Newsgroup: it.scienza.biologia
Titolo: Re: acidi grassi saturi (era: acqua potabile e cloro)


 
-- 
bye
!(!1|1)
 

 doesn't cause heart disease.
 
permettimi di ribattere con quest'altra:
 
 
http://www.ncbi.nlm.nih.gov/pubmed/23388667
  (2013)
 
    Diet and risk of chronic diseases: results from the first 8 years
    of follow-up in the EPIC-Potsdam study.
 
   (...) The paradoxical findings concerning the potential health
   benefit of coffee as well as cakes and cookies are interesting
   and should be investigated further.
 
Sarebbe benefico il consumo di torte (cakes) e biscotti (cookies)?
Beh, io mi sono sempre sentito meglio dopo una fetta di Saint Honorï¿½
di pasticceria, ma non credevo che fosse tanto salutare. F/up altrove,
grazie: la chimica non puï¿½ spiegare questi misteri dell'alimentazione.
 
Bye,
 
   *GB*

    and should be investigated further.
 
riguardo il caffè negli ultimi due anni ho letto diversi articoli che 
ne evidenziavano gli effetti benefici sia per il diabete che per altre 
patologie quindi la cosa non mi sorprende, riguardo il resto sarebbe 
il caso di aspettare ulteriori riscontri...
 
(ovviamente il caffè fa bene nelle dosi giuste... ci sono stati 
diversi decessi per overdose di caffeina anche se non da caffè, ma da 
bevande energetiche o assunta pura come integratore)
-- 
bye
!(!1|1)
 

 the link between food sources of saturated fat and mortality.
 
Domanda: rispetto agli studi precedenti, ï¿½ cambiato qualcosa riguardo
alle modalitï¿½ di cottura degli alimenti contenenti quei grassi saturi?
Voglio dire che secondo me il burro crudo su un panino con marmellata
non fa male, mentre il burro bruciato sulla superficie di un quarto
di manzo alla griglia, sï¿½. In questo tipo di studi, ci sono sempre
troppe variabili, e ogni volta ci si concentra solo su parte di esse.
 
Forse sarebbe il caso di formulare ipotesi strane, e verificare in che
misura i dati epidemiologici e sperimentali collimino con esse.
 
Esempio 1: Il danno vascolare ï¿½ causato da un danno al fegato. Pertanto
lo stesso alimento puï¿½ favorire o no un danno vascolare a seconda di
quanto ï¿½ cucinato pesante.
 
Esempio 2: Il cancro ï¿½ causato dall'attivazione incongrua di retrovirus
endogeni. Pertanto radiazioni, agenti chimici, mutazioni, accorciamento
dei telomeri, agiscono tutti provocando tale attivazione retrovirale.
 
Bye,
 
   *GB*

 dei telomeri, agiscono tutti provocando tale attivazione retrovirale.
 
il cancro è stato riscontrato anche negli organismi più semplici
ormai si ipotizza sia semplicemente un effetto collaterale dell'essere 
organismi pluricellulari
 
-- 
bye
!(!1|1)
 
 
 
 

 organismi pluricellulari
 
Giï¿½, ma come spieghi il paradosso di Peto? Le balene non dovrebbero
nemmeno esistere se le cose fossero cosï¿½ semplici. Infatti, sebbene
animali piï¿½ grossi abbiano un numero di cellule corrispondentemente
piï¿½ grande, l'incidenza del cancro non aumenta affatto con il numero
delle cellule, ma si mantiene mediamente quasi costante (anzi a volte
specie piï¿½ grosse mostrano un'incidenza minore): eppure tante cellule
in piï¿½ significano altrettante probabilitï¿½ in piï¿½ di mutazioni casuali.
Al riguardo leggiamo, anche se ï¿½ in tedesco:
 
   http://de.wikipedia.org/wiki/Petoï¿½s_paradox
 
da cui estraggo:
 
   Bei im Labor aufgezogenen Hausmï¿½usen (Mus musculus) haben etwa 46 %
   beim Tod Tumore entwickelt.[6] Bei Hunden (Canis lupus familiaris)
   liegt dieser Wert bei ungefï¿½hr 20 %[7] und beim Menschen bei 22 %
   (in den USA, durch Krebs verursachte Todesfï¿½lle).[8]
 
Interessante questo articolo, che considera il cancro evolutivamente
conservato per spazzar via i portatori di mutazioni nocive alla specie:
 
 
http://protein.bio.msu.ru/biokhimiya/contents/v70/full/70091277.html
 
 
   The hypothesis introduces the idea that there is a critical level
   of mutagenesis that triggers a program of organism death by means
   of proliferation of killer cells. Similarly to apoptosis, which is
   an altruistic suicidal act of a faulty cell threatening the stability
   of a multicellular organism, a malignant tumor is an altruistic
   suicide of an individual carrier of harmful alleles threatening
   genetic stability of the population.
 
