Michael's Quotidian Diet

one more question: which type of green tea do you prefer? what do u think about roobios tea? are there other good teas/beverages with similar properties?

No, I hadn't noticed -- thanks! And my P is already arguably too high ... good catch, thanks. I shall alert Aaron. Are there any other examples?

.....

I take both to hedge my bets, because both have different targets, and because I am too ignorant of the microbiology to know if CMV replicates by the same arginine-dependent mechanism as HSV (see my book on why CMV is bad). The animal evidence for lysine is also superior to that for arginine, as I document. I would be pleased, in general, if lysine were keeping my GH release low; as to the glycemia claim:

No, don't have any other examples. I see that you still take quite a bit of IP6, are you not worried about the phosphate levels (and do you not get enough from your diet?).

Also, what book is this?

First, in case anyone has missed it, I've recently posted my latest supplement regimen.

Second: I don't know how I missed these last ffew posts:
 

aren't macadamia nuts better source of MUFA, with almost zero n-6 (but also more saturated fats)?

 

Yes .
 

one more question: which type of green tea do you prefer? what do u think about roobios tea? are there other good teas/beverages with similar properties?

 

I prefer Japanese sencha, and post-Fukushima, I prefer sources further away from the disaster: Uji, Kagoshima (on the island of Kyushu), or other areas substantially south of Shizuoka. No, I am not going to name a brand ...

[Edit: should read, "The various studies on which health benefits are claimed for"] Rooibos [are] test-tube and-or carcinogen-soaked nonsense; there are no in vivo studies showing actual health benefits in healthy rodents or humans.
 

 

No, I hadn't noticed -- thanks! And my P is already arguably too high ... good catch, thanks. ...

I see that you still take quite a bit of IP6, are you not worried about the phosphate levels (and do you not get enough from your diet?).

"Yes," and "I think no," respectively, tho' it's hard to say. Remember, I consume very, very little grains; also, of course, when it's in my diet it gets bound up with minerals in my food.

 

 

I take both to hedge my bets, because both have different targets, and because I am too ignorant of the microbiology to know if CMV replicates by the same arginine-dependent mechanism as HSV (see my book on why CMV is bad).

Also, what book is this?

 

 

Ending Aging.

Edited by Michael, 29 June 2014 - 03:17 PM.

Lentil Curry

I see you eat quite a lot of lentils and others legumes and no things like pasta.

Is that to reduce methionine, cisteine & leucine ? White Pasta has also low levels ... maybe not so low total methionine+cisteine+leucine/proteins... but -pairing calories- is much lower in proteins than lentils.

Is that to have less glucose & insuline ? White Pasta (welll not too much cooked as it must be done) stimulates lower levels of insuline and has lower glucose index than lentils... specially if well dressed with olive oil and tomato and other vegetables is IMHO a really healty food.... I'm Italian :-)

http://en.wikipedia....i/Insulin_index

Is that finally becouse you are gluten intollerant ?! That is a problem...

I understand to avoid white bread... becouse it's really high both in insuline and glicemic index... but withe pasta isn't IMHO so bad... totally different story.

Tomatos are specially well suited with pasta…

An increase in the acidity of a meal can greatly lower its GI. Increasing the amount of vinegar in a meal, for instance, will affect the glucose response. The addition of sourdough bread to a meal can result in different GIs, depending on its content of organic acids (48). These foods apparently affect the glucose response, at least partially, by slowing gastric emptying. So, should we alert consumers to check how much vinegar they put on their food and how much acid is in their bread?

http://www.ajcn.org/...76/1/290S.short

Edited by brunotto, 02 March 2012 - 05:13 PM.

Rooibos is test-tube and-or carcinogen-soaked nonsense...

Maybe it is nonsense, but carcinogen-soaked? Not so fast. It has been a staple in my extended family (by blood and by marriage) for generations (I am South African), and yet cancer is something completely unknown to us. Nobody has ever gotten cancer, to my knowledge, for generations, despite the tradition of daily consumption of rooibos tea. I know absence of evidence is not evidence of absence, but still this is not what one would expect if we all have been consuming even a weak carcinogen for the past couple of centuries.

Edited by viveutvivas, 02 March 2012 - 06:49 PM.

Michael
With its favorable n-3 to n-6 ratio, have you considered the sacha inchi as a "nut" in your diet rotation? http://en.wikipedia....netia_volubilis

Michael, I'd like to know what your top calorie sources are. Would you be able to rank calorie sources by food groups and/or specific foods. Looks like maybe legumes take first place, then maybe nuts and extra-virgin olive oil, and then perhaps vegetables.

Edited by Brett Black, 19 March 2012 - 02:59 AM.

