[quote name='niner' timestamp='1343568836' post='526370']
I have three that I would really like to see: One is high quality EVOO, to attempt a replication of Baati's extraordinary results feeding Wistar rats a Tunisian Chemlali, which probably qualifies as high quality.[/quote]
I greatly doubt that on two grounds. First, in terms of quality
per se (freshness, flavorfulness; how well the olives were handled and how good the milling technique was), Tunisia has a deserved reputation for producing low-quality oil (tho' of course, there is good oil and bad oil produced everywhere). Second, in terms of healthfulness, Chemlali is a low-phenolic, low-oleic, high-linoleic, (relatively) high-palmitic varietal.
[quote name='Luminosity' timestamp='1363328061' post='572019'][quote name='dasheenster']
Responding to dasheenster:According to
one study, Japanese and British vegetable consumption levels have remained stable over the past 45 years. However, the average Japanese person consumes vegetables with 2 out 3 meals, while the average British person consumes vegetables with only 1 out of 5 meals. [...] I think sufficient evidence to cast doubt on your unsupported claim that "they don't actually eat that many fresh veggies". -- dasheenster[/quote]
According to actual life, where I have been surrounded by Japanese people my whole life, they eat a small amount of pickled vegetables or perhaps little bit of seaweed, or a small amount of raw vegetables as part of some of their meals. By volume they don't actually eat that many vegetables on average. ... Okinawans here are roughly analogous. The amount of vegetables that Japanese nationals eat is probably stable for the last 45 years, it's just low. -- [/quote]The Okinawan diet of today's Okinawans should not be taken as representative of the Okinawan diet that produced record-breaking centenarianship rates: whatever is going on in the rest of Japan, Calories and meat intake have been climbing steeply, and vegetable intake declining, in Okinawa since the 1960s; concomitantly, its edge in life expectancy has faded in sequential Okinawan birth cohorts.(1,3) In 1880,
93% of the Calories in the common people's everyday diet (as opposed to the festival diet, which contained more pork) was Satsuma sweet potatoes.2) The remarkably high incidence of centenarians occurred between the 1970s and the early 2000s, reflecting the diets of the late 19th century up to the 1960s:(1,2) it's not informative to look at what Okinawans eat today. And Okinawan expats have long eaten much poorer diets -- and had much poorer health -- than Okinawan natives.(4)
[quote name='dasheenster']When you say, "they drink a lot of green tea", I have to assume you've looked into the national statistics (and are not merely judging based on Japanese with whom you have personal acqauintence), which reveal a per capita consumption of tea leaves equal to
three cups of tea per week per person? There are many who drink it like water, 8-10 cups per day. But they are balanced out by people who drink only water, or people who prefer coffee to tea. In fact,
Japan consumes half the per capita tea leaves as Britain(1 kg yearly vs 1.9 kg yearly)! And you want to attribute their longevity to tea consumption? [/quote]
In addition to the fact, already mentioned by Luminosity, that the kinds of tea are different, you're each emphasizing the flaw in the other's thinking and thus missing the fact that no matter whether average consumption is high or low, it's
always a mistake to look
per capita rates of consumption of
anything in a given geographical area to draw conclusions about health effects of that single item. The Japanese
as a nation also smoke more than Americans
as a nation and die less of less lung cancer
as a nation: that doesn't mean that smoking doesn't cause lung cancer. This is the problem with the China Study. The question is whether the
individuals with high or low exposure to something (green tea, tobacco) have higher or lower risk of some outcome (lung cancer death, longevity). In a real prospective epidemiological study, you take a group of individuals and ask each of them INDIVIDUALLY about hir dietary and other exposures at time X, and then follow them all up for several years and see their health outcomes; then, you correlate specific exposures to specific outcomes. If you see such correelations (eg, people who consumed more cooked tomato products were less likely to develop aggressive prostate cancer), then because you have a range of other information about EACH of these people as INDIVIDUALS, you can double-check for false positives on an individual-by-individual basis: eg, you can say, "were cooked tomato product users mostly of Italian descent (possible genetic influence)? Were they less likely to smoke, or eat a lot of saturated fat? Did they tend to have their cooked tomato products with salads, or eat more vegetables generally?" Etc. The combination of a prospective design and the existence of a range of info about EACH PERSON'S lifestyle gives such studies great power to test for real causal connections -- not definitive proof, but strong evidence.