     ï¿½The Samurai lawï¿½: It is better to die than to be wrong!
 
E proprio quell'articolo spiega meglio il paradosso di Peto (notare che
la probabilitï¿½ di ammalare di cancro a 60-80 anni non ï¿½ quella media
del 22% sull'intera esistenza):
 
   The Peto paradox. Fifty years ago a fundamental concept of oncology
   was formulated that carcinogenesis is a multistage process [7].
   On analyzing statistics of age dependence of cancer incidence in
   humans, seven stages were revealed (today it is clear that they are
   associated with accumulation in the cellular DNA of mutations which
   induce discrete and irreversible changes in the cell genotype and,
   respectively, phenotype). Obviously, the more stages are required
   for the cell transformation, the higher is its anticancer defense [8];
   thus, this value (the number of stages and, respectively, mutations
   which underlie them) may be used to quantitatively characterize
   ï¿½transformational resistanceï¿½ of the cell.
 
   The multistage pattern of carcinogenesis shows a very low probability
   of transformation of a normal cell to a cancer cell: mutations (which
   are extremely rare events, ~10^-7 gene/division [9-11]) have to hit
   several times a very small target (~300 genes, or ~1% of the genome )
   and be accumulated in the genome of the same cell. Nevertheless,
   cancer is rather common in humans (the probability of the illness
   during the lifetime is ~20% and 40-50% at the age of 60-80 years ).
   The discrepancy between the low probability of cancer transformation
   of the cell and the high probability of cancer morbidity in humans
   is explained by a high number of proliferating cells in the human body
   (~10^-12-10^-13) and a prolonged lifetime: even a highly improbable
   event can occur under such conditions. In accordance with this logic,
   cancer should not occur in small and short-living animals (such as
   mice), whereas big and long-living animals (elephants, whales)
   should be ill even in uterus and die out as species. However, these
   theoretical predictions do not correspond to the reality: cancer
   occurs in all animals, independently of size and longevity, but,
   on the other hand, cancer does not threaten the existence of species
   (the known Peto paradox [14]).
 
Ma ne dï¿½ questa spiegazione esclusivamente evolutivo-selettiva:
 
   The Peto paradox is also true for different tissues of the same
   organism [15]. Thus, man has ~100 types of tissues, which considerably
   vary in both number of cells and their proliferative activity,
   but they all are susceptible to cancer transformation. The
   transformational resistance depends on both the species and tissue
   (table) [19]. Thus, the anticancer defense of the cell adapts to
   conditions of its existence in the body not only on the genome level
   (as it seems to be for species-associated differences), but also
   on the transcriptional level, which is markedly more changeable.
   Therefore, if the cancer phenomenon had even a slight negative effect
   on the species survival and reproduction, it would be easily
   eliminated during evolution. By contrast, the stubborn maintaining
   of this phenomenon in Nature (proved by its universality) suggests
   its evolutionary reasonability. It seems that the anticancer defense
   on the organism's level is balanced by the opposite tendency (i.e.,
   directed for its preservation), which acts on the level of the
   population (see below).
 
Mentre a mio parere si potrebbe anche spiegare piï¿½ meccanicisticamente
con due fattori: la maggiore importanza dell'aneuploidia (che inizia a
manifestarsi massivamente quando con l'etï¿½ i telomeri si sono accorciati
abbastanza da rendere collose le estremitï¿½ dei cromosomi) rispetto alle
mutazioni puntiformi, e il fatto che i mammiferi piï¿½ grossi espellono
attivamente gli ERV (retrovirus endogeni) dal loro genoma. Infatti il
numero di ERV sembra inversamente proporzionale alle loro dimensioni.
Si pensa che se non lo facessero, piï¿½ ï¿½ grosso un animale (le sue
dimensioni dipendono dal numero delle sue cellule, che in generale
hanno circa tutte le stesse dimensioni nel topo come nell'elefante)
e piï¿½ probabilitï¿½ esso avrebbe di morire presto di cancro (paradosso
di Peto). Per cui un quarto degli esseri umani o degli elefanti
morirebbero di cancro entro l'etï¿½ in cui ne muore un quarto dei topi.
E gli altri tre quarti ne morirebbero in max un lustro o poco piï¿½,
per cui le specie troppo grosse si estinguerebbero, a meno di non
espellere attivamente gli ERV dal loro genoma, che quindi diventa
piï¿½ piccolo di quanto ci si aspetterebbe. Altri riferimenti:
 