Michael

Do you prefer a particular type of orange? And what is the average size of the orange (weight in grams or diameter)?

Michael

Do you prefer a particular type of orange? And what is the average size of the orange (weight in grams or diameter)?

blood oranges have the highest level of naringin and hesperidin, if that matters to you.

You seem to eschew saturated fat. What are your thoughts on coconut oil? Just as bad as any other saturated fat source?

You seem to eschew saturated fat. What are your thoughts on coconut oil? Just as bad as any other saturated fat source?

Here is an argument MR wrote a while ago about saturated fat. (for starters)

APBT wrote:
UPDATE: After contacting Amphora Nueva, I was told that a Website was in the works, with on-line sales to follow, stay tuned.....http://www.amphoranueva.com/

Yup, they've been saying that for ~8 months now . IAC, as I said, if you call or contact them on FB, VF will give you client stores in your area, most of which are already set up for online sales.

They're up and runnin' now! http://www.amphoranueva.com/

There are studies suggesting toxicity from Mn in water but not food. Do you worry at all and have you checked your water levels?

To add to our coffee discussion: maybe low-ish doses do have some worthwhile benefits and you could add it somehow? (cut back on a few 100ml dr pepper & gr tea?) Is it possible to do a good extract of brewed coffee w/o the liquid? isn't that pretty much what instant coffee is? (tho, IIRC it may be prepared from unfiltered coffee and have the side-effect of raising cholesterol)

http://www.theheart....on (Prevention)

not really fitting, maybe you could do a lifestyle and(blood)testing thread one day:
what do you think about my idea:
Helicobacter pylori: should we test-and-treat in the very healthy?

do you watch your serum phosphate?

Salt (12 shakes ~900 mg from my shaker; this varies wildly from one to another)

why is this necessarey in your chili?
arent many people cutting back on salt cause of the high sodium

 

Salt (12 shakes ~900 mg from my shaker; this varies wildly from one to another)

why is this necessarey in your chili?
arent many people cutting back on salt cause of the high sodium

 

I will direct you to the post I made earlier in the thread in which I addressed this question.
 

There are studies suggesting toxicity from Mn in water but not food. Do you worry at all and have you checked your water levels?

It does concern me, at least a bit. There are some studies suggesting Mn neurotoxicity from food. Most of these are in neonatal rodents, whose Mn metabolism is apparently not yet properly-developed, but see (1), in humans (weak, case-control, high-Fe interaction probably doesn't apply to me or anyone not eating a ton of red meat). During past efforts, I have found it very hard to meaningfully lower my Mn intake in the context of a vegetarian, grain-averse CR diet.

I haven't had my water tested, Slapping myself on the forehead, I see that Mn is included in my standard municipal water report. Without giving the number of samples taken >:( , it says the samples ranged from ND to 150 ppb. I think this is probably all right: EPA has an aesthetic-based limit (taste and clothes staining) of 50 ppb; "California has set a health-based notification level of 500 ppb" ; New York has a Maximum Contaminant Level for manganese of 300 ppb, and "If iron and manganese are present, the total concentration of both should not exceed 0.5 mg/L [ie, 500 ppb]" (my local tap water Fe tested between ND and 100 ppb).

IAC, most of my water is reverse osmosis (the remainder being run thru' a PUR filter, which AFAIK doesn't attenuate Mn).
 

To add to our coffee discussion: maybe low-ish doses do have some worthwhile benefits and you could add it somehow? (cut back on a few 100ml dr pepper & gr tea?)

Done! I'm now at 1.25 L green tea and 4 C instant coffee (moving from full-caff at the first dose to half-and-half at the second, and decaf at the last two) per day. Beverage regimen is laid out in gloriously anal detail in my supplement regimen, since the beverages are taken concomitantly with pills. Thank you (and Dr. Lyle Dennis) for the evidence-backed encouragement . (And no, the yeast study that is currently at the top of his blog played no role in this transition).
 

Is it possible to do a good extract of brewed coffee w/o the liquid? isn't that pretty much what instant coffee is? (tho, IIRC it may be prepared from unfiltered coffee and have the side-effect of raising cholesterol)

I consume instant coffee, which (when it's been explicitly tested) seems to have the same positive health associations as brewed coffee, and contains "negligible" amounts of the diterpenes responsible for that effect.(2) Starbucks actually puts some pure, finely-ground coffee bean in their Via instant drek, so it must have some, tho' whether it's meaningful or couldn't say.
 

maybe you could do a lifestyle and (blood)testing thread one day:

I wouldn't post my medical records ...
 

what do you think about my idea:
Helicobacter pylori: should we test-and-treat in the very healthy?

