisce con la mia flora batterica e...si scambiano per cosi dire informazioni. il batterio muta e per caso muta in un super bug...che in una piccola comunita della foresta amazzonica, uccide un paio di persone epoi sparisce..ma in una supercolonia umana come Milano si distribuisce e continua amutare.
Insomma come al solito non c'e'una sola risposta. e'l'insieme che conta.

Grazie Roberto,

leggendo la parte dei virus mi è venuto in mente, come un flash, che un certo Arnold Ehret (ho un certo disagio nel nominarlo) sosteneva che i virus in se non sono pericolosi e che in un organismo sano transitano indisturbati svolgendo dentro di noi svariate utili funzioni. Questi virus vengono paragonati a dei topi che nutrendosi della spazzatura ripuliscono il territorio (i virus il nostro organismo). Se la spazzatura e poca tutto va bene ma se tanta allora le tossine che scaturiscono da questo processo di pulizia non vengono espulse causando la malattia. Credo che Ehret si riferisse a Bechamp, infatti lui ha scoperto che i germi non sono la causa della malattia ma si occupano solo di decomporre i tessuti in degrado e sono prodotti dall'organismo; di fatto sono gli spazzini dell'organismo. Quindi quando noi, con i farmaci, uccidiamo i virus è come se uccidessimo i topi lasciando che la montagna di spazzatura continui a crescere. Così dopo che l'effetto del farmaco svanisce e i virus ritornano, si troveranno una super montagna di spazzatura da metabolizzare con un effetto ancora più drammatico per il nostro organismo. Lo stesso Pasteur in punto di morte disse ad un suo assistente: "Claude Bernard aveva ragione, il terreno è tutto, il microbo è nulla".
Anche un certo dr. Hamer disse: Se fossero i germi o i virus le cause delle malattie noi saremmo già morti perché ne abbiamo in gran quantità nel nostro organismo.

Articolo molto interessante
ZoekresultatenThe Neuroscience of the Gut: Scientific Americanwww.scientificamerican.com/article.cfm?id...gutIn cache - Vertaal deze pagina
U heeft dit openbaar een +1 gegeven. Ongedaan maken
19 Apr 2011 – For example, gut bacteria may have an influence on the body's use of ... way of phrasing it- how much of epigenetics is controlled by bacteria?

Grazie di cuore per le tue risposte, Roberto. Questo argomento mi interessa moltissimo e mi piacerebbe che Tu continuassi a tenerci aggiornati. Ciao:-)

Articolo molto interessante
ZoekresultatenThe Neuroscience of the Gut: Scientific Americanwww.scientificamerican.com/article.cfm?id...gutIn cache - Vertaal deze pagina
U heeft dit openbaar een +1 gegeven. Ongedaan maken
19 Apr 2011 – For example, gut bacteria may have an influence on the body's use of ... way of phrasing it- how much of epigenetics is controlled by bacteria?

Non riesco a trovare l'articolo. Per favore potresti postare l'indirizzo corretto. Grazie!^_^

Grazie di cuore per le tue risposte, Roberto. Questo argomento mi interessa moltissimo e mi piacerebbe che Tu continuassi a tenerci aggiornati. Ciao:-)

---

Articolo molto interessante
ZoekresultatenThe Neuroscience of the Gut: Scientific Americanwww.scientificamerican.com/article.cfm?id...gutIn cache - Vertaal deze pagina
U heeft dit openbaar een +1 gegeven. Ongedaan maken
19 Apr 2011 – For example, gut bacteria may have an influence on the body's use of ... way of phrasing it- how much of epigenetics is controlled by bacteria?

Non riesco a trovare l'articolo. Per favore potresti postare l'indirizzo corretto. Grazie!^_^

Scusa, errore mio, ho copiato il sito...che il mio server poi ha tradotto in olandese.
e'un articolo semplice che va bene come introduzione.
Hai mai pensato che l'epigenetica potrebbe essere il risultato della azione dei batteri? insomma una conseguenza.Che i batteri influenzini il cervello, gli ormoni etc e'oramai quasi certo e se influenzassero anche il genoma? saremmo di fronte ad una specie di Matrix, noi saremmo gli schiavi ignari dei batteri.

L'articolo e'
Scientific American the neuroscience of the gut

Scientific American
The Neuroscience of the Gut
Strange but true: the brain is shaped by bacteria in the digestive tract

By Robert Martone

Researchers track the gut-brain connection

The Best Science Writing Online 2012
Showcasing more than fifty of the most provocative, original, and significant online essays from 2011, The Best Science Writing Online 2012 will change the way...

Read More »
.People may advise you to listen to your gut instincts: now research suggests that your gut may have more impact on your thoughts than you ever realized. Scientists from the Karolinska Institute in Sweden and the Genome Institute of Singapore led by Sven Pettersson recently reported in the Proceedings of the National Academy of Sciences that normal gut flora, the bacteria that inhabit our intestines, have a significant impact on brain development and subsequent adult behavior.

We human beings may think of ourselves as a highly evolved species of conscious individuals, but we are all far less human than most of us appreciate. Scientists have long recognized that the bacterial cells inhabiting our skin and gut outnumber human cells by ten-to-one. Indeed, Princeton University scientist Bonnie Bassler compared the approximately 30,000 human genes found in the average human to the more than 3 million bacterial genes inhabiting us, concluding that we are at most one percent human. We are only beginning to understand the sort of impact our bacterial passengers have on our daily lives.

Moreover, these bacteria have been implicated in the development of neurological and behavioral disorders. For example, gut bacteria may have an influence on the body’s use of vitamin B6, which in turn has profound effects on the health of nerve and muscle cells. They modulate immune tolerance and, because of this, they may have an influence on autoimmune diseases, such as multiple sclerosis. They have been shown to influence anxiety-related behavior, although there is controversy regarding whether gut bacteria exacerbate or ameliorate stress related anxiety responses. In autism and other pervasive developmental disorders, there are reports that the specific bacterial species present in the gut are altered and that gastrointestinal problems exacerbate behavioral symptoms. A newly developed biochemical test for autism is based, in part, upon the end products of bacterial metabolism.

But this new study is the first to extensively evaluate the influence of gut bacteria on the biochemistry and development of the brain. The scientists raised mice lacking normal gut microflora, then compared their behavior, brain chemistry and brain development to mice having normal gut bacteria. The microbe-free animals were more active and, in specific behavioral tests, were less anxious than microbe-colonized mice. In one test of anxiety, animals were given the choice of staying in the relative safety of a dark box, or of venturing into a lighted box. Bacteria-free animals spent significantly more time in the light box than their bacterially colonized littermates. Similarly, in another test of anxiety, animals were given the choice of venturing out on an elevated and unprotected bar to explore their environment, or remain in the relative safety of a similar bar protected by enclosing walls. Once again, the microbe-free animals proved themselves bolder than their colonized kin.

Pettersson’s team next asked whether the influence of gut microbes on the brain was reversible and, since the gut is colonized by microbes soon after birth, whether there was evidence that gut microbes influenced the development of the brain. They found that colonizing an adult germ-free animal with normal gut bacteria had no effect on their behavior. However, if germ free animals were colonized early in life, these effects could be reversed. This suggests that there is a critical period in the development of the brain when the bacteria are influential.
Consistent with these behavioral findings, two genes implicated in anxiety -- nerve growth factor-inducible clone A (NGF1-A) and brain-derived neurotrophic factor (BDNF) -- were found to be down-regulated in multiple brain regions in the germ-free animals. These changes in behavior were also accompanied by changes in the levels of several neurotransmitters, chemicals which are responsible for signal transmission between nerve cells. The neurotransmitters dopamine, serotonin and noradrenaline were elevated in a specific region of the brain, the striatum, which is associated with the planning and coordination of movement and which is activated by novel stimuli, while there were there were no such effects on neurotransmitters in other brain regions, such as those involved in memory (the hippocampus) or executive function (the frontal cortex).

When Pettersson’s team performed a comprehensive gene expression analysis of five different brain regions, they found nearly 40 genes that were affected by the presence of gut bacteria. Not only were these primitive microbes able to influence signaling between nerve cells while sequestered far away in the gut, they had the astonishing ability to influence whether brain cells turn on or off specific genes.