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4102558/
 
 
    Larger Mammalian Body Size Leads to Lower Retroviral Activity
 
   Retroviruses have been infecting mammals for at least 100 million
   years, leaving descendants in host genomes known as endogenous
   retroviruses (ERVs). The abundance of ERVs is partly determined by
   their mode of replication, but it has also been suggested that host
   life history traits could enhance or suppress their activity. We show
   that larger bodied species have lower levels of ERV activity by
   reconstructing the rate of ERV integration across 38 mammalian
   species. Body size explains 37% of the variance in ERV integration
   rate over the last 10 million years, controlling for the effect of
   confounding due to other life history traits. Furthermore, 68% of
   the variance in the mean age of ERVs per genome can also be explained
   by body size. These results indicate that body size limits the number
   of recently replicating ERVs due to their detrimental effects on
   their host. To comprehend the possible mechanistic links between body
   size and ERV integration we built a mathematical model, which shows
   that ERV abundance is favored by lower body size and higher
   horizontal transmission rates. We argue that because retroviral
   integration is tumorigenic, the negative correlation between body
   size and ERV numbers results from the necessity to reduce the risk
   of cancer, under the assumption that this risk scales positively with
   body size. Our model also fits the empirical observation that the
   lifetime risk of cancer is relatively invariant among mammals
   regardless of their body size, known as Petoï¿½s paradox, and indicates
   that larger bodied mammals may have evolved mechanisms to limit
   ERV activity.
 
    Endogenous Viral Elements in Animal Genomes
 
   Integration into the nuclear genome of germ line cells can lead
   to vertical inheritance of retroviral genes as host alleles. For
   other viruses, germ line integration has only rarely been documented.
   Nonetheless, we identified endogenous viral elements (EVEs) derived
   from ten non-retroviral families by systematic in silico screening
   of animal genomes, including the first endogenous representatives
   of double-stranded RNA, reverse-transcribing DNA, and segmented RNA
   viruses, and the first endogenous DNA viruses in mammalian genomes.
   Phylogenetic and genomic analysis of EVEs across multiple host
   species revealed novel information about the origin and evolution
   of diverse virus groups. Furthermore, several of the elements
   identified here encode intact open reading frames or are expressed
   as mRNA. For one element in the primate lineage, we provide
   statistically robust evidence for exaptation. Our findings establish
   that genetic material derived from all known viral genome types and
   replication strategies can enter the animal germ line, greatly
   broadening the scope of paleovirological studies and indicating a
   more significant evolutionary role for gene flow from virus to animal
   genomes than has previously been recognized.
 
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060950
 
 
    Petoï¿½s Paradox: Evolutionï¿½s Prescription for Cancer Prevention
 
   The evolution of multicellularity required the suppression of cancer.
   If every cell has some chance of becoming cancerous, large,
   long-lived organisms should have an increased risk of developing
   cancer compared to small, short-lived organisms. The lack of
   correlation between body size and cancer risk is known as Petoï¿½s
   Paradox. Animals with 1,000 times more cells than humans do not
   exhibit an increased cancer risk, suggesting that natural mechanisms
   can suppress cancer 1,000 times more effectively than is done in
   human cells. Because cancer has proven difficult to cure, attention
   has turned to cancer prevention. In this review, like pharmaceutical
   companies mining natural products, we seek to understand how
   evolution has suppressed cancer to ultimately develop improved
   cancer prevention in humans.
 
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925786/
 
 
    Endogenous retroviruses and the development of cancer
 
   Mammalian genomes include a considerable number of endogenous
   retroviruses (ERVs), relics of ancestral infectious retroviruses,
   whose proviruses have invaded the germ-line. The documented ability
   of infectious retroviruses to cause cancer has greatly contributed
   to the discovery of ERVs. It also reinforced the concept that ERVs
   are causative agents of many cancers, a notion that historically
   has not always stood up to experimental scrutiny. The recent greater
   appreciation of the complexity of ERV biology and the identification
   of dedicated host mechanisms controlling ERV activity have revealed
   novel interactions between ERVs and their hosts with the potential
   to cause or contribute to disease. In this review, the involvement
   of ERVs in cancer initiation and progression is discussed, as well
   as their contribution to our understanding of the process of
   transformation and to the invention of innovative preventive
   and therapeutic cancer treatments.
 