It's interesting and well-laid-out. From a relatively brief look, it seems to me that the evidence for a benefit of screening in asymptomatic individuals is fairly modest, and would be reluctant to undergo (or endorse) the implied followup treatment in identified cases (antibiotics and PPI). I have very few risk factors for gastric cancer (including blood type); moreover, my risk factors for H. pylori infection seem to be low. So, I would at least say that I wouldn't do it without clearer evidence of benefit.
 

do you watch your serum phosphate?

In the sense that I look at it and wish it were lower, yes . I don't know what to do about it, tho' clearly dropping the IP-6 supplements would help.
 

You seem to eschew saturated fat.

(I did provide links in my opening post explicitly stating my eschewal, and the reasons for it).
 

What are your thoughts on coconut oil? Just as bad as any other saturated fat source?

More or less, yes. The available data suggests (for mechanistically rational reasons) that coconut oil is less likely to worsen the lipid profile than other saturated oils. That suggests that coconut oil might be less harmful than other saturated fat sources. But putting aside the silly "Polynesians don't get heart disease" "argument," we have exactly zero prospective epidemiology or long-term clinical trials with health outcomes on the stuff. There's no reason to slip your host's Thai coconut curry shrimp to the dog under the table, but there's certainly no evidential basis for treating it like it was health food.
 

Do you prefer a particular type of orange?

Not really: there's usually only only one kind of organic orange available at the store. If there are more, I buy what's cheapest.
 

And what is the average size of the orange (weight in grams or diameter)?

I cut off 80 g of orange no matter how big the orange is to begin with; this is usually about half an orange, tho' again it depends on how big the orange was to begin with.
 

With its favorable n-3 to n-6 ratio, have you considered the sacha inchi as a "nut" in your diet rotation? http://en.wikipedia....netia_volubilis

They've got too much omega-6 for me — and if I did want something with that fatty acid profile, I'd buy walnuts, which (a) are cheaper; (b) are probably more environmentally sound due to economies of scale (and "food miles" — tho' food miles are an extremely unreliable metric); and ( c) are not "exotic health foods." Generally, little real research (prospective epidemiology, or lifelong toxicity or supplementation studies in animals) has been done on foods like these, and also (as some wise person pointed out on the CR list a little while ago) they have generally only ever had their nutritional contents assayed once or twice, often by a party with a vested financial interest, and often the data are unpublished except in promotional materials, giving little idea of whether the data are a representative sample or of regional, seasonal, or other variations (vs. USDA doing such work independently, and often doing multiple samples over several years — eg., most nutrients in the entry for walnuts had at least 7 samples used for testing, and some had as many as 13, and most nutrients for broccoli being based on 20-40 samples).
 

 

Rooibos is test-tube and-or carcinogen-soaked nonsense...

Maybe it is nonsense, but carcinogen-soaked? Not so fast. It has been a staple in my extended family (by blood and by marriage) for generations (I am South African), and yet cancer is something completely unknown to us. Nobody has ever gotten cancer, to my knowledge, for generations, despite the tradition of daily consumption of rooibos tea. I know absence of evidence is not evidence of absence, but still this is not what one would expect if we all have been consuming even a weak carcinogen for the past couple of centuries.

 

Sorry: I phrased that very poorly, and I can fully understand why you'd mistake my intended meaning. I wasn't intending to indicate that rooibos is soaked in carcinogens (any more than that it is raised in test tubes): I was saying that the studies cited to assert that rooibos has all these amazing health properties are based on meaningless data (in vitro studies, and studies of animals coadministered rooibos along with hideous chemicals humans don't actually encounter in their real lives and that in no way reflect the etiology or pathogenesis of "normal," age-related cancer). There is no good evidence that rooibos is good for one's health (and, AFAIK, no good evidence that it's bad for one, either).

That said: as regards your family history: I'm glad your rellies have not come down with the Big C (tho' I don't of course know whether what did kill them was any less ugly), but ... anecdotes, shmanecdotes. Even if rooibos were as carcinogenic as tobacco (and again: I have no reason to think that it is carcinogenic at all!!), it could still be the case that no one in your rooibos-drinking family would have gotten cancer. Even smoking tobacco only leads to cancer in 17.2% of male users and 11.6% of women, and few things in the diet or ordinary lifestyle are as potent a risk factor for cancer as tobacco. My paternal grandfather smoked a pack a day from age 13, and two packs a day most of his senior years; after my grandmother died, he smoked more, and started getting up in the middle of the night for an extra, and he still made it to 93 with no lung cancer. And we all know about George Burns. Maybe your ancestors have good genes; maybe they've eaten some food that neutralizes the (again, purely stipulated for argument's sake) nasty carcinogen in the stuff. Maybe they were just lucky (or unlucky enough to die of something else first. Heck: maybe some of them did die of cancer, and it wasn't diagnosed.
 

