per Marlin e Julien, parere

juliensorel

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http://www.informaworld.com/smpp/content~db=all~content=a785830330
http://inhumanexperiment.blogspot.com/2009/05/soy-isoflavones-reduce-dht-increase.html
http://inhumanexperiment.blogspot.com/2009/06/soy-protein-isolate-reduces-dht-in.html

Credo che il trucco per avere isoflavoni biodisponibili a partire da derivati della soia sia ferentare il latte di soia con i fermenti lattici, che è ciò che faccio con successo da 3 settimane. Addirittura i fermenti lattici fermentano meglio e più rapidamente la soia del latte stesso. Nel processo le proteine vengono degradate i svariati peptidi ad attività biologica e gli isoflavoni glicosilati scarsamente assobibili) divengono agliconi (assobibili in maniera eccellente) http://www.ncbi.nlm.nih.gov/pubmed/15796581


http://www.naturalnews.com/025513_soy_food_soybeans.html
http://jn.nutrition.org/cgi/content/full/136/1/45

In conclusion, these studies show that the bioavailability and pharmacokinetics of isoflavones are influenced mainly by the type of food matrix or form in which they are ingested. A liquid matrix, such as soy milk, yields a faster absorption rate and higher peak plasma concentrations than a solid matrix, whereas aglycones in a fermented food such as tempeh are absorbed more rapidly than glucoside conjugates. Although these data are suggestive of an influence of gender, there was no major influence of age.

utile l'associazione alimentare col tè verde. http://jn.nutrition.org/cgi/content/full/133/2/516
(in sostanza penso che sia l'associazione alimentare più efficace e utile del palmetto, del cocco e di tutti i ritrovati a base di acidi grassi.)

Per chi volesse provare uso latte si soia non agm della soyasun con i ferminte bionova per il kefir di latte. Il risultato è uno yogurt a base di soya dal gusto delicato. Fermneta in meno di 7 ore e con appena 3 cucchiai se ne riforma un litro, basta aggiungere il latte e lasciare a temperatura ambiente.
 

kaspar hauser

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Julien scrisse:

>> non voglio eliminarlo, voglio avere il tasso di un H202 di un neonato.

Allora perché bevi così tanto tè verde? Non sapevi che:

Free Radic Biol Med. 2010 Aug 11. [Epub ahead of print]
Hydrogen peroxide mediates EGCG-induced antioxidant protection in
human keratinocytes.
Elbling L, Herbacek I, Weiss RM, Jantschitsch C, Micksche M, Gerner C,
Pangratz H, Grusch M, Knasmüller S, Berger W.
Institute of Cancer Research, Department of Medicine I, Medical
University of Vienna, Vienna, Austria.
Abstract
Health beneficial effects of (-)-epigallocatechin-3-gallate (EGCG),
the main catechin of green tea, have been attributed to complex
interactions with a focus on antioxidative properties. Susceptibility
to auto-oxidation and production of cytotoxic reactive oxygen species
(ROS), mostly H(2)O(2), has been suggested to occur in vitro but also
in vivo [1]. In this study, we address whether auto-oxidation-derived H
(2)O(2) may be involved in the cytoprotective effects of EGCG. To that
end we investigated keratinocyte-derived HaCat and Hl-60 promyelocytic
leukaemia cells with significantly different sensitivities against H(2)
O(2) (IC50 117.3 versus 58.3muM, respectively) and EGCG (134.1 versus
84.1muM). HaCat significantly resisted cytotoxicity and DNA damage
based on enhanced H(2)O(2) clearance, improved DNA repair and reduced
intracellular ROS generation. Cumulative versus bolus EGCG and H(2)O
(2) treatment and H(2)O(2) pretreatment prior to subsequent high-dose
EGCG and vice versa significantly reduced DNA damage and cytotoxicity
in HaCat cells only. Addition of catalase abolished protective
activities of low-dose H(2)O(2) and EGCG. In summary, our data suggest
that auto-oxidative generation of low-dose H(2)O(2) is a significant
player in the cell-type-specific cytoprotection mediated by EGCG and
support the hypothesis that regular green tea consumption can
contribute as prooxidant to increased resistance against high-dose
oxidative stressors.
PMID: 20708679 [PubMed - as supplied by publisher]


Un altro punto a favore della teoria ormetica, un altro a sfavore di quella dei radicali liberi.
 

marlin

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Nulla di nuovo sotto...la soia[:D]....i prodotti utilizzati a base di isoflavoni sono infatti titolati (e non poco) in agliconi.