Now, I suspect this is actually part of what you mean (and part of what Luminosity is neglecting) when you point out that while some Japanese drink a lot of green tea, they are counterbalanced by those who drink little or none. The question is whether
As I discussed in some detail
earlier in the thread, prospective epidemiological studies do show that people consuming high levels of (Japanese) green tea do live longer, apparently due to lower CVD mortality (and not, notably, cancer).
[quote name='dasheenster']My claim that they are inconsistent is based on the facts that many Japanese today drink tea less than one cup of tea per month, that many of them prefer black or oolong tea, that some pick up or drop the habit of tea drinking in the middle of life, and that there're 40,000 other variables that you can't control during their life which will interfere with the data collection.[/quote]
But that isn't really the question.
[quote name='Kevnzworld' timestamp='1363360367' post='572078']
One of the lifespan tables from the ITP study:
Table 1 Medium
[Sic! -- Median -- MR] Survival for each Intervention pooled across sites for each gender.
Group Males Females
Control 786 (742-826) 866 (832- 891)
Curcumin 808 (744-838) 905 (836-933)
Green Tea 822 (769-880) 923 (887-939 )
Oxaloacetic acid 819 (756-857) 889 (859-937)
Resveratrol 813 (763-863) 907 (871-938)
In the female mice group fed resveratrol, all of the mice lived longer than the medium survival of the controls.
In the female mice group fed GTE , all of the mice survived longer than the longest living control.
I thin that its important to consider that some of the beneficial actions attributed to these supplements may work on maladies that longer lived mammals suffer and die from, like cardiovascular disease and dementia. So one wouldn't expect to see the same longevity benefit in short lived mammals.
Yet given the table and data above....I would STILL rather be a supplemented mouse than a control mouse.
The full study....
http://resveratrolce...ngevitStudy.pdf[/quote]
What's actually notable here is that the control group was abnormally short-lived, not that there was any special longevity advantage too the supplemented group. As I keep hammering at, a normal, well-husbanded, well-fed, genetically-normal, non-toxin-fed colony of mice will live 900 d on average, 1100 max. In their previous,
landmark study on rapamycin, the control females (of the same heterogeneous strain, in the same labs) had a median survivals ranging from 881–895 days at different sites in the consortium (University of Michigan, The Jackson Laboratories, University of Texas Health Sciences Center), and it was acknowledged that there was a problem with short-lved animals in the males at UTexas. Eg. in (8), median longevity of controls was 983 d; max not specifically reported, but from eyeballing, approaching 1400 d).The fact that all of the supplemented groups in
this study lived longer than the short-lived control group is more likely telling us that there was something wrong with the controls (and, possibly, with the colony as a whole), than that there was something beneficial about
all of these supplements.
Additionally:
•Most of the stuff in this study has been tested by others, and has also been found to have no meaningful effect on lifespan. Resveratrol, notably, has now failed to extend lifespan in normal, healthy mice when tested at
six different doses and combinations of ages of onset (including the study currently under discussion, plus (5) and (6)), and also in rats.(7) Curcumin (bioavailability-enhanced microencapsulated curcumin at 1000 and 2000 mg/kg diet) and green tea extract (alone (931 mg/kg food) or in combination with black tea extract and morin (931, 440, 500 mg/kg food, respectively)) both failed in the very competent hands of Dr. Steven Spindler.(8) Indeed, with folks getting excited about not-statistically-significant better-than-short-lived-control median LS from green tea in
this study, Spindler found that green tea extract NS
shortened median LS (median survival, 943 days, vs 983 d in controls (note:
• the numerical differences people are highlighting in the table were not statistically significant IAC (ie, individually likely to be flukes, if indeed there is not a systematic error introduced by the controls being unusually short-lived).