A 10-year retrospective study (1986-1995) of all autopsies performed at the Medical Center of Louisiana at New Orleans ... excluding preterm fetuses, ... Of ... 1105 cases, 654 were male and 451 were female. The mean age was 48.3 years (range, 1-98 years). A total of 433 neoplasms were diagnosed, 250 of which were malignant. One hundred eleven malignant neoplasms in 100 patients had been either undiagnosed or misdiagnosed, and in 57 patients, the immediate cause of death could be attributed to the malignant neoplasm. The discordance between clinical and autopsy diagnoses of malignant neoplasms in this study is 44%, which is similar to previously reported studies.

Just to break that down: nearly half of malignant cancers were not identified at time of death, and in 1105 people autopsied, 111 (10%!) died with a cancer no one knew was there -- and 57 of them (more than 1 in 20!) died of that undiagnosed cancer. Now recall that this was in 1986-1995, in the USA. Do you suppose that medical diagnosis of cancers was likely better, or worse, in SA at the time of your relatives' deaths?
 

Cancer remains a major killer throughout the developed and developing world, including South Africa. Cancer incidence rates in South Africa are among the highest reported in Africa. ... Some cancers are suboptimally reported because of a lack of tissue diagnoses. An important example is hepatocellular carcinoma, which is diagnosed clinically and by blood tests (alpha-fetoprotein)—without tissue diagnosis—but still remains among the top 15 most common cancers. Approximately 700,000 new cases yearly are diagnosed worldwide, especially in southern Africa and the Far East, which are endemic for hepatitis B virus. [HebB is rare in the USA outside of immigrant populations from SE Asia and other areas where it's endemic -MR]. Future population-based registries, as well as better cancer diagnoses, especially in rural areas, will give us a more accurate picture of this usually fatal malignancy, as well as other pathologically underdiagnosed cancers.

We really, really need to work to free our minds of the bias introduced into our thinking by our anecdotal observations.
 

I see you eat quite a lot of lentils and others legumes and no things like pasta.

Is that to reduce methionine, cisteine & leucine ?

No: it's because pasta is a high-Calorie, low-volume, low-nutrition carb bomb. [Edit: to be clear, one of the reasons I favor lentils and other legumes as protein sources is the fact that they contain low levels of Met, Cys, and Leu per unit protein. Of course, pasta has even less of these aminos, primarily because it has little protein in it, period. The reason why I avoid pasta and other grain products is because they are "high-Calorie, low-volume, low-nutrition carb bomb[s]."]
 

Is that to have less glucose & insuline ? White Pasta (welll not too much cooked as it must be done) stimulates lower levels of insuline and has lower glucose index than lentils...

http://en.wikipedia....i/Insulin_index

The numbers for the glucose score for these foods in the study from which these data are taken are quite surprising, and discordant from their glycemic index. The glucose score was calculated as 120 minute postprandial glucose AUC per 238 Calories, whereas GI is measured per 50 g of available carbohydrate. Certainly, the glycemic index of red lentils is 18-21, whereas the glycemic index for spaghetti boiled for only 5 minutes (!) is 32, and most entries for spaghetti arel >40. I'm not sure if the GS numbers in this one study were a fluke, or if (for instance) something about the glucagon elicited by the lentils actually drives higher postprandial glucose per calorie than pasta, even though it yields less per gram of carb.

That doesn't, however, mitigate the enormous bomb of total carb in pasta, or the lack of nutrients. Compare the nutritional content of 100 g of lentils and spaghetti, and note that the lentils have 27% fewer Calories.
 

White Pasta ... stimulates lower levels of insuline and has lower glucose index than lentils... specially if well dressed with olive oil and tomato and other vegetables [MR emphasis]

Sure, but the same is true of lentils. You'll note the EVOO in all of my legume recipes (and, indeed, in almost everything I eat), and the tomato products (sauce and salsa) in my chili.
 

An increase in the acidity of a meal can greatly lower its GI. Increasing the amount of vinegar in a meal, for instance, will affect the glucose response.

http://www.ajcn.org/...76/1/290S.short

I'd be interested to see how you're working vinegar into your white pasta recipes . By contrast, nearly all of my legume dishes make very complementary use of organic acids (mostly lemon or lime juice). But actually, despite the promising early data, later studies have found that adding organic acids to foods doesn't actually do much for normoglycemic people, and that most of the effect is lost in meals that are low-GI to begin with:

http://www.nature.co...jcn201089a.html
http://care.diabetes...t/27/1/281.full
http://www.sciencedi...002822305012228
 

I understand to avoid white bread... becouse it's really high both in insuline and glicemic index... but withe pasta isn't IMHO so bad... totally different story.