Trovo invece illuminante il filone inaugurato sopra cui manca questo articolo precedente:

http://www.impactaging.com/papers/v2/n4/pdf/100139.pdf

...veramente chiaro (sperando che non sia iper-semplificato o meglio semplicistico[:D]).

Ciao

MA - r l i n
 

kaspar hauser

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> buone notizie dai pesticidi naturali.

Una review non è una notizia. E' solo rimasticatura di vecchie notizie.
Inoltre nemmeno gli estensori metterebbero la mano sul fuoco. Nelle conclusioni leggiamo infatti:
[...]Clinical studies so far have not undoubtedly succeeded in pointing out any specific polyphenols or food products in reducing the risk of insulin resistance.

P.S. La tua H202 come se la passa? Con tutta quella produzione EGCG-mediata mi preoccupi ... [}:)]
 

kaspar hauser

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J Agric Food Chem. 2010 Jul 29. [Epub ahead of print]

Quercetin and Ferulic Acid Aggravate Renal Carcinoma in Long-Term Diabetic Victims.
Hsieh CL, Peng CC, Cheng YM, Lin LY, Ker YB, Chang CH, Chen KC, Peng RY.

Graduate Institute of Biotechnology, National Changhua University of Education, 1 Jin-De Road, Changhua, Taiwan 500.

Abstract
Many phytoantioxidants have therapeutic drawbacks due to their potent prooxidant bioactivity. It is hypothesized that phytoantioxidants (PAO) are beneficial only to the early-stage diabetes mellitus (DM) and will become ineffective once renopathy occurs. Gallic acid, rutin, EGCG, ferulic acid (FA), and quercetin were tried on the streptozotocin (STZ)-induced DM rat model for a 28 week experimental period. All of these PAO were shown to be ineffective for hypoglycemic action. The incidence of cataract (50%), injured glomerules, and renal cell carcinoma (RCC) was very common, among which the most severely affected involved the quercetin- and the FA-treated groups. The tumorigenicity of ferulic acid is still unclear. However, for quercetin, this can be attributted to (i) the prooxidant effect, (ii) the insulin-secretagogue bioactivity, and (iii) the competitive and noncompetitive inhibition on the O-methyltransferase to enhance the estradiol-induced tumorigenesis. Conclusively, quercetin and FA are able to aggravate, if not induce, nephrocarcinoma. It is time to reevaluate the tumorigenic detrimental effect of PAO, especially those exhibiting prooxidant bioactivity.

Come si può ben vedere la riduttiva e semplicistica equivalenza fitoestratti=antiossidanti non regge e questi risultati apparentemente contraddittori trovano la loro spiegazione all'interno dell'ipotesi ormetica.
Ovvero un po' di veleno (ops, pesticida) stimola la produzione endogena di antiossidanti, troppo ha effetto contrario. Quindi fitoestratti si, ma con moderazione (molta) e precauzione (moltissima) nei soggetti con funzionalità renale o epatica compromessa.



 

juliensorel

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>>risultati apparentemente contraddittori trovano la loro spiegazione all'interno dell'ipotesi ormetica.
>>Ovvero un po' di veleno (ops, pesticida) stimola la produzione endogena di antiossidanti

E' falso che una sostanza prossidante sia un veleno per il motivo stesso della definizione di antiossidante. Un antiosssidante in una soluzione è una sostanza che si ossida (ovvero accetta elettroni) prima di atre sostanze in soluzione. Il punto è che semplicemente non esistono antiossidanti puri, la maggior parte delle molecole in particolari condizioni diventa a sua volte ossidante, cioé ricede le specie radicaliche. Il punto quindi non sta nemmeno nell'ossidazione in sé, ma in che misura alcune sostanze interrompono la cascata ossidativa. (una specie ossida una specia che a sua volta ne ossida un'altra e un'altra ancora, ripetutamente). l'acido ascorbico, ad esempio, che non è una fitoalessina né un polifeoloha si comporta come riducente (ossidandosi) ma può a sua volta ossidare e ciò nonostante non può essere considerato un veleno in accordo con LD50.
L'effetto ormetico inoltre è solo un piano d'analisi che non esaurisce l'effetto farmacologico dei fitonutraceutici, che interagiscono su più livelli biomecolare (le chiamano dirty molecules perché interagiscono con vari tipi di proteine con funzini differenti.). Pure, va precisato, le molecole vengono metabolizzate a livello epatico ed intestinale in metaboliti secondari, e non si sa con esattezza se siano questi ultimi o le prime ad essere responsabili degli effetti farmacologici.