How, then, do these single-celled intestinal denizens exert their influence on a complex multicellular organ such as the brain? Although the answer is unclear, there are several possibilities: the Vagus nerve, for example, connects the gut to the brain, and it’s known that infection with the Salmonella bacteria stimulates the expression of certain genes in the brain, which is blocked when the Vagus nerve is severed. This nerve may be stimulated as well by normal gut microbes, and serve as the link between them and the brain. Alternatively, those microbes may modulate the release of chemical signals by the gut into the bloodstream which ultimately reach the brain. These gut microbes, for example, are known to modulate stress hormones which may in turn influence the expression of genes in the brain.

Regardless of how these intestinal “guests” exert their influence, these studies suggest that brain-directed behaviors, which influence the manner in which animals interact with the external world, may be deeply influenced by that animal’s relationship with the microbial organisms living in its gut. And the discovery that gut bacteria exert their influence on the brain within a discrete developmental stage may have important implications for developmental brain disorders.

.

Grazie di cuore per le tue risposte, Roberto. Questo argomento mi interessa moltissimo e mi piacerebbe che Tu continuassi a tenerci aggiornati. Ciao:-)

---

Articolo molto interessante
ZoekresultatenThe Neuroscience of the Gut: Scientific Americanwww.scientificamerican.com/article.cfm?id...gutIn cache - Vertaal deze pagina
U heeft dit openbaar een +1 gegeven. Ongedaan maken
19 Apr 2011 – For example, gut bacteria may have an influence on the body's use of ... way of phrasing it- how much of epigenetics is controlled by bacteria?

Non riesco a trovare l'articolo. Per favore potresti postare l'indirizzo corretto. Grazie!^_^

Scusa, errore mio, ho copiato il sito...che il mio server poi ha tradotto in olandese.
e'un articolo semplice che va bene come introduzione.
Hai mai pensato che l'epigenetica potrebbe essere il risultato della azione dei batteri? insomma una conseguenza.Che i batteri influenzini il cervello, gli ormoni etc e'oramai quasi certo e se influenzassero anche il genoma? saremmo di fronte ad una specie di Matrix, noi saremmo gli schiavi ignari dei batteri.

L'articolo e'
Scientific American the neuroscience of the gut

Scientific American
The Neuroscience of the Gut
Strange but true: the brain is shaped by bacteria in the digestive tract

By Robert Martone

Researchers track the gut-brain connection

The Best Science Writing Online 2012
Showcasing more than fifty of the most provocative, original, and significant online essays from 2011, The Best Science Writing Online 2012 will change the way...

Read More »
.People may advise you to listen to your gut instincts: now research suggests that your gut may have more impact on your thoughts than you ever realized. Scientists from the Karolinska Institute in Sweden and the Genome Institute of Singapore led by Sven Pettersson recently reported in the Proceedings of the National Academy of Sciences that normal gut flora, the bacteria that inhabit our intestines, have a significant impact on brain development and subsequent adult behavior.

We human beings may think of ourselves as a highly evolved species of conscious individuals, but we are all far less human than most of us appreciate. Scientists have long recognized that the bacterial cells inhabiting our skin and gut outnumber human cells by ten-to-one. Indeed, Princeton University scientist Bonnie Bassler compared the approximately 30,000 human genes found in the average human to the more than 3 million bacterial genes inhabiting us, concluding that we are at most one percent human. We are only beginning to understand the sort of impact our bacterial passengers have on our daily lives.

Moreover, these bacteria have been implicated in the development of neurological and behavioral disorders. For example, gut bacteria may have an influence on the body’s use of vitamin B6, which in turn has profound effects on the health of nerve and muscle cells. They modulate immune tolerance and, because of this, they may have an influence on autoimmune diseases, such as multiple sclerosis. They have been shown to influence anxiety-related behavior, although there is controversy regarding whether gut bacteria exacerbate or ameliorate stress related anxiety responses. In autism and other pervasive developmental disorders, there are reports that the specific bacterial species present in the gut are altered and that gastrointestinal problems exacerbate behavioral symptoms. A newly developed biochemical test for autism is based, in part, upon the end products of bacterial metabolism.

But this new study is the first to extensively evaluate the influence of gut bacteria on the biochemistry and development of the brain. The scientists raised mice lacking normal gut microflora, then compared their behavior, brain chemistry and brain development to mice having normal gut bacteria. The microbe-free animals were more active and, in specific behavioral tests, were less anxious than microbe-colonized mice. In one test of anxiety, animals were given the choice of staying in the relative safety of a dark box, or of venturing into a lighted box. Bacteria-free animals spent significantly more time in the light box than their bacterially colonized littermates. Similarly, in another test of anxiety, animals were given the choice of venturing out on an elevated and unprotected bar to explore their environment, or remain in the relative safety of a similar bar protected by enclosing walls. Once again, the microbe-free animals proved themselves bolder than their colonized kin.

Pettersson’s team next asked whether the influence of gut microbes on the brain was reversible and, since the gut is colonized by microbes soon after birth, whether there was evidence that gut microbes influenced the development of the brain. They found that colonizing an adult germ-free animal with normal gut bacteria had no effect on their behavior. However, if germ free animals were colonized early in life, these effects could be reversed. This suggests that there is a critical period in the development of the brain when the bacteria are influential.
Consistent with these behavioral findings, two genes implicated in anxiety -- nerve growth factor-inducible clone A (NGF1-A) and brain-derived neurotrophic factor (BDNF) -- were found to be down-regulated in multiple brain regions in the germ-free animals. These changes in behavior were also accompanied by changes in the levels of several neurotransmitters, chemicals which are responsible for signal transmission between nerve cells. The neurotransmitters dopamine, serotonin and noradrenaline were elevated in a specific region of the brain, the striatum, which is associated with the planning and coordination of movement and which is activated by novel stimuli, while there were there were no such effects on neurotransmitters in other brain regions, such as those involved in memory (the hippocampus) or executive function (the frontal cortex).

When Pettersson’s team performed a comprehensive gene expression analysis of five different brain regions, they found nearly 40 genes that were affected by the presence of gut bacteria. Not only were these primitive microbes able to influence signaling between nerve cells while sequestered far away in the gut, they had the astonishing ability to influence whether brain cells turn on or off specific genes.

How, then, do these single-celled intestinal denizens exert their influence on a complex multicellular organ such as the brain? Although the answer is unclear, there are several possibilities: the Vagus nerve, for example, connects the gut to the brain, and it’s known that infection with the Salmonella bacteria stimulates the expression of certain genes in the brain, which is blocked when the Vagus nerve is severed. This nerve may be stimulated as well by normal gut microbes, and serve as the link between them and the brain. Alternatively, those microbes may modulate the release of chemical signals by the gut into the bloodstream which ultimately reach the brain. These gut microbes, for example, are known to modulate stress hormones which may in turn influence the expression of genes in the brain.

Regardless of how these intestinal “guests” exert their influence, these studies suggest that brain-directed behaviors, which influence the manner in which animals interact with the external world, may be deeply influenced by that animal’s relationship with the microbial organisms living in its gut. And the discovery that gut bacteria exert their influence on the brain within a discrete developmental stage may have important implications for developmental brain disorders.

.

Un articolo che lascia intravedere la possibilita che la nostra durata della vita potrebbe essere influenzata dai batteri intestinali. Interessante nel testo il punto in cui descrive, tabella lifespan e tipi di batteri o flora completamente assente, che i ratti senza flora batterica vivevano in media 10 settimane in piu degli altri. da 78 quelli con flora completa a 87 quelli con flora ricca di bifido a 97 se sterili.

Intestinal flora and human health

Tomotari Mitsuoka, DVM, PhD

Professor Emeritus, The University of Tokyo, Japan

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There is a growing interest in intestinal flora and human health and disease. The intestines of humans contain 100 trillion viable bacteria. These live bacteria, which make up 30% of the faecal mass, are known as the intestinal flora. There are two kinds of bacteria in the intestinal flora, beneficial and harmful. In healthy subjects, they are well balanced and beneficial bacteria dominate. Beneficial bacteria play useful roles in the aspects of nutrition and prevention of disease. They produce essential nutrients such as vitamins and organic acids, which are absorbed from the intestines and utilised by the gut epithelium and by vital organs such as the liver. Organic acids also suppress the growth of pathogens in the intestines.