It's really only a very moderately different story.

References
1: Powers KM, Smith-Weller T, Franklin GM, Longstreth WT Jr, Swanson PD,
Checkoway H. Parkinson's disease risks associated with dietary iron, manganese,
and other nutrient intakes. Neurology. 2003 Jun 10;60(11):1761-6. PubMed PMID:
12796527.

2. Gross G, Jaccaud E, Huggett AC. Analysis of the content of the diterpenes
cafestol and kahweol in coffee brews. Food Chem Toxicol. 1997 Jun;35(6):547-54.
PubMed PMID: 9225012.

Edited by Michael, 29 June 2014 - 03:31 PM.

Michael, would you mind telling us how much you weigh now? In an interview you gave several years ago you reportedly said that at ~6 feet you weighed ~115 lbs. The other burning question is, what is your fasting glucose? I am sure you saw the thread http://www.longecity...ciety-members/. What's your comment?

aren't macadamia nuts better source of MUFA, with almost zero n-6 (but also more saturated fats)?

Yes .

What is your take on this?
http://www.ncbi.nlm....pubmed/23386268

Michael, thank you all the time you put a side to post all this valuable info here. I can see that you drink a fair amount of green tea. I do too, and was looking into what is the best way to brew the tea. Lately I'm doing a "cold brew" especially when preparing the white tea - I just put the tea leaves in a room temperature water for two hours. It seems that cold white tea brewing extracts less caffeine and more antioxidants compared to a standard hot brewing:

Hot vs. cold water steeping of different teas: Do they affect antioxidant activity?

A new popular way of making tea, especially in Taiwan, is to steep leaves in cold water. Here we investigate whether antioxidant activity of teas may be affected by hot or cold water steeping and if this correlates with their polyphenol content and metal-chelating activity. A set of five loose tea samples, consisting of unblended and blended teas, was analysed following their infusion in either hot water (90 °C, 7 min) or cold water (room temperature, 2 h). Antioxidant activity, measured as hydrogen-donating ability, using the ABTS· and DMPD assays, showed no significant differences among hot or cold teas, except in the case of white tea, where significantly higher values were obtained after cold water steeping, a recurrent finding in this study. The antioxidant activity of the teas correlates well with their total phenolic content and metal-chelating activity. Cold teas were, however, generally better inhibitors of in vitro LDL conjugated diene formation and of loss in tryptophan fluorescence. The results of this study contribute to gaining further knowledge on how the potential health benefits of this popular beverage may be maximised by the different methods of preparation.

Link to the study:
http://www.sciencedi...308814609011091

Another study I found shows that recovery of tea catechins significantly improves when mixing green tea with lemon (lime, grapefruit) juice:

Common tea formulations modulate in vitro digestive recovery of green tea catechins.

Abstract
Epidemiological evidence suggests a role for tea catechins in reduction of chronic disease risk. However, stability of catechins under digestive conditions is poorly understood. The objective of this study was to characterize the effect of common food additives on digestive recovery of tea catechins. Green tea water extracts were formulated in beverages providing 4.5, 18, 23, and 3.5 mg per 100 mL epicatechin (EC), epigallocatechin (EGC), epigallocatechin-gallate (EGCG), and epicatechin-gallate (ECG), respectively. Common commercial beverage additives; citric acid (CA), BHT, EDTA, ascorbic acid (AA), milk (bovine, soy, and rice), and citrus juice (orange, grapefruit, lemon, and lime) were formulated into finished tea beverages at incremental dosages. Samples were then subjected to in vitro digestion simulating gastric and small intestinal conditions with pre- and post-digestion catechin profiles assessed by HPLC. Catechin stability in green tea was poor with <20% total catechins remaining post-digestion. EGC and EGCG were most sensitive with less, not double equals 10% recovery. Teas formulated with 50% bovine, soy, and rice milk increased total catechin recovery significantly to 52, 55, and 69% respectively. Including 30 mg AA in 250 mL of tea beverage significantly (p<0.05) increased catechin recovery of EGC, EGCG, EC, and ECG to 74, 54, 82, and 45% respectively. Juice preparation resulted in the highest recovery of any formulation for EGC (81-98%), EGCG (56-76%), EC (86-95%), and ECG (30-55%). These data provide evidence that tea consumption practices and formulation factors likely impact catechin digestive recovery and may result in diverse physiological profiles.


Link to the study:
http://www.ncbi.nlm....pubmed/17688297

Unfortunately, the exact amount of juice they added to the tea (or pH of the tea afterwords) is not available in the abstract. If someone has the access to the full text of the study, please share that info.

Cheers !

Edited by rikelme, 05 May 2013 - 08:54 PM.