in merito alla quercitina non si possono non citare i più recenti studi in biotecnologie.
http://dx.doi.org/10.1016/j.mad.2008.07.001
http://www.springerlink.com/content/2g6qn7u258056744/
http://www.ncbi.nlm.nih.gov/pubmed/18024103
http://www.ncbi.nlm.nih.gov/pubmed/17376580
http://dx.doi.org/10.1016/j.exger.2010.07.001
 

juliensorel

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Non e' tutto male cio' che e' alcol, ma moderare e' d'obbligo.

http://www.ncbi.nlm.nih.gov/pubmed/16962100

acetaldehyde significantly reduced mTOR phosphorylation without affecting total mTOR expression.

We also evaluated the effect of acetaldehyde on phosphorylation of 4E-BP1, a signaling molecule downstream of mTOR. Data in Fig. 6 show that acetaldehyde (ACA, 150 ¦ÌM) inhibited 4E-BP1 phosphorylation

Our current study revealed that short-term incubation of acetaldehyde interferes with basal and insulin-stimulated Akt phosphorylation, basal phosphorylation of mTOR and 4E-BP1 but enhanced basal (not insulin-stimulated) p70S6K phosphorylation in the absence of overt abnormality in IRS-2, glucose uptake and cell survival in SH-SY5Y human neuroblastoma cells. These results suggested possible interruption of insulin signal at levels of Akt, mTOR and 4EBP1, which may be countered by some compensating mechanisms leading to enhanced p70S6K phosphorylation and glucose uptake.

Acetaldehyde is the very first metabolic product of ethanol from alcohol dehydrogenase and is considered one of the toxins contributing to the pathogenesis of alcoholic complications due to its high reactivity. The role of acetaldehyde in the neurobehavioral effects of ethanol: a comprehensive review of animal studies. Nonetheless, our data revealed that acetaldehyde may interrupt Akt, mTOR and 4E-BP1 signaling, three critical components in post-insulin receptor signaling cascade, in the absence of overt cell death

 

kaspar hauser

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http://www.livescience.com/health/cancer-fighting-foods-diet-nutrition-100812.html

Interessante. I fondatori della dieta macrobiotica, i coniugi kushi, prolifici scrittori e divulgatori della dieta anticancro (http://www.ibs.it/code/9788827215326/kushi-michio/dieta-per-prevenzione.html)
sono morti di cancro in (relativamente) giovane età.
Per la signora Kushi:
1) donna
2) giapponese

morire a 78 anni di cancro è un risultato piuttosto deludente. La figlia (cresciuta in accordo con i principi della macrobiotica) è morta a 41 anni di cancro.

Morale della favola: se qualcuno ti propone una dieta anticancro mettiti a correre. Se non altro correre, dati epidemiologici alla mano, sembra essere un fattore di prevenzione.
 

kaspar hauser

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x Marlin, appassionato cultore di rimedi fitoterapici:

cardamomo http://www.cryonet.org/cgi-bin/dsp.cgi?msg=32606
cumino http://www.cryonet.org/cgi-bin/dsp.cgi?msg=32583
 

marlin

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Però la macrobiotica è considerata un approccio molto spannometrico e poco sicentifico.

Tanto per fare un esempio i macro aborrono i minerali-metalli, non andate a chiedere sostanze di questo tipo in un punto macrobiotico (io l'ho fatto....). Anche se poi vendono magari piante che li contengono....

http://it.wikipedia.org/wiki/Macrobiotica

Comunque non si confonda il vegetarianismo con questa dieta, anche se hanno punti di contatto.

Il cardamomo l'ho usato come salva alito, funziona, ma vanno bene pure liquirizia e, notoriamente, menta. Proprio ieri mi veniva in mente, perché sto utilizzando aglio marinato e questo quando è preparato bene non da problemi, solo che non sempre si trova preparato a regola d'arte. Dovrebbe infatti essere bollito per almeno 10 min e tenuto sotto conserva per un mese, ma questi tempi sono contro la logica industriale. Diciamo che l'ultimo problema che può restare è appunto un appesantimento dell'alito, da qui il pensiero al cardamomo[:)]

Comunque sono studi che erano un po' nell'aria su questo tipo di piante (apiacee) che ho utilizzato anche topicamente come essenze e che peraltro contengono potenti sostanze volatili che in alte concentrazioni portano a reazioni cutanee avverse (e penso anche a qualche altro problem, tipo sviluppo di tumori, se assunte sistemicamente in dosi esagerate).