Other intestinal bacteria produce substances that are harmful to the host, such as putrefactive products, toxins and carcinogenic substances. When harmful bacteria dominate in the intestines, essential nutrients are not produced and the level of harmful substances rises. These substances may not have an immediate detrimental effect on the host but they are thought to be contributing factors to ageing, promoting cancer, liver and kidney disease, hypertension and arteriosclerosis, and reduced immunity. Little is known regarding which intestinal bacteria are responsible for these effects. A number of factors can change the balance of intestinal flora in favour of harmful bacteria. These include peristalsis disorders, surgical operations of stomach or small intestine, liver or kidney diseases, pernicious anaemia, cancer, radiation or antibiotic therapies, immune disorders, emotional stress, poor diet and ageing.

However, more importantly, the normal balance of intestinal flora may be maintained, or restored to a normal from an unbalanced state, by oral bacterio-therapy or by a well balanced diet. Oral bacterio-therapy using intestinal strains of lactic acid bacteria, such as lactobacillus and bifidobacteria, can restore normal intestinal balance and produce beneficial effects. Benefits include suppression of intestinal putrification so as to reduce constipation and other geriatric diseases; prevention and treatment of diarrhoea including antibiotic-associated diarrhoea; stimulation of the immune system; and increased resistance to infection.

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Ecological significance of intestinal flora

A single individual harbours in the intestine 100 trillion viable bacteria and so 1000 me 100 different bacterial species, which constitute the intestinal flora. In mutual symbiotic or antagonistic relationships, these organisms grow on ingested food components and those secreted into the alimentary tract by the host, and excreted. In the past, most of these organisms have been considered to be dead, but marked advances in culturing techniques for anaerobic bacteria enable cultivation of over 70% of the microscopic count of bacteria in human faeces, and often more than 90%.

Major bacterial groups composing the intestinal flora

The major bacterial groups detected in the intestinal flora are roughly divided into the following three groups:

the lactic acid bacteria group (LAB), including Bifidobacterium, Lactobacillus and Streptococcus including Enterococcus;
the anaerobic group, including Bacteroidaceae, anaerobic curved rods, Eubacterium, Peptococcaceae, Veillonella, Megasphaera, Gemmiger, Clostridium, and Treponema; and
the aerobic group, including Enterobacteriaceae, Staphylococcus, Bacillus, Corynebacterium, Pseudo-monas, and yeasts (Table 1) 1.
Development of the intestinal flora of infants

The fetus exists in a sterile environment until birth. After birth it rapidly becomes colonised by bacteria. On the 1st to 2nd days of life, the large intestine of neonates fed with breast milk and supplementary cow’s milk is colonised by enterobacteriaceae, streptococci including enterococci, and clostridia. On the 3rd day, bacteroides, bifidobacteria and clostridia occur in 40% of infants. Between days 4 and 7, bifidobacteria become predominant accounting to 1010 to 1011 organisms per gram faeces, and clostridia, bacteroides, enterobacteriaceae, streptococci, and staphylococci decrease. Thus, nearly 100% of all bacteria cultured from stools of breast-fed infants were bifidobacteria (Fig.1) 1.

Figure 1. Development of the faecal flora of neonates.

Table 1. Differentiation of major intestinal bacterial groups
Bacterial group Gram-staining
Aerobic growth
Spore
Major fermentation products

LAB group
Lactobacillus +
+
--
Lactic acid

Bifidobacterium +
--
--
Acetic acid + lactic acid

Streptococcus +
+
--
Lactic acid

Anaerobic group
Bacteroidaceae --
--
--
Various products

Anaerobic curved rods --
--
--
Succinic acid, butyric acid

Eubacterium +
--
--
Various products

Peptococcaceae +
--
--
Various products

Veillonella --
--
--
Acetic acid + propionic acid

Megasphaera --
--
--
Caproic acid + butyric acid

Gemmiger --
--
--

Clostridium +/--
--
+
Various products

Treponema --
--
--

Aerobic group
Enterobacteriaceae --
+
--

Staphylococcus +
+
--

Bacillus +
+
+

Corynebacterium +
+
--

Pseudomonas --
+
--

Yeasts +
+
--

Morphology

The intestinal flora of children and adults

Although bifidobacteria have been considered to be the most important organisms for infants and lactobacilli and Escherichia coli are more numerous bacteria for children and adults than bifidobacteria, it has now become clear that bifidobacteria also constitute a member of the major organisms in the colonic flora of healthy children and adults. During weaning, when an adult diet is consumed, the stools of infants shifted to the Gram-negative bacillary flora of adults: bifidobacteria decrease by 1 log, the numbers of bacteroidaceae, eubacteria, peptococcaceae, and usually clostridia outnumber bifidobacteria, which constitute 5 to 10% of the total flora. The counts of enterobacteriaceae, and streptococci decrease to less than 108 per gram faeces. Lactobacilli, megasphaerae, and veillonellae are often found in adult faeces, but the counts are usually less than 107 per gram faeces. The species and biovars alter from infant-type such as B. infantis and B. breve to adult-type such as B. adolescentis and B. longum (Fig.2) 1.

Figure 2. Composition of the faecal flora in adults.

The intestinal flora of elderly persons

In elderly persons bifidobacteria decrease or diminish, clostridia including C. perfringens significantly increase, and lactobacilli, streptococci and enterobacteriaceae also increase. This phenomenon is considered to be a result of ageing, but it might accelerate senescence (Fig.3) 1.

Figure 3. Changes in the faecal flora with increased age.

Disturbances in the intestinal flora

Although the composition of the intestinal flora is rather stable in healthy individuals, it can be altered by many endogenous and exogenous factors such as peristalsic disorders, cancer, surgical operations of stomach or small intestine, liver or kidney diseases, pernicious anaemia, blind loop syndrome, radiation therapy, emotional stress, disorders of immune systems, administration of antibiotics, and ageing.

Disturbances in the intestinal flora are non-specific: the small intestine harbours large numbers of bacteria, particularly anaerobes, enterobacteriaceae and strepto-cocci; bifidobacteria disappear or considerably decrease in the large intestine, while enterobacteriaceae and strepto-cocci remarkably increase and, some times, Clostridium perfringens also increase.

These ecological evidences would suggest that bifidobacteria should exist in the large intestine for maintenance of health and are far more important than Lactobacillus acidophilus as the beneficial intestinal bacteria throughout human life. In other words, the reduction or disappearance of bifidobacteria in human intestine would indicate an "unhealthy" state.

Role of the intestinal flora in human health

Metabolic profile of the intestinal flora

The intestinal flora is composed of different bacterial species, and thus, contains a variety of enzymes that perform the extremely varied types of metabolism in the intestine, and influence the host’s health and resistance to disease (Fig. 4). This includes such factors as: nutrition, physiological function, drug efficacy, carcinogenesis, ageing, immunological response and resistance to infection, endotoxins, and various other stresses. Within the intestine, the bacteria are implicated in the conversion of various substances that produce both beneficial and detrimental products to the host. In addition, bacterial toxins and cell components produced by some bacterial species modify the host’s immune responses, enhancing or inhibiting immune function. The beneficial intestinal flora protect the intestinal tract from proliferation or infection of harmful bacteria, while the detrimental bacteria manifest pathogenicity when the host’s resistance is decreased.

Figure 4. Enzymatic activities of intestinal bacteria.

The intestinal flora may play an important role in the causation of cancer and ageing

Dietary factors are considered important environmental risk determinants for colorectal cancer development. From epidemiological observations, a high fat intake is associated positively and a high fibre intake negatively with colorectal cancer. This is thought to occur by the following mechanisms. From food components in the gastrointestinal tract, organisms produce various carcinogens from the dietary components and endogenous substances, detoxify carcinogens, or enhance the host’s immune function, which results in changes in the incidence of cancers. The ingestion of large amounts of animal fat enhances bile secretion, causing an increase in bile acid and cholesterol in the intestine. These increased substances are converted by intestinal bacteria into secondary bile acids, their derivatives, aromatic polycyclic hydrocarbons, oestrogen and epoxides derivatives that are related to carcinogenesis. Various tryptophan metabolites (indole, skatole, 3-hydroxykinurenine, 3-hydroxyanthranilic acid, etc.) phenols, amines, and nitroso compounds produced by intestinal bacteria from protein also participate in carcinogenesis (Fig. 5). However, some intestinal bacteria reportedly inactivate noxious substances in the intestine.