I managed to access the "Common tea formulations modulate in vitro digestive recovery of green tea catechins." study. It is too big to be attached, so I'm embedding a graph and some parts of interest:

1 Introduction
Epidemiological studies have associated green tea (Camellia sinensis) consumption with a reduced risk of several chronic diseases including cancer and cardiovascular disorders [1 – 7]. Among the most commonly consumed beverages worldwide, teas and tea mixes could be of great value in reducing disease severity and risk if factors associated with its protective activity are identified. Catechins, including (–)-epicatechin (EC), (–)-epigallocatechin (EGC), (–)-epigallocatechin-gallate (EGCG), and (–)-epicatechingallate (ECG) (Fig. 1), are the most abundant polyphenols in tea accounting for approximately 80% of the flavonoid content of brewed tea. Catechins have attracted the interest of medical and nutritional researchers as their documented biological activities include scavenging of reactive oxygen and nitrogen species, chelation of redox active metals, inhibition of cancer-related transcriptional factors, and inhibition of oxidative enzymes [8 – 12].
A limiting factor is the poor bioavailability of tea catechins resulting from instability under digestive conditions, poor transcellular transport, and rapid metabolism followed by excretion [13 – 15]. Catechin losses of approximately 80%, including almost total degradation of EGCG, have been observed during simulated digestion of simple tea infusions [16]. Instability of catechins in authentic intestinal juice and buffered systems above pH 7.4 has also been previously demonstrated [17, 18], indicating that degradation in the small intestine limits catechin uptake and bioavailability.
While the study of plain tea infusions has been useful in estimating the digestive fate of catechins, tea is commonly consumed in combination with additional ingredients such as sweeteners, juices, and creamers. For ready-to-drink (RTD) tea products, food additives are often included to modify sensory characteristics, provide process and storage stability, and aid in preserving color, flavor, and catechin
content of the finished beverages. Common and effective food additives formulated within RTD tea beverages include citric acid (CA), EDTA, 2,6-di-tert-butyl-4-methyl-phenol (BHT), and ascorbic acid (AA) [19]. Furthermore, milk and citrus juices are increasingly being utilized as adjuncts to RTD and fresh brewed tea products to modify the sensory characteristics of the finished product. While the impact of these common formulation factors on the stability of tea catechins in beverage systems has been investigated, information on their ability to modulate catechin digestive behavior is still unknown.
The specific objective of this study was to determine the effect of common food additives and tea adjuncts on in vitro digestive recovery of catechins from tea in preparation for future assessments of food formulation factors that modulate catechin bioavailability in vivo.
...
2.2 Tea beverage preparation
Powdered green tea extract (A gift from Nestle R & D, Marysville, OH, USA) was dissolved in boiling water (1008C) to provide l50 mg total catechins per 100 mL and combined with prescribed amounts of AA (6 – 80 mg/ 100 mL), EDTA (1 – 100 mg/100 mL), CA (12 – 80 mg/100 mL), and BHT (0.5 – 10 mg/100 mL). Citrus juices (grapefruit, lemon, lime, and orange) and creamers (bovine, rice, and soy milks) were prepared at 10, 20, and 50% (v/v) displacing water in the formulation and maintaining constant catechin levels between formulated and plain green tea preparations. Total AA content of each juice was determined by the 2,6-dichloroindophenol titration method and total solids of creamers and juices was determined by microwave moisture analysis (CEM Smart System 5, Matthews, NC) as previously reported [20]. Creamers were further analyzed for phenolic acid (methanol extract) and protein content using the Folin-Ciocalteau and Bicinchoninic acid (BCA) methods, respectively [21].
...

3.3 Impact of citrus juice on catechin digestive recovery
The impact of common tea adjuncts on digestive recovery of catechins from green tea was investigated by formulating green tea preparations with citrus juices (grapefruit, lemon, lime, and orange) prior to in vitro digestion. Juices were prepared and formulated from 10 – 50% (v/v) displacing water in the formulation in order to maintain constant catechin levels between formulated and plain green tea preparations. For citrus juices, significant increases in individual and total catechin recoveries were noted with increased level of juice in the formulations (Fig. 5). Significant increases in individual catechins were generally noted after addition of 20 and 50% juices and were most notable among the relatively instable EGC and EGCG. Maximum total catechin recoveries were observed for lemon (77.9 l 2.9%)
followed by orange (71.2 l 1.5%), lime (67.1 l 6.8%) and grapefruit juice (62.3 l 4.1%) at the 50% juice relative to the RM values. With the exception of orange juice, the AA content (Table 1) appears to account for only a small percentage of the observed enhancement in digestive recovery of catechins in tea-juice formulations (Fig. 6) indicating that other factors from juice may be responsible, in part, for
observed digestive stabilization. Other components such as flavonols (kaempherol, myricetin, quercetin), flavanones (hesperetin, naringenin), or terpenes (d-limonene) are known to be abundant in citrus juices [34 – 36]. These phytochemicals may be capable of stabilizing catechins by quenching catechin free radicals formed under high pH conditions of the small intestine or indirectly by synergistically sparing AA from oxidative damage. While, possible the extent to which specific citrus polyphenols may stabilize digestive catechin reactions is still unknown and remains to be investigated.
Furthermore, juices also contain a small amount of natural proteins, of which have potential to interact strongly with polyphenols [37] physically trapping individual catechins and limiting their availability for reaction. Nondigestible fiber and polysaccharides present in the fresh squeezed juices may also prove to aid in recovery of catechins with similar mechanistic approaches. Further analysis of the specific component and combinations on tea catechin recoveries remains to be completed.