Buona comunque la conferma della funzione anti-diabetica, anche perché se restiamo orfani dei polifenoli e non siamo pronti a prendere la metformina, serve una soluzione alternativa [:)]

Ciao

MA - r l i n

 

kaspar hauser

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Vecchia storia, ma da tenere sempre a mente quando si parla di diete e longevità.


Man lives to 112 despite sausage-and-waffles diet
By JEFF WILSON, Associated Press Writer> Friday, September 1, 2006

George Johnson, considered California's oldest living person at 112 and
the state's last surviving World War I veteran, had experts shaking their
heads over his junk food diet.

He had terrible bad habits. He had a diet largely of sausages and
waffles Dr. L. Stephen Coles, founder of the Gerontology Research Group
at the University of California, Los Angeles, said Friday.

The 5-foot-7, 140-pound Johnson died of pneumonia Wednesday at his
Richmond home in Northern California.

A lot of people think or imagine that your good habits and bad habits
contribute to your longevity, Coles said. But we often find it is in
the genes rather than lifestyle.

Johnson, who was blind and living alone until his 110th birthday when a
caregiver began helping him, built the Richmond house by hand in 1935. He
got around using a walker in recent years.

Johnson was the only living Californian considered a
supercentenarian, a designation for those ages 110 or older, Coles
said. His group is now in the process of validating a Los Angeles
candidate who claims to be 112 years old.

Coles participated in an autopsy Thursday that was designed to study
Johnson's health.

All of his organs were extremely youthful. They could have been the
organs of someone who was 50 or 60, not 112. Clearly his genes had some
secrets, Coles said.

Everything in his body that we looked at was clean as a whistle, except
for his lungs with the pneumonia, Coles said. He had no heart disease,
he had no cancer, no diabetes and no Alzheimer's.

This is a mysterious case that someone could be so healthy from a
pathology point of view and that there is no obvious cause of death.

The family was in favor of an autopsy. Relatives said Johnson wanted them
to allow it if it would help science.

Born May 1, 1894, Johnson's father managed the Baltimore and Ohio Railway
station in Philadelphia.

Johnson was working in 1917 as a mail sorter for the U.S. Post Office
when he was drafted into the Xxxxx. The war ended a year later, and he
never served in combat.

Two years later, he and his wife moved to Northern California.

It was a great adventure in those days. We were young and wanted the
experience, Johnson said in a March interview with the Contra Costa
Times.

The couple settled in Fresno and remained there until 1935, when they
bought property in Richmond. They used lumber salvaged from dismantled
buildings to build their house.

During World War II, Johnson worked at the Kaiser shipyard in Richmond
and later managed the heating plant at Oak Knoll Naval Hospital in
Oakland.

He remained in good health and continued driving until he was 102, when
his vision began to fail.

Johnson's wife died in 1992 at the age of 92. The couple had no children.
 

juliensorel

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http://www.youtube.com/watch?v=iU3d-_7FDcA
http://www.youtube.com/watch?v=byQ6l_bjIUo
http://www.youtube.com/watch?v=FtApUZmXA3o
http://www.springerlink.com/content/c428xw01574g50n4/fulltext.pdf

(gli daranno il Nobel, prima o poi per la medicina o per la chimica).
 

kaspar hauser

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Inibizione dell'mTOR = depressione? Se aggiungiamo anche la sarcopenia, il quadro che ne esce è a tinte fosche. Camperemmo 150 anni, ma depressi e sarcopenici ... ouch!