Figure 5. Relationships among diet, intestinal bacteria and cancer.

Recent epidemiological studies have revealed that insufficient intake of dietary fibre is associated with high incidences of Western dis 1000 eases such as colorectal cancer, obesity, heart disease, diabetes, and hypertension. Ingested dietary fibre causes increased volume of faeces, dilution of noxious substances, and shortening of the transit time of intestinal contents, resulting in early excretion of noxious substances such as carcinogens produced by intestinal bacteria.

The cell components of intestinal bacteria modify the host’s immune function; some enhance immune response and others suppress it, involving them indirectly in the suppression or enhancement of carcinogenesis.

It is completely unknown at present which of these mechanisms plays the key role in carcinogenesis. Our studies with gnotobiotic mice showed that the presence of bacteria in the intestine can have marked effect on the incidence of liver tumours in C3H/He mice. Mice with conventional microflora had a much higher incidence of hepatic tumours (about 75% after 1 year) than their germfree counterparts (30% incidence after 1 year).

Table 2. Incidence of liver tumour in germfree (GF), conventionalised (CV), and gnotobiotic (GB) C3H/He male mice associated with human intestinal bacteria Group Bacteria NB
Liver tumour (%)*

GF Germfree 0
30

CV Conventionalised 75

GB6 Mitsuokella multiacida A4052 9.7
75

GB2 Enterococcus faecalis M266TA 9.7
67

GB1 Escherichia coli M66 10.3
62

GB13 Bifidobacterium longum E194b 10.1
47

GB20 Escherichia coli M66 10.2
100

Enterococcus faecalis M266TA 10.2

Clostridium paraputrificum VPI1586 9.5

Clostridium paraputrificum VP16558

GB7 Escherichia coli M66 9.9
88

Clostridium perfringens MAC521 9.5

GB9 Escherichia coli M66 9.7
80

1000 Enterococcus faecalis M266TA 9.9

Bacteroides vulgatus M45 10.1

GB21 Escherichia coli M66 9.3
46

Enterococcus faecalis M266TA 10.2

Clostridium paraputrificum VPI1586 9.6

Clostridium paraputrificum VP16558
Bifidobacterium longum E194b 9.8

NB= number of bacteria established log/g faeces ; * = percentage of animals

Table 3. Comparison of lifespan of germfree (GF) conventional (CV) female mice and gnotobiotic (GB) CF#1 female mice associated with human intestinal bacteria. Animals

Bacterial strains used GF
CV
GB-1
GB-2
GB-3

Bifidobacterium longum E194b --
*
9.8a
--
9.8

Clostridium perfringens MAC521 --
*
8.6
8.6
--

Escherichia coli 123 --
*
9.1
10.0
9.4

Enterococcus faecalis 1-12 --
*
10.1
10.1
10.1

Bacteroides vulgatus M-64 --
*
10.3
10.1
10.3

Eubacterium aerofaciens 151 --
*
10.3
10.3
10.3

Lifespan 96.3
78.2
87.1
80.7
87.1

(Means ± SD of age in weeks) ± 14.6
± 22.2
± 19.9
± 21.5
± 17.6

*: Conventional rat flora. a: No. of bacteria established (log/ g faeces)

Furthermore, when germfree mice were contaminated with specific intestinal bacteria, isolated from humans, the tumour incidence ranged up to 100%; of the mono-contaminated mice Mitsuokella multiacidatumours in 75% of the mice, Enterococcus faecalis gave in 67%, Escherichia coli in 62%, and B. longum in 47%. When mixtures of strains were used, high rates of tumour production were observed with mixtures of E. coli + E. faecalis + C. paraputrificum (100%), coli + C. per-fringens (88%), or E. coli + E. faecalis + B. E. vulgatus(80%). However, this promoting effect was suppressed by 46% by the addition of Bifidobacterium longum to the first promoting combination (Tabl 1000 e 2) 3,4.

These two studies suggested that intestinal bacteria are related to both promotion and prevention of cancer and ageing. The mechanism of the suppressive effect of bifidobacteria on liver tumours might be related to detoxifying carcinogens by bifidobacteria.Dietary control of intestinal flora for human health

Evidence that the intestinal flora is closely related to the host’s health and disease indicates the importance of the balance of the intestinal flora for health and longevity. In other words, the increase of harmful bacteria in the intestine may ultimately lead to various disorders, such as liver and kidney disorders, atherosclerosis, hypertension, cancer, and ageing. A satisfactory balance of the intestinal flora is possibly achieved by a nutritionally varied diet, and inclusion of dietary fibre and fermented milk which promote useful bacteria or suppress harmful bacteria.

Effect of intake of dietary fibre or oligosaccharides

Human digestive enzymes have little or no effect on raw starch and polysaccharides such as cellulose, pectin, hemicellulose, and pentosan; and oligosaccharides such as melibiose, raffinose, stachyose, fructo-oligosaccharides, isomalto-oligosaccharides, and galacto-oligosaccharides. These substances are hydrolysed to varying degrees and digested by colonic bacteria with the production of organic acids, mainly volatile fatty acids (acetate, propionate, and butyrate), and gas (carbon dioxide and hydrogen). Small amounts of lactic, formic and succinic acids are also produced. Methane may be produced in some people.

Figure 6. Changes in faecal bifidobacteria by the administration of FOS. FOS (8g/ day) were administered to aged subjects.

Most Bifidobacterium species metabolise a wide rage of indigestible polysaccharides and oligosaccharides to acetic and lactic acids and subsequently act as effective scavengers in the large intestine, when many oligosaccharides are ingested in the diet, while E. col 1000 i and C. perfringens do not.

In this way several commercially available oligosaccharides including raffinose, stachyose, fructo-oligosaccharides, isomalto-oligosaccharides, galacto-oligosaccharides are effective for proliferation of resident or implanted bifidobacteria in intestine and cause the reduction of faecal ammonia and pH as well as serum cholesterol and triglyceride level of the host5-8.

In our studies with volunteers, improvement of intestinal flora as well as intestinal environment were observed by oral administration of various oligosaccharides, including fructo-oligosaccharides, palatinose condensate, raffinose, and soybean oligosaccharides. Table 4 shows utilisation of five oligosaccharides by intestinal bacteria. Most of the oligosaccharides stimulated the growth of bifidobacteria in vitro and in vivo (Fig.6), and caused reduction of faecal pH, beta-glucuronidase, azoreductase, and indole, serum cholesterol and triglycerides levels as well as the blood pressure of elderly patients with hyperlipidaemia. From the results presented here, it may be concluded that oligosaccharides are considered to enhance the intestinal bifidobacteria, to promote the intestinal flora, the consistency of stool, and lipid metabolism.

We also studied the effect of dietary fibre on the faecal flora and faecal metabolite in eight healthy adult volunteers fed with low cholesterol (LC) diet, high cholesterol (HC) diet and high cholesterol supplemented with polydextrose (15g/day) (HC-P) diet for a 12 day interval. While a decrease (ca. 25%) of the faecal weight was observed during HC diet, HC-P diet led to a ca. 30% increase of the faecal weight. The faecal pH increased (ca. 0.2) during HC diet and decreased (ca. 0.6) during HC-P diet. Faecal putrefactive products including phenol, p-cresol, indole, iso-butyric and iso-valeric acids remarkably decreased by the administration of polydextrose (Fig. 7). In addition, the occurrence of clostridia, including Clostridium perfringens was higher during HC diet than during HC-P diet. These results suggested that polydextrose has a beneficial effect on the intestinal environment and human health through changing the balance and metabolic activity of the intestinal flora and physiologic activity of the host and that intestinal clostridia are involved in putrefactive activity in the intestinal content9.

Effect of yoghurt on human health

Yoghurt and other fermented milk products may enhance human health by the following mechanisms10.