Edited by rikelme, 07 May 2013 - 07:12 AM.

You seem to eschew saturated fat. What are your thoughts on coconut oil? Just as bad as any other saturated fat source?

Here is an argument MR wrote a while ago about saturated fat. (for starters)

This is a very poor condemnation of SFA, IMO, and lacks any meat. His one tentpole study against SFA is based on a Mediterranean diet, in which the study authors say is low in both SFA and PFA. We KNOW PFAs are bad for humans and cause CDV -- I even provided links in the comments section of MR's blog post.

Saturated fat has been in hominid diets for nearly 2 million years. It wouldn't make sense that we are not adapted to SFAs, because that would mean we are not adapted to meat.

These things are not in question anymore:

o Most plant oils are inflammatory, and pro-CVD. (Yet, the medical community still promotes these oils as heart healthy, based on the false assumption that lowered LDL is CDV friendly.)

o Saturated fats are healthy, and in fact necessary to good human health. (Yet, the medical community still promotes saturated fat as potentially artery clogging, despite zero evidence. The evidence has always been indirect, misunderstood evidence, based on false assumptions, such as the raising of total cholesterol.)

o Grains are inflammatory to humans, mostly because of lectins and gluten. We are not adapted to grain consumption. (Yet, the medical community still promotes "whole grains" healthy, mostly based on the obviously biased USDA recommendations.)

o Hominids began eating meat at some point roughly 1.7 million years ago, and it's the consumption of nutrient and calorically dense meat (note that practically all plant foods are naturally low in nutrients and calories, which is why vegetarian animals must eat practically all day) that allowed us to develop metabolically expensive bigger brains, by allowing our digestive plumbing to shrink in size accordingly. This is a required trade-off based on Kleiber's Law: (good explanation here: http://tinyurl.com/m59rwx)

o Given that humans are adapted to eating meat, it doesn't make sense that eating meat would be unhealthy. No meat-eating wild animals that eats meat develops CVD. Studied hunter-gather groups that eat meat not develop CVD.

o An estimated 70% of calories most American's consume come from sources that didn't exist 10,000 or so years ago, such as processed plant oils, processed sugar, and grains. All three of these are known to be unhealthy to humans.

Edited by DukeNukem, 08 May 2013 - 09:29 PM.

You seem to eschew saturated fat. What are your thoughts on coconut oil? Just as bad as any other saturated fat source?

Here is an argument MR wrote a while ago about saturated fat. (for starters)

This is a very poor condemnation of SFA, IMO, and lacks any meat. His one tentpole study against SFA is based on a Mediterranean diet, in which the study authors say is low in both SFA and PFA. We KNOW PFAs are bad for humans and cause CDV -- I even provided links in the comments section of MR's blog post.

Saturated fat has been in hominid diets for nearly 2 million years. It wouldn't make sense that we are not adapted to SFAs, because that would mean we are not adapted to meat.

These things are not in question anymore:

o Most plant oils are inflammatory, and pro-CVD. (Yet, the medical community still promotes these oils as heart healthy, based on the false assumption that lowered LDL is CDV friendly.)

o Saturated fats are healthy, and in fact necessary to good human health. (Yet, the medical community still promotes saturated fat as potentially artery clogging, despite zero evidence. The evidence has always been indirect, misunderstood evidence, based on false assumptions, such as the raising of total cholesterol.)

o Grains are inflammatory to humans, mostly because of lectins and gluten. We are not adapted to grain consumption. (Yet, the medical community still promotes "whole grains" healthy, mostly based on the obviously biased USDA recommendations.)

o Hominids began eating meat at some point roughly 1.7 million years ago, and it's the consumption of nutrient and calorically dense meat (note that practically all plant foods are naturally low in nutrients and calories, which is why vegetarian animals must eat practically all day) that allowed us to develop metabolically expensive bigger brains, by allowing our digestive plumbing to shrink in size accordingly. This is a required trade-off based on Kleiber's Law: (good explanation here: http://tinyurl.com/m59rwx)

o Given that humans are adapted to eating meat, it doesn't make sense that eating meat would be unhealthy. No meat-eating wild animals that eats meat develops CVD. Studied hunter-gather groups that eat meat not develop CVD.

o An estimated 70% of calories most American's consume come from sources that didn't exist 10,000 or so years ago, such as processed plant oils, processed sugar, and grains. All three of these are known to be unhealthy to humans.