http://www.sciencedaily.com/releases/2010/08/100819141913.htm

Secrets of 'Magic' Antidepressant Revealed
ScienceDaily (Aug. 20, 2010) ‹ Yale researchers have discovered how a
novel anti-depressant can take effect in hours, rather than the weeks or
months usually required for most drugs currently on the market. The
findings, described in the August 20 issue of the journal Science,
should speed development of a safe and easy-to-administer form of the
anti-depressant ketamine, which has already proven remarkably effective
in treating severely depressed patients.
The Yale scientists found that, in rats, ketamine not only quickly
improves depression-like behaviors but actually restores connections
between brain cells damaged by chronic stress.
It's like a magic drug -- one dose can work rapidly and last for seven
to 10 days, said Ronald Duman, professor of psychiatry and pharmacology
at Yale and senior author of the study.
Ketamine traditionally has been used as a general anesthetic for
children, but a decade ago researchers at the Connecticut Mental Health
Center found that, in lower doses, the drug seemed to give patients
relief from depression, Duman said. In these initial clinical studies,
which have been replicated at the National Institute of Mental Health,
almost 70 percent of patients who are resistant to treatment with all
other forms of antidepressants were found to improve within hours after
receiving ketamine. However, its clinical use has been limited because
it has to be delivered intravenously under medical supervision and in
some cases can cause short-term psychotic symptoms. It has also been
used as a recreational drug, known as Special K or sometimes just K.
So Duman, colleague George Aghajanian and the Yale team set out to map
the molecular action of the drug in the prefrontal cortex of rats that
could lead to potential targets for a safer and more easily used drugs.
The team discovered that ketamine acts on a pathway that rapidly forms
new synaptic connections between neurons -- a process called
synaptogenesis.
The pathway is the story. Understanding the mechanism underlying the
antidepressant effect of ketamine will allow us to attack the problem at
a variety of possible sites within that pathway, Aghajanian said.
The team identified a critical point in the pathway, the enzyme mTOR,
which controls protein synthesis required for new synaptic connections.
There are already promising leads on ways to sustain the initial rapid
effect of ketamine by intervening at specific downstream targets.
An estimated 40 percent of people suffering depression do not respond to
medication. And many others only respond after many months or years of
trying different treatments. The authors note that ketamine also has
been tested as a means to rapidly treat people with suicidal thoughts, a
benefit usually not seen until weeks of treatment with traditional
antidepressants.
Other Yale authors of the paper are Nanxin Li, Boyoung Lee, Rong-Jian
Liu, Mounira Banasr, Jason M. Dwyer, Masaaki Iwata and Xiao-Yuan Li.
National Institute of Mental Health, the Connecticut Mental Health
Center and Yale University School of Medicine funded the work.
------------------------------------------------------------------------
Story Source:
The above story is reprinted (with editorial adaptations by ScienceDaily
staff) from materials provided by Yale University, via EurekAlert!, a
service of AAAS.
------------------------------------------------------------------------
Journal Reference:
1. Nanxin Li, Boyoung Lee, Rong-Jian Liu, Mounira Banasr, Jason M.
Dwyer, Masaaki Iwata, Xiao-Yuan Li, George Aghajanian, and Ronald S.
Duman. mTOR-Dependent Synapse Formation Underlies the Rapid
Antidepressant Effects of NMDA Antagonists. Science, 2010; 329 (5994):
959-964 DOI: 10.1126/science.1190287
Science. 2010 Aug 20;329(5994):959-64
mTOR-dependent synapse formation underlies the rapid antidepressant
effects of NMDA antagonists.
* Li N,
* Lee B,
* Liu RJ,
* Banasr M,
* Dwyer JM,
* Iwata M,
* Li XY,
* Aghajanian G,
* Duman RS.
Laboratory of Molecular Psychiatry, Center for Genes and Behavior,
Department of Psychiatry, Yale University School of Medicine, 34 Park
Street, New Haven, CT 06508, USA.
The rapid antidepressant response after ketamine administration in
treatment-resistant depressed patients suggests a possible new approach
for treating mood disorders compared to the weeks or months required for
standard medications. However, the mechanisms underlying this action of
ketamine [a glutamate N-methyl-D-aspartic acid (NMDA) receptor
antagonist] have not been identified. We observed that ketamine rapidly
activated the mammalian target of rapamycin (mTOR) pathway, leading to
increased synaptic signaling proteins and increased number and function
of new spine synapses in the prefrontal cortex of rats. Moreover,
blockade of mTOR signaling completely blocked ketamine induction of
synaptogenesis and behavioral responses in models of depression. Our
results demonstrate that these effects of ketamine are opposite to the
synaptic deficits that result from exposure to stress and could
contribute to the fast antidepressant actions of ketamine.
PMID: 20724638

 

juliensorel

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http://www3.lastampa.it/benessere/sezioni/ricerca/articolo/lstp/309732/
http://www.newsfood.com/q/d637021f/il-riso-nero-piu-antiossidanti-dei-frutti-di-bosco/
 

marlin

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Non ricordo Julien, tu assumi riso nero o solo integrale ? Comunque immagino che la crusca non sia disponibile (almeno da noi).

Ciao

MA - r l i n
 

juliensorel

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il riso nero è un riso solo integrale. al 90 mangio quello o il basmati integrale per il suo G.I molto basso (comparabile a quello della pasta integrale). L'ho trovato oltre che in farmacia da Carrefour, Ipercoop, e finanche librerie coop nella varietà padana coltivata dalla cascina falasco. http://web.tiscalinet.it/AgricolaCirio/venere.htm non mi risulta che vi sia commercio di crusca di riso nero.