Effect of milk used for yoghurt production: Milk protein prevents stomach cancer. Lactose increases indigenous bifidobacteria in the intestine. Calcium and iron prevent osteoporosis and anaemia, respectively. Vitamin A may prevent certain cancers.
Effect of fermentation products of yoghurt: Lactate prevents constipation and inhibits putrefactive bacteria. Peptone and peptides promote liver function. Effect of lactic acid bacteria (LAB): LAB detoxify carcinogens, stimulate immune response, and lower serum cholesterol.
Several recent studies have focused on bifidobacteria to establish the importance of these bacteria in influencing certain normal functions of the intestinal tract and in exploring its role in human health and diseases. In Japan, bifidobacteria now-a-days have been used as dietary supplements or as starter culture for yoghurt and other cultured milk products with the thought that such products may help the promotion of health. The effects of the daily intake of such products are reported as follows:

to suppress the putrefactive bacteria as well as intestinal putrefaction, for the prevention of constipation, geriatric diseases, including cancer,
to prevent and treat antibiotic-associated diarrhoea,
to stimulate immune response,
to contribute to a greater resistance to infection.
Figure 7. Influence of low cholesterol (LC) diet, high cholesterol (HC) diet supplemented with polydextrose. (HCP) on b -glucoronidase, b -glucosidase, nitro-reductase and tryptophanase activity in human faeces.

Effect of oral administration of bifidobacteria on intestinal flora and intestinal metabolites

We observed that oral administration of 109 Bifidobacterium longum preparation per day for 5 weeks to 5 healthy volunteers from 25 to 35 years old resulted in the increase of the counts of bifidobacteria and the remarkable decrease of the counts and frequencies of occurrence of clostridia in stools. This result also reflected a decrease of ammonia concentration and beta-glucuronidase activity in both faeces and serum11.

Serum cholesterol in Hartley male rabbits fed with 0.25% cholesterol diet supplemented with 1010/day of B. longum for 13 weeks were compared with the control diet group. In 2 of 3 rabbits fed with diet supplemented with B. longum there was a remarkably suppressed increase in cholesterol level, but 1 of 3 rabbits showed no effect.

Table 4. Utilisation of 5 sugars by various intestinal bacteria. Bacterial species Number of strains
SOR
RAF
STA
FOS
GLU

Bifidobacterium:
B. bifidum 6
--
--
±
--
++

B. longum 8
+++
++
+++
++
+++

B. breve 4
+++
+++
+++
+
+++

B. infantis 2
+++
+++

1000 +++
++
+++

B. adolescentis 9
++
++
++
++
+++

Lactobacillus:
L. casei 2
--
--
--
--
+

L. acidophilus 3
±
±
±
+
++

L. gasseri 1

1000 +
+
--
+
+

L. salivarius 2
++
++
++
+
++

Bacteroides:
B. vulgatis 9
±
±
+
+
++

B. fragilis 3
+
+
+
+
++

1000 B. distasonis 5
+
±
+
±
+

B. ovatus 4
+
+
+
+
++

B. thetaiotamicron 2
±
±
±
+
+

B. uniformis 1
+
+
+
+
+

B. melaninogenicus 1
+
+
+
+
+

Fusobacterium:
F. varium 1
--
--
--
--
±

F. necrophorum 1
--
--
--
--
--

Mitsuokella multiacida 4
++
++
++
+
++
1000
Megamonas hypermegas 1
++
++
++
+
+++

Eubacterium:
E. limosum 3
--
--
--
±
++

E. aerofaciens 2
±
±
±
±
++

E. nitritogenes 1
--
--
--
--
++

E. lentum 1
--
--
--
--
--

Clostridium:
C. perfringens 6
--
--
--
--
+

C. paraputrificum 4
--
--
--
--
+++

C. difficile 4
--
--
--
--
+

C. butyricum 2
++
++
++
++
+++

C. clostridiforme 2
±
±
±
--
+

C. innocuum 1
--
--
--
±
+++

C. ramosum 1
±
+
±
++
+++

C. sordelli 1
--
--
--
--
±

C. septicum 1
--
--
--
--
+++

C. cadaveris 1
--
--
--
--
±

C. sporogenes 1
--
--
--
--
1000 ±

Propionibacterium acnes 1
--
--
--
--
++

Peptostreptococcus:
P. magnus 1
--
--
--
--
--

P. anaerobius 1
--
--
--
--
±

P. productus 2
±
±
±
+
++

P. asaccharolyticus 1
--
--
--
--
±

P. prevotti 1
±
±
±
--
+

Veillonella:
V. dispar 1
--
--
--
--
--

V. parvula 1000 2
--
--
--
--
--

Megashaera elsdenii 1
--
--
--
--
±

Escherichia coli 6
--
±
--
--
++

Klebsiella pneumoniae 3
+
+
+
+
++

Enterobacter aerogenes 1
+
±
±
±
±

Enterococcus
E. faecalis 1
±
±
±
+
+++

E. faecium 1
+
±
+
+
+++

Streptococcus pyogenes 1
--

Ricapitolando, quindi, Alla base di un buona "salute intestinale" (che poi si ripercuote su quella generale) c'è una dieta nutrizionalmente variata (come strutturarla?); l'ingestione di fibra alimentare e latte fermentato (per i fermenti lattici).
Il latte fermentato sotto forma di kefir sarebbe una buona scelta? Tempo fa avevo letto che anche nel latte crudo, a dispetto di quello trattato termicamente, anche se non fermentato, sono contenuti dei fermenti lattici. So che l'inulina, essendo un oligosaccaride, è "gradita" a certi batteri benefici, promuovendone la proliferazione... cosa ne pensi della sua integrazione?
Hai già individuato qualche prodotto da assumere, veramente efficace, per poter favorire una corretta colonizzazione dell'intestino? Tu come ti stai muovendo, dieta inclusa, per promuovere/migliorare la salute nel tuo nucleo familiare?

Ricapitolando, quindi, Alla base di un buona "salute intestinale" (che poi si ripercuote su quella generale) c'è una dieta nutrizionalmente variata (come strutturarla?); l'ingestione di fibra alimentare e latte fermentato (per i fermenti lattici).
Il latte fermentato sotto forma di kefir sarebbe una buona scelta? Tempo fa avevo letto che anche nel latte crudo, a dispetto di quello trattato termicamente, anche se non fermentato, sono contenuti dei fermenti lattici. So che l'inulina, essendo un oligosaccaride, è "gradita" a certi batteri benefici, promuovendone la proliferazione... cosa ne pensi della sua integrazione?
Hai già individuato qualche prodotto da assumere, veramente efficace, per poter favorire una corretta colonizzazione dell'intestino? Tu come ti stai muovendo, dieta inclusa, per promuovere/migliorare la salute nel tuo nucleo familiare?

Ricapitolando, quindi, Alla base di un buona "salute intestinale" (che poi si ripercuote su quella generale) c'è una dieta nutrizionalmente variata (come strutturarla?); l'ingestione di fibra alimentare e latte fermentato (per i fermenti lattici).
Il latte fermentato sotto forma di kefir sarebbe una buona scelta? Tempo fa avevo letto che anche nel latte crudo, a dispetto di quello trattato termicamente, anche se non fermentato, sono contenuti dei fermenti lattici. So che l'inulina, essendo un oligosaccaride, è "gradita" a certi batteri benefici, promuovendone la proliferazione... cosa ne pensi della sua integrazione?
Hai già individuato qualche prodotto da assumere, veramente efficace, per poter favorire una corretta colonizzazione dell'intestino? Tu come ti stai muovendo, dieta inclusa, per promuovere/migliorare la salute nel tuo nucleo familiare?

Ciao Fabietto, scusa di nuovo..ma penso avrai capito che spesso non trovo il tempo di rispondere in tempo alle domande.
Prima di risponderti ho io una domanda ...per cosi dire tecnica. Io ho inviato 3 distinti “replay”che il sito ha provveduto, ma non era il mio scopo, ha incorporare insieme. Come fare per spedire 3 distinti replay?

Ora le tue domande.
Il latte contiene gia tutti i fermenti necessari per l’acidificazione. Purtroppo il latte che compriamo al negozio e’filtrato e pastorizzato quindi e’sterile. Ma qui andiamo sul post del latte.
Io mi regolo sulla dieta dei miei avi anche per i miei figli. Seguendo le teorie/risultati di Price e dell’imprint genetico ho capovolto la mia dieta a favore di quelli che erano le abitudini alimentari dei miei bis/bis nonni che attraverso mio padre ho ricercato. Ad esempio oggi si fa un gran parlare della dieta mediterranea e dell’olio di oliva. Beh io quel prof americano, Ancel Keys, l’ho per caso conosciuto quando ero piccolo, non sapendo chi cavolo era. Ho speso i miei primi 15 anni, 1964-1980, di vacanze al mare a ..Pioppi. ...giocando sulla spiaggia di fronte casa sua. Mio padre mi disse che suo padre e i suoi nonni non usavano molto l’olio di oliva come alimento, era per le lucerne. Il grasso di maiale era molto ricercato. Che non si mangiasse carne e’una favola. Mio nonno andava a caccia 2 volte la settimana. Carne e pesce erano la base accompagnati da verdure, cavoli/cavolacae oramai non piu coltivate, pane nero , dove c’erano un bel po di sementi diverse, e frutta di stagione salvo per le mele.
Il maiale era il principe della tavola, si uccideva una volta/due all’anno e si utilizzava tutto. Le bistecchine non c’erano mica. Chi era cosi scemo da uccidere il bue che trainava l’aratro? Carne di montone, pecora, capra e molta selvaggina.