I agree with the rationale of all your points Duke, and in the opposite corner of the argument most of the rationale for fat=bad cholesterol=bad is specious and built upon the foundation of viral memes that have infiltrated large segments of the medical community, however, I think what Michael would like to see (especially with regards to coconut oil), is more population studies or some large double blind studies showing neutral or beneficial effects.

One other point of "rationale", it would seem odd that saturated fat would be the worst, unholy, toxic, disease-promoting macro nutrient known to man, when it is our body's preferred method of storing excess energy. If it was so god awful for health, you would think we would have quickly evolved some other method of long term caloric storage. I know it is unhealthy to carry around too much white adipose tissue, and that our ancestors perhaps did not live long enough to feel negative effects from storing too much fat, however, is it actually the "fat" that is the problem, or the fat cells that store it? Is saturated fat extra-super-duper-bad for health outside of the context of it being stored to excess in tissues?

I find it strange when discussions on saturated fat come up here and Apo E genotype isn't mentioned at all. Saturated Fat = very bad for Apo E 4/4 people, and probably isn't that great for many 3/4 people. So overlooking population studies, evolutionary theory, whatever ... the simple fact remains that about 25% of the population doesn't do that great with saturated fats. Saying things like saturated fats are healthy, may be true for some (that is a different debate) ... I just don't like blanket statements that seem to imply it's great for everyone.

Nameless, what are the negative health effects of saturated fat on people with ApoE, which is about 14% of the population, based on what I've read?

Based on this study, LDL is increased given a higher saturated fat diet:
http://www.ncbi.nlm....pubmed/18494374

Is this the primary concern?

Higher levels of LDL, higher incidents of CVD, stroke etc ... so yep, that is a concern. ApoE 4/4 (and 3/4 to a lesser extent) also have increased risks of alzheimer's, although I am not sure if fat intake plays a role.

I am not sure where the 14% number came from. From what I recall, it's about 20% 3/4 and 5% 4/4. I don't think 2/2s do that great with fats either, although they are sort of rare.

Saturated Fat = very bad for Apo E 4/4 people, and probably isn't that great for many 3/4 people. So overlooking population studies, evolutionary theory, whatever ... the simple fact remains that about 25% of the population doesn't do that great with saturated fats

This also brings up a point for discussion. How many past population studies involving saturated fat controlled for ApoE 4/4 and 3/4 people? None, I would venture to guess, which might skew the results negative, based on genetics, not because the macro nutrient (SFA) is "bad".

Edited by Mind, 10 May 2013 - 05:27 PM.

I've not seen any study evidence that Apo 4/4 or 3/4 plus saturated fat equals reduced lifespan. Higher LDL is the canard that drives the useless statin industry. Whenever anything is seen as bad just because it raises LDL, MUCH more digging is required: What type of LDL does it raise? If it's the large particle LDL, then that's a GOOD thing. (Saturated fat raises large particle LDL, and also HDL.)

So, I'm still waiting for something that shows saturated fat is actually bad for people with these ApoE alleles.

This study shows that the LDL receptor is required for ApoE4 to induce atherosclerosis, while ApoE3 doesn't induce atherosclerosis either way. You may argue that it's the sugar content of the diet inducing the atherosclerosis, but this still shows that it's mediated through LDL, and is much worse in ApoE4. There are a number of other studies that can probably fill in the gaps, but I think this is a good start.

As an aside, I'd recommend focusing on LDL particle count rather than size, as size generally only alters atherosclerotic activity through its relation to particle count. That is, larger particles for same concentration of means lower particle count.

Apolipoprotein E4 in Macrophages Enhances Atherogenesis in a Low Density Lipoprotein Receptor-dependent Manner

http://www.ncbi.nlm....pubmed/17234631
http://www.jbc.org/c...1/7817.full.pdf

and the diet info, since people will ask (pdf link in page)
http://www.harlan.co..._research_diets

What brand of Brewers yeast do you get? Ive been trying to increase my folate intake and thought this may be a good source.

Michael, why do you prefer flaxseed oil over flaxseeds?

What does COM stand for? Useful to explode acronyms, like papers do for the first time it is used in any post and then can acronymise it after.