• there was no effect on maximum lifespan.
[quote name='AgeVivo' timestamp='1363389654' post='572169']
@Methos000: indeed the title of the thread is very bad to me. it is great to have some robust proofs of increase mouse lifespan already, even if it is not by 50%. The increase could be tuned with improved dosage and combinations, certainly.[/quote]
I cannot make out what you're trying to say here.
[quote name='AgeVivo' timestamp='1363389654' post='572169']
- the past consumption of tea in Japan is to be compared with the past tea consumption of tea in English. How does it compare? (some say that the milk absorbs much of the tea good content; not sure how true that might be)[/quote]
As Luminosity already noted, green and black teas are quite different in their composition, and probably can't be compared. (Note that, as already mentioned, neither green tea extracts alone nor in combination with black tea and morin extracts had an effect on LS in (8))
[quote name='AgeVivo' timestamp='1363389654' post='572169']- it is possible that extracts tea (including teanine and cafeine) is better for health than tea, but perhaps we should stay with tea as much as possible to avoid other confounding interpretations[/quote]
... or, at least, they should be tested separately. There's pretty convincing evidence that caffeine per se has some health benefits; I'm not nearly so convinced for theanine.
[quote name='Kevnzworld' timestamp='1363400614' post='572203'][quote name='Methos000' timestamp='1363385300' post='572163']Judging by the chart, I'm not sure why this topic contains the words ''More Supplement Failures". These results look at worst like modest successes to me. I wonder what the outcome would be for combinations of all the substances .[/quote]
It makes you wonder if the people who wrote the conclusion for the study, let alone the OP ( a CR advocate ) have a bias or agenda. [/quote]
Compare my reaction
when something actually works.
[quote name='Kevnzworld' timestamp='1363400614' post='572203']Humans die from illnesses that mice never live long enough to get.[/quote]
That isn't really true. Mice get (most of) the same diseases of aging that humans get -- they just get them
at a more rapid pace. If you think about it, saying that
"Humans die from illnesses that mice never live long enough to get" is backward: mice die sooner precisely because they age faster, and thus get the diseases of aging faster. If they didn't age faster and get the diseases of aging faster, they live as long as humans do (unless squished in their cages or eaten by foxes). CR increases their lifespan because it decelerates the accumulation cellular and molecular lesions of aging, and thereby delays or decelerates teh onset and progression of age-related disease.
It's true that mice don't die of some things that humans do die of, but not because they're short-lived: it's because of differing molecular structure of the underlying proteins that make them more vulnerable to disease, or other aspects of metabolism. For instance, wild-type mice don't get atherosclerosis because "rapid murine hepatic LDL clearance results in a total serum cholesterol level of approximately 85 mg/dL, mostly carried as high-density lipoproteins (HDL), a lipid profile significantly different from that of humans."(9) If you had that lipid profile, I doubt you'd get a heart attack in the next 200 years. Another example: the sequence of TTR and amyloid precursor protein in mice is much less vulnerable to misfolding (and causing senile cardiac amyloidosis and Alzheimers') than in humans. But mice do still develop amyloid diseases, neuronal aggregates, and cognitive decline in an age-related manner.
[quote name='Kevnzworld' timestamp='1363400614' post='572203']Illnesses and conditions that these supplements have been shown to address to some degree..[/quote]
... under very artificial conditions that don't tell you much of anything about the natural course of the disease.
[quote name='Kevnzworld' timestamp='1363400614' post='572203']But if I was a mouse, given the chart above, I would be taking all of those supplements.
[/quote]
If I was a mouse, given the chart above, I would be packing my bags for new digs with Spindler.
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More details
here.
7. da Luz PL, Tanaka L, Brum PC, Dourado PM, Favarato D, Krieger JE, Laurindo FR. Red wine and equivalent oral pharmacological doses of resveratrol delay vascular aging but do not extend life span in rats. Atherosclerosis. 2012 Sep;224(1):136-42. doi: 10.1016/j.atherosclerosis.2012.06.007. Epub 2012 Jun 26. PubMed PMID: 22818625.
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