Mi regolo cosi per me stesso, esempio menu giornaliero:
Colazione: a)uova, pancetta, latte caldo/b) uova, latte di cocco (con moderazione essendo nuovo per i miei geni) frullati con frutta/ c)gallette di riso o pane e burro e miele/ avanzi di carne e verdure della sera prima. Li alterno. Uova da galline razzolanti all’aperto, burro e pancetta biologico. Insomma non una colazione amidacea/ricca di carb..non li sopporto bene la mattina. Non mi viene fame fino alle 11.30 circa.

Meta giornata; frutta di stagione 1-2 pezzi
Pranzo: insalata mista, 100-150 gr, o verdure cotte miste etc , con 100-150 gr di pollo, salmone, carne di manzo o agnello. Pezzetto di cioccolato fondente 85-90%

Meta pomeriggio : frutta
Sera: riso, mais (polenta con burro e latte), patate con burro, tutto eccetto graminacee con glutine 100-150 gr e piu, dipende se mi sono allenato. Accompagno con carne, pesce, formaggi stagionati e fatti latte crudo, ed un bicchiere di vino rosso. Pezzetto di cioccolato fondente 85-90%
Della fibra non me ne preoccupo tanto. Anzi mangiando meno fibra ho meno problemi intestinali, gas, che ricompaiono se esagero con le verdure crude. Prediliggo le crucifere, cavoli vari, carote e tuberi vari.
Mangiare yogurt per favorire la flora intestinale e’solo una teoria..da provare. Nello stomaco i batteri vengono uccisi dai succhi gastrici.
Integrare inulina...non sono d’accordo. Mangia frutta, verdure e carciofi che ne sono ricchi.
Io mi sto ricredendo sugli integratori. Ne uso pochissimi. Vitamina D, anche per i miei figli, e per me Ginko biloba e taurina ( ma questo e’un retaggio del mio periodo fibromialgico).

Per i miei piccoli come dicevo prodotti quanto piu naturali.
Latte caldo e miscela di mais/riso/orzo/segale/miglio etc, per una pappa, colazione . Pane, burro miele/marmellate. Abbiamo bandito da sempre, coca cola, bibite varie, uso la centrifuga se voglio fare un succo di frutta, pasticcini e schifezze da supermercato.
Legumi li usiamo pochi e ci troviamo bene..ma la questione e’personale e lo sai.
Quindi pochissimi cibi gia pronti, merendine..biscotti etc, il meno possibile. Io sono per gli alimenti “originali”per cosi dire. Pane, quello vero fatto con il lievito madre, burro
Ma non sono un tipo psico...la domenica se facciamo la lasagna la mangio, se a volte ad un compleanno c’e’la torta fatta in casa la mangio, in estate sui monti, amiamo scalare e salire in montagna, portiamo per facilita pane e prosciutto crudo/formaggi. Mai avuto problemi.
Quindi ti direi di guardare un po come stavano i tuoi nonni/bis in salute, i miei sono morti a 98-102 anni in perfetta salute, e di cercare la loro dieta. E’quella che ti ha dato l’imprint genetico piu prossimo.
Ciao
Roberto

I miei nonni/bisnonni sono vissuti poco e con malattie che li ha portati alla morte, a parte mia nonna paterna che sfiora i 90 ma ha avuto anche lei ictus.
Ecco, io allora non dovrei seguire il loro esempio alimentare :not:
Comunque da quello che so l'olio di oliva era una rarità, ne usavano poco, si usava molto più il lardo/strutto, si usava tutto il maiale, anche organi come il cervello, galline e uova e diversi cereali e legumi autoctoni, tipo la cicerchia.

Dei miei bisnonni dovrei chiedere ai miei genitori. Mio nonno paterno non aveva nemmeno un dente cariato, aveva una vista perfetta, era magro ma a 72 anni gli venne il primo ictus e un po' si riprese; a 75 anni seconda ricaduta che lo costrinse al letto fino all'età di 82 anni dove morì. Mia nonna paterna è morta di brucellosi all'età di 40 anni. Mio nonno materno era cicciottello, con la dentiera e con gli occhiali, è morto di blocco renale all'età di 82 anni, era affetto da diabete dall'età di 40 anni, da glaucoma, ipertrofia della prostata e nella sua vita aveva avuto anche 3 infarti. Mia nonna materna era magra, miope quasi cieca, soffriva di dolori reumatici, aveva la dentiera, è morta a 73 anni sotto i ferri mentre la operavano per un aneurisma dell'aorta. I miei nonni erano tutti pastori e agricoltori come anche i miei bisnonni.

I miei nonni/bisnonni sono vissuti poco e con malattie che li ha portati alla morte, a parte mia nonna paterna che sfiora i 90 ma ha avuto anche lei ictus.
Ecco, io allora non dovrei seguire il loro esempio alimentare :not:
Comunque da quello che so l'olio di oliva era una rarità, ne usavano poco, si usava molto più il lardo/strutto, si usava tutto il maiale, anche organi come il cervello, galline e uova e diversi cereali e legumi autoctoni, tipo la cicerchia.

interpertando la epigenetica/genetica significa che in parte i tuoi avi non erano in un equilibrio biologico. Non ti chiedo ovviamente di che sono morti ma potresti partire da questo e correggere i loro eventuali errori alimentari. l'olio era costoso, si facevano le unzioni, confermo il lardo era ricercato. Mia nonna non ha mai disegnato il fatto di aver mangiato lardo e dolciumi, miele..torroni etc, ma all'eta di 60 anni aveva tutti i denti.( mori durante il terremoto).nemmeno una carie. Ma mica mangiavano la pasta al sugo...quella e'arrivata nel dopoguerra.
Io ricordo di aver mangiato il sanguinaccio da bambino. fatto con il sangue del maiale e cioccolato...buonisimo. cervelli, polmoni, milza fritta fegato si mangiava tutto. io ritengo questi cibi sani, lo so che ora sono pieni di immondizie dovuto al tipo di allevamenti, ma sono alimenti completi.

Nel DNA i segreti della dieta efficace
Alcune donne sono geneticamente 'programmate' per dimagrire seguendo una determinata dieta piuttosto che un'altra.
Ecco perchè la dieta Atkins funziona solo su alcune e una ricca di carboidrati è efficace solo per altre.
E' quanto emerso da uno studio della Stanford University presentato in occasione dell'annuale conferenza dell'American Heart Association.
Per arrivare a queste conclusioni i ricercatori hanno analizzato il DNA di 100 donne in sovrappeso che avevano provato diverse diete. L'attenzione degli scienziati si è concentrata su 5 geni in particolare, tutti legati al modo in cui il corpo utilizza i grassi e i carboidrati. Ebbene, i ricercatori hanno scoperto che le donne che seguono una dieta 'compatibile' con il proprio patrimonio genetico, sono riuscite a perdere circa 6,35 chili in un anno, cioè quasi il triplo di quello che sono riuscite a perdere le altre donne.
Inoltre, il girovita delle partecipanti che hanno seguito una dieta 'su misura' per il proprio DNA è diminuito in media di circa 6,5 centimetri contro i 3 centimetri delle altre.
"La diversità nella perdita di peso per gli individui che seguivano una dieta abbinata al loro genotipo rispetto a una che non è stato abbinata", ha spiegato Christopher Gardner, ricercatore che ha coordinato lo studio, "è molto significativa e rappresenta un approccio alla perdita di peso che non è mai stato segnalato in letteratura".
Utilizzare le informazioni genetiche per le diete, ha concluso l'esperto, "potrebbe contribuire a risolvere il problema del peso eccessico nella nostra società".

www.nutrigene.it

I miei nonni/bisnonni sono vissuti poco e con malattie che li ha portati alla morte, a parte mia nonna paterna che sfiora i 90 ma ha avuto anche lei ictus.
Ecco, io allora non dovrei seguire il loro esempio alimentare :not:
Comunque da quello che so l'olio di oliva era una rarità, ne usavano poco, si usava molto più il lardo/strutto, si usava tutto il maiale, anche organi come il cervello, galline e uova e diversi cereali e legumi autoctoni, tipo la cicerchia.