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864273/
 
 
    Broad-scale phylogenomics provides insights into retrovirusï¿½host
    evolution
 
   Retroviruses, such as HIV, are important pathogens of vertebrates,
   including humans. They are capable of crossing species barriers
   to infect new hosts, but knowledge about the evolutionary history of
   retroviruses is limited. However, genomic traces of past retrovirus
   activities known as ï¿½endogenous retrovirusesï¿½ can be screened from
   sequenced genomes and analyzed to improve understanding of retrovirus
   evolution. Here we use a unique approach to address the evolution of
   one group of retroviruses in a screen of 60 diverse vertebrate host
   genomes. We find evidence of rampant host-switching across mammalian
   orders by members of this group throughout their evolutionary
   history. We also find evidence that the spread of infective
   retroviruses from this group may be facilitated by rats.
 
Quindi i retrovirus entrano continuamente nel genoma (rappresentano
l'8% del genoma umano), e le cellule degli organismi pluricellulari
li estromettono per ridurre l'incidenza di cancro. Quei retrovirus
che non provocano il cancro non vengono eliminati e importano da altre
specie elementi di nuove funzionalitï¿½ che dï¿½nno luogo all'evoluzione.
 
Il meccanismo dell'espulsione selettiva degli ERV potrebbe avvenire
con il monitoraggio della funzionalitï¿½ di determinati geni, effettuato
ad es. da geni residenti sull'altro allele. Se un certo gene risulta
non piï¿½ funzionante (quantitï¿½ di proteina corrispondente dimezzata),
si provvede a tagliar via un breve tratto di DNA prima di esso. Cosï¿½
se la causa non era un'inserzione dentro il gene, la sua funzionalitï¿½
ï¿½ ripristinata. Se invece l'inserzione ï¿½ avvenuta in un punto in cui
non danneggia la funzionalitï¿½ di geni essenziali, il DNA di quell'ERV
non viene tagliato via. La ragione per cui tale meccanismo ï¿½ piï¿½ attivo
negli animali piï¿½ grossi potrebbe essere semplicemente che essi hanno
un maggior numero di cellule e gli enzimi taglia-DNA una volta prodotti
vengono diffusi anche nelle cellule circostanti, per cui maggiore ï¿½
il numero di cellule dell'organismo e piï¿½ intensa ï¿½ l'attivitï¿½ di
eliminazione degli ERV. Quanto agli organismi piï¿½ complessi, in media
sono anche piï¿½ grossi (confronta le dimensioni medie di un vertebrato
con quelle di un invertebrato, o pensa a quante formiche schiacci
quando cammini).
 
D'altronde l'eliminazione degli ERV puï¿½ non essere l'unico meccanismo
che spiega il paradosso di Peto:
 
 
http://icb.oxfordjournals.org/content/47/2/317.long
 
 
    Why donï¿½t all whales have cancer? A novel hypothesis resolving
    Petoï¿½s paradox
 
   Larger organisms have more potentially carcinogenic cells, tend to
   live longer and require more ontogenic cell divisions. Therefore,
   intuitively one might expect cancer incidence to scale with body
   size. Evidence from mammals, however, suggests that the cancer risk
   does not correlate with body size. This observation defines ï¿½ï¿½Petoï¿½s
   paradox.ï¿½ï¿½ Here, we propose a novel hypothesis to resolve Petoï¿½s
   paradox. We suggest that malignant tumors are disadvantaged in larger
   hosts. In particular, we hypothesize that natural selection acting on
   competing phenotypes among the cancer cell population will tend to
   favor aggressive ï¿½ï¿½cheatersï¿½ï¿½ that then grow as a tumor on their
   parent tumor, creating a hypertumor that damages or destroys the
   original neoplasm. In larger organisms, tumors need more time to
   reach lethal size, so hypertumors have more time to evolve. So,
   in large organisms, cancer may be more common and less lethal.
   We illustrate this hypothesis in silico using a previously published
   hypertumor model. Results from the model predict that malignant
   neoplasms in larger organisms should be disproportionately necrotic,
   aggressive, and vascularized than deadly tumors in small mammals.
   These predictions may serve as the basis on which to test the
   hypothesis, but to our knowledge, no one has yet performed a
   systematic investigation of comparative necrosis, histopathology,
   or vascularization among mammalian cancers.
 
In conclusione, piï¿½ un organismo ï¿½ piccolo e meno rischia il cancro
a paritï¿½ di fattori (ha meno cellule e minor durata della vita), per cui
gli conviene avere tanti geni diversi e un piï¿½ alto tasso mutazionale.
Invece un organismo molto piï¿½ grande e complesso deve controllare
continuamente i suoi geni, per cui gli conviene averne il numero minimo
essenziale e operare per via post-trascrizionale. Ciï¿½ non solamente
per la faccenda degli ERV, ma anche perchï¿½ il rischio di cancro risulta
proporzionale anche al numero di geni (c'ï¿½ una maggiore probabilitï¿½ di
mutazioni oncogeniche in un set di 50.000 geni che in uno di 20.000).
 
Bye,
 
   *GB*