Qui un buon articolo per continuare la discussione

BRAIN GUT 7: INTRO TO YOUR GUT MICROBIOME
August 5, 2012 By Jack Kruse 199282 Commentshttp%3A%2F%2Fwww.jackkruse.com%2Fbrain-gut-7-intro-to-your-gut-microbiome%2FBRAIN+GUT+7%3A++INTRO+TO+YOUR+GUT+MICROBIOME2012-08-05+18%3A01%3A48Jack+Krusehttp%3A%2F%2Fjackkruse.com%2F%3Fp%3D1992

READERS SUMMARY:

1. WHAT CONTROLS OUR LOOK OR BODY COMP?

2. IS LEPTIN TIED TO THE GUT FLORA?

3. WHAT IS THE PURPOSE OF THE GUT MICROFLORA IN HUMANS?

4. IS OUR GUT LIKE A MONOPOLY BOARD?

5. HOW ARE PREGNANCY AND OBESITY ALIKE, YET QUITE DIFFERENT?

In the human gut and mouth, two other domains of microbial life are involved in human physiology. Archaea and Eukaryotic fungi and possibly protozoa, likely play an as-yet-undetermined role in optimal health maintenance. The human mouth and gut are a teeming microbial cauldron of life, which covers such intimate vital tissues, like our teeth and gut that remain exposed to our current environment. No longer can a human being be viewed as simply an individual produced from a diploid genome from its parents germ cells (Mom and Dad). Throughout the last 15 years, paradigm-shifting studies have shown the how gut microbial metabolism can truly alter human health and disease states. Today we will discuss how pregnancy and obesity are very closely related but yet different because of the hormone surges that each present with in humans. That hormone difference is all that separates a normal physiologic state (pregnancy) from a neolithic disease state (obesity). Because of this new knowledge, I now recognize that modern man is a cyborg like “superorganism” colonized with a huge variety of microbial life that can positively and negatively alter the course of health and well-being. Understanding the anatomy or the physiology in textbooks often just falls short of the entire story of human metabolism. It is complex and is tied to modern epigenetics, and this ultimately determines “our look and body composition.”

THE LEPTIN LINK OF “GUT FLORA” TO OBESITY:

Many of you know I believe obesity if an inflammatory disease of the brain. Where this disease begins may surprise some of you. It begins in our gut flora. How does this happen? Read this link! Sub optimal bacteria which contain bacterial toxins called lipopolysaccharides (LPS) which are found in bacterial cell membranes. As gut LPS rises, it has been shown to cause a rise in serum leptin levels. Once leptin levels are raised high enough it stimulates SOCS 3 signaling in the hypothalamus to cause LR. The overweight seem to physiologically ‘guard’ their elevated weight once it has transpired. In many mammal models of diet-induced obesity, leptin resistance is seen initially at and within the signaling though the vagal afferents into the area postrema. This blunts the actions of satiety incretin hormones centrally, and causes low brain dopamine levels. These things, along with the gastrointestinal bacterial-triggered SOCS3 signaling, are all implicated in the etiology of human obesity. In humans, dietary fat and fructose elevate systemic lipopolysaccharide, while dietary glucose also strongly activates SOCS3 signaling. Protein seems immune to this signaling of SOCS3 and it is why protein is the key macronutrient in my Leptin Rx.

This information implies that the gut flora can directly induce leptin resistance and be a cause of obesity. Gut bacterial LPS also raises blood levels of triglycerides as do simply refined dietary sugars and industrial seed oils found in most western diets. Both of these things are the modern principal causes of leptin resistance at the blood-brain barrier near the hypothalamus. It is also clearly established that eating a diet high in refined carbohydrates with or without a combo of industrial seed oils “simplifies the gut flora” in both species and in shear numbers, and these changes selects out for bacteria that cause inflammation at the blood brain barrier by increasing SOCS3 signaling.

NON GEEKS: Low numbers and amounts of bacteria happen to people who eat lots of processed foods and industrial seed oils. This leads to constipation and hard stools like we see in grade 1 and 2 of the Bristol Stool Chart.

So far in the Brain Gut series we have focused mostly on the brain side of this equation. Today we begin to work a bit on the other side of the equation were the gut is located. We are going to talk about the gut microflora. The key frontier questions now for scientists and clinicians are to figure out what is the purpose of the gut microflora? In Brain Gut one and two, I make the case, that the gut microflora is our casino dealer who shuffles the deck of genes that we collect from viruses. It also appears that the gut microflora helps in presenting these viral components to the immune system and they are neutralized and made less virulent so that we can carry their spare parts in our genome to use at a later date when we see fit based upon our genomic and epigenomic needs. These viral genes are ‘humans junk yard’ for new gene creation. We learned from Barbara McClintock’s work that these collected genes are then purposefully and systematically inserted into parts of genome where we have the most genomic or epigenomic needs based upon the stresses the organism faces in its current environment. The human body is roughly made up of one trillion cells. The latest number science gives us about the numbers of bacteria in our gut now is close to 100 trillion! Just a few years ago we thought this number was ten trillion cells. This means we have 100 times as many bacteria in our own guts that we do in our body. What might this imply? When you are on a process of discovery you always want to ask really good questions and try to avoid old answers with dead ends. So todays blog asks this question, “What is the purpose of the gut microflora in humans?” It is a loaded question for sure, but let us explore it.

When we consider the non-digestive microbiota benefits, they can be broadly segregated into two large areas:

1. gut homeostasis

2. immune system education.

What is becoming clear to clinicians and scientist alike now, is that human beings are truly a cyborg like creatures. Our genome and things that make us humans unique are made up from large amounts of retrotransposons from viruses and the bacteria in our gut truly take this concept to a new level as we explored in Brain Gut 2. We technically are “super-organisms.” As a result of this co-evolution, our guts shortened in length from our immediate ancestors, and our gut bacteria ecology became quite complex, to offset the change in length to facilitate the dietary changes we saw in the East Rift zone to make a human brain. These evolutionary moves also dramatically also improved our immune system’s ability to present antigens to our cellular immunity arm to better protect us from the ecology that the transitional apes found themselves in. We explored this in Brain Gut 5 in some detail. The immune system had to undergo great expansion because of how we evolved using viruses and bacteria as our path to our humanness. By once again harnessing the power of diversity of bacteria from our vertebrate ancestors with in our own guts, it allowed us to digest more new food sources that we used to fuel the blueprint to build a human brain. This diet is called the Epi paleo Rx.

While 99% of the adult gut microbiota is dominated by two bacterial phyla Bacteroides and Firmicutes, a full-term infant who is breast-fed, has a radically different gut microbiota from adults which is dominated by Bifidobacterium species along with Lactobacillus species for the first few months of post natal life. This persists until solid food ingestion begins and a transition to a normal adult microbiota occurs. Moreover, the human microbiota also evolves as we age as well.

Recent studies have shown that delivery type (Cesarean versus vaginal), birth weight, breast feeding, and diet all influence which gut microbes colonize the sterile newborn gut. This implies that the early colonization window of an infant is environment-dependent (epigenetic) rather than host-dependent action in humans.

Moreover, this gut microbial plasticity is quite temporary because shortly after birth, at approximately 100-300 days, most of the infant’s gut microbiota transforms to a more adult-like composition mentioned above.

GUT REAL ESTATE:

All along the gastrointestinal tract, there is a distinct gradient of immune tissue type, chemical acidity, and a specific rate of transit that controls the microbiota composition. I consider the GI tract as a “monopoly board” where some places are very different like the Boardwalk and Oriental Avenue properties found in the board game. I have recently began to mention this in many of my educational consults I have done recently. For example, in the stomach, Proteobacteria dominate, but in the distal gut (colon), Firmicutes and Bacteroides, which are barely detectable in the upper GI tract, become the dominant super organisms in a normal gut. This transition is very likely epigenetically and host-mediated (by antimicrobial peptide production). The precise physiologic and immunologic mechanisms which control these compositional changes have not yet been delineated by modern science, but we now know this happens in health and in disease states.

The microbiota composition, in the distal gut at least, is probably evolutionarily ancient, given the dominance of Bacteroides and Firmicutes amongst all mammals studied so far to date by science. This implies it is a highly conserved finding in the mammalian clade for an evolutionary reason. The parasympathetic nervous system controls the connections between the gut and the brain in humans. On each end of this conduit are two specialized membranes to control the optimal health milieu of both the gut and the brain at all times. The policeman of this system is the vagus nerve. In humans, the distal gut is also not innervated by the vagus nerve which is the tenth cranial nerve. The remainder of the gut is innervated by this nerve. This means the distal gut has no direct conduit to the brain. This is why most neolithic disease happens in this area. This is a direct connection of the gut to the brain in 90% of its length. The fact that most neolithic diseases occur in this uncovered gut real estate by this cranial nerve seems to imply that the brain directly is involved with monitoring the gut microbiotic mix in health.

I mentioned earlier in this series that I believe their has been a massive co-evolution of the gut microbiota with the host immune system. I believe this arrangement has allowed the host physiology to become optimized for survival of some bacterial lineages over others, but no direct scientific evidence for this effect has yet been presented as far as I know of today. The findings we have found today in the lab in humans are now strongly pointing in this direction.

Microbiota and Progesterone:

The bacterial survival issue also appears to be carried directly over to reproductive fitness too in humans. Women’s gut microbe populations change as pregnancy advances, becoming more like those of people who might develop diabetes. It now appears there is a special microbiota for pregnant women that develops during the first 5 months of pregnancy to allow them to put on massive amounts of weight without developing diabetes in a normal pregnancy. The reason they do not appear to develop diabetes is because during pregnancy their progesterone levels are massively raised (by their placenta if it is functioning well) while their cortisol levels stay flat to decreased. This is true of most normal pregnancies, but today in the modern world due to the older age of women at conception, now infertility issues and obesity are skyrocketing and as a result those switches no longer work well. Many obese, infertile, and older women have low progesterone and high cortisol’s before they get pregnant and this radically alters the gut flora to favor an obeseogenic status as their pregnancy progresses. This is why we often see gestational diabetes develop in these women with low progesterone levels as their fetus gets larger.

Morevover, if you go back and re read point 12 in Brain Gut 5 you will see another hormone, called E3 or estriol, has a massive affect on the gut microbiota. This diminishes the risk or cancer development both to the fetus and to the mother’s breast. This is precisely how epigenetics has direct actions on a fetus and mom.

WHAT MAKES METABOLIC SYNDROME AND PREGNANCY DIFFERENT?

In pregnant women overall, the diversity of their gut bacteria declines between the first and third trimesters. Simultaneously there is a massive change in species. Certain types, such as the Proteobacteria and Actinobacteria, are increased dramatically from pre-pregnancy to pregnancy states. The Proteobacteria are a major group (phylum) of bacteria. They include a wide variety of pathogens, such as Escherichia, Salmonella, Vibrio, Helicobacter, and many other notable genera. Actinobacteria are a group of Gram-positive bacteria with high guanine and cytosine content. They can be terrestrial or aquatic.

These species, ironically, are also more common in people who are obese or have metabolic syndrome associated with T2D. Proteobacteria in particular are often the bad guys in research studies checking stool samples of pregnant women. They are associated with inflammation, elevated cytokines and lowering of DHEA and progesterone further. They also are implicated in causing leptin resistance. This also allows for even higher cortisol levels to develop quickly. Remember what I told you in the Hormone 101 blog post about high cortisol levels? A high cortisol level can not be sustained forever and eventually adrenal fatigue is the end result. Go re-read the blog to understand what is happening both in a suboptimal pregnancy and in obesity.

Dr. Kjersti Aagaard, an OB/GYN from Baylor University, published some data comparing vaginal microbiomes in pregnant and non-pregnant women; those in the pregnant women were dominated by Lactobacillus species, which are thought to prevent the growth of harmful bacteria and help aid human digestion. Many probiotics are loaded with these bacteria but in too few a dose to make a ton of immediate help in a diseased state without the help of higher progesterone and lower cortisol levels. The ideal way to have both of these situations is to have an optimal hormone panel that pays strict attention to circadian light and dietary signals.

Furthermore the research also shows that the process is reversible after birth. It appears the shifts in microbial diversity did not affect mothers’ health during pregnancy. What it did show is that their stools (PCR analysis) collected during the third trimester contained more inflammatory markers than those collected during the first trimester. These trends held firm thoughout whether or not the women were of normal weight or overweight before falling pregnant, had actually developed diabetes, or had taken antibiotics or probiotics (supplements taken to provide or boost populations of ‘healthy’ bacteria) during pregnancy. Meanwhile, after birth, the children’s microbiota’s resembled those of the mothers’ first trimester samples. This implies the status of mom’s gut health and pre pregnancy and her hormone panels are of primary importance to the developing fetal brain. In my opinion, this link best explains why we are seeing record increases in autism and spectrum disorders today. I don’t believe that vaccines are the major issue in spectrum disorders as some do. I believe hormone changes in the mother prenatally are to blame. This is due to sub optimal circadian biology (light and diet) which cause subsequent changes to the gut microflora pre-pregnancy are of primary importance in these epigenetic diseases. This also implies it is reversible and can be made optimal before a child is conceived if the mother decides to become proactive and understands how much power her decisions truly yield in forming an optimal brain for her child.

When researchers transplanted gut bacteria from stool samples into mice that had been raised under sterile conditions, they found that mice receiving microbiota from third-trimester samples became fatter and insulin resistant than mice that were given first-trimester samples. This was not a surprising result to me because there is quite a bit of information in the literature today that obesity has its own inherent gut microbiota that is highly inflammatory and blocks normal gut signals and eventually leptin at the blood brain barrier.

The reality appears today that that the microbiome is a contributing factor to this change. Some of us believe that it maybe the driving force behind it completely. It may be that obesity is due to a change in signaling between the gut microbiome and the leptin receptor in the brain. The link is both ingenious and fascinating and of course how it ties the hormone panels together is something that modern medicine remains quite blind too. You no longer should be blind to this link. It maybe the critical first link in reducing your risk for obesity. CT helps destroy inflammation while increasing energy expenditure and it too changes your gut flora.

It appears in pregnancy direct hormone surges dramatically alter the gut microbiota, and these changes give you the changes in metabolism to foster massive growth of the body and brain of a fetus. This implies that food and hormones are cut from the same cloth with regards to physiology. This eerily sounds like the quote I made in Brain Gut 5. It said, “Think of food as hormone information, not as a metabolic fuel. Think of the Epi-paleo template as human jet fuel for the human nervous system.”

Here is another piece of the QUILT in how the gut and brain are married and dance a beautiful dance together when circadian biology is optimally matched.

You should mind your gut health and it might help you repair your hormones and all this can help heal an adult ‘bad brain’ or one that is forming your own uterus right now!

Bè si ovviamente parto dalle loro malattie per capire dove sono più a rischio, le 2 nonne entrambe di ictus, nonno materno morto per tubercolosi renale e quindi perdita della funzione renale, nonno paterno per tumore al retto. Mio padre,in vita, tumore alla prostata, suo fratello (mio zio) ancora in vita ma con tumore al retto. Il quadro grossomodo è questo.
Da quel che mi ricordo e mi dicono tutti grossi mangiatori di cereali tranne nonno paterno che amava la carne (anche cruda) ed il vino, molto vino.

Per me è molto difficile risalire a cosa mangiassero i miei nonni, vivendo nella povertà e campagna comunque penso mangiassero prodotti propri, brodi, cerali pane, latte di capra e mucca, verdure e quando disponibile la carne.
Nonna materna ha avuto 2 ictus, in seguito è morta. Nonno materno è morto di infarto abbastanza giovane (sulla sessantina).
Nonno paterno non ricordo, mentre nonna paterna ha avuto un ictus ed in seguito è morta di tumore all'intestino.

L'ostruzione delle vene mi pare vada per la maggiore tra infarti ed ictus. La "mediterranea" dei nostri nonni non era tutto sto granchè.