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mccoy

Low fat and tocopherols

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Hi everyone,

I wonder how you meet the tocopherol requirements when on a low-fat diet. Last week I averaged 32% fats, wich is not very low (but low for me) and I was only at 95% vitamin E requirement.

I'm eating very few almonds and less EVOO now than usual. I'm planning to eat routinely maybe 20 grams of sunflower seeds to hit the full target.

What makes me wonder though is that with 10% fats it would appear just impossible to meet vitamin E requirements naturally. 

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Leafy greens such as spinach and from brassicas I think are the richest low fat sources.  Doable calorie wise but not volume wise for me.  I normally get much of my vit. E from high fat foods such as seeds, nuts and avocados.  I think wheat germ oil is much richer in vit. E. per gram of fat then those whole food sources and might help the fat phobic make goal.  But I just take a weekly high quality mixed tocopherols supplement during periods of restriction when I come up significantly short.

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Thanks Todd, true enough, I just veryfied that some vegetables like spinach and turnip greens, which I ate tonight,  have a fat fraction very rich in tocopherols. Kiwifruit also appears to be a contributor, if eaten in largish amounts. I reckon that's just one of the aspects one must learn to manage if on a really low fat diet. But I've been nonplussed for a couple of days, seeing my cronometer bar remaining on the yellow...I also bought two bags of sunflower seeds, just to be on the cautious side.

I'll carry out some simulations in cronometer though, to ascertain if a strict 10% fat diet, 1800 kcal for example, can provide enough vitamin E or if supplementation is necessary.

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According to cronometer 5 grams of wheat germ oil provides 50% of daily vit. E for only 45 fat calories of a daily 180 fat calories of 1800 cal at 10% fat.  Add 5 g each of sunflower seeds, almonds and evoo and you would be at 75%.  Add in 200 g spinach and you've got 101% of daily vit. E and another 5 grams of fat to squander as you please.

 

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This is the results of my first attempt of a cronometer simulation. Tocopherols are not a problem with spinach and whole grain breads, but to fully hit the target of 10% fats the only fat foot allowed is...one small almond!!! No kidding, numbers speak by tehmselves. I wonder if there are really people, aside Dr. Mc Dougall, who are able to follow such a diet. 10% fats, 18% protein, 72% carbs 

I included nonfat greek yogurt for protein, without that maybe a 10% fats, 10% protein may be achieved.

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Edited by mccoy

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The major contributors of the fat quota, 19.5 grams, are the breads (wheat and buckwheat), garbanzo beans, spinach. No room for oils, seeds, nuts, except a single small almond, is left. This is an example of an extreme diet which may be justified by particular targets. both omega 3s and omega 6s are far below the RDAs. According to cronometer the only supplementation in addition to the polyunsaturated fats would be B12, D, calcium, maybe choline.

by excluding breads and incuding more simple sugars we may perhaps make room to very few oils, maybe...

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2 hours ago, mccoy said:

but to fully hit the target of 10% fats the only fat foot allowed is...one almond!!!

Careful!!!  DON'T eat the entire almond!  Your Cronometer plan allows for 1 g almond.  A typical almond weighs 1.2 g.

 

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4 hours ago, Todd Allen said:

Careful!!!  DON'T eat the entire almond!  Your Cronometer plan allows for 1 g almond.  A typical almond weighs 1.2 g.

 

Right, I edited the post: one small almond

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Broccoli sprouts are rich in E. Asparagus, too. And of course, Almonds.

Here is my Cronometer from yesterday, 25% fat intake, 61% carbs (285% of daily recommended fiber) and 13% protein.

The fat is mostly from:

Flax seeds, not fortified: 16%

Walnuts: 13%

Cacao Nibs: 12%

Avocado: 10%

Almonds, raw: 7%

Black gram, quinoa, black rice, black lentils: 3%

Steel cut oatmeal: 2%

 

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Edited by Ron Put

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Ron, 25% fat is a reasonable amount, far above the extremes of 10% suggested by Dr. Esselstyn and Mc Dougall, and as you show it provides ample tocopherols and more than meets the omega 3 and 6 requirements.

It seems that a 10% fat diet cannot allow nuts and oils (unless nonfat carbs-simple sugars- are eaten in abundance).

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Yeah, I am not on a low fat diet, although as I mentioned elsewhere, I cut out extra virgin olive oil from my daily intake (now I eat it when my willpower fails me at an Italian restaurant, maybe a couple of times a month, and at home another couple of times). In fact, the reason I cut out EVOO is because my diet was already heavy on fat, from nuts, , cacao nibs, avocados and whole grains. Now I hover between 20% and 35% on most days. My total cholesterol has dropped, while my my HDL has shot up, so I am happy with the change (and my doctor is impressed :)

But I also don't have cardiovascular issues. I can see the reasoning for an extremely low fat diet for someone who already has been diagnosed.

I think munching on ample quantities of sprouted broccoli seeds, asparagus and spinach would supply enough vitamin E without the fat. And yams.

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Ron, of course the result in your own example of dropping EVOO is positive, but it should be investigated if it is an individual, atypical reaction, we are talking a n=1 case after all.

Even in VLF diets, no nuts no oils, some people exhibit high cholesterol and have to take statins (as per Dr. Esselstyn reports in one of his podcasts). Often lipids homeostasis works (or goes wrong) independently of the kind and amount of lipids we eat...

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12 hours ago, mccoy said:

Often lipids homeostasis works (or goes wrong) independently of the kind and amount of lipids we eat...

Nor is there consensus about what aspects of a lipid profile are most important.  What is most commonly measured and calculated in standard lipid panels doesn't have tight correlation to healthspan or lifespan.  There are studies showing reduced all cause mortality in some populations with increasing LDL-C at levels well above those considered ideal.  I haven't seen any evidence that centenarians have low or even normal cholesterol and some evidence among small samples of elevated cholesterol such as https://www.sciencedirect.com/science/article/abs/pii/0167494396869676

I heard in a podcast that in the NHANES data all 5 of the people who have so far survived past 100 each had LDL-C greater than 130 mg/dl upon entry into the studies when they were in their 70s or younger..

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I don't want to turn this into another argument about EVOO, but as I stated elsewhere, I made the dramatic reduction in my EVOO intake precisely because I did some research. For me, the studies clearly showed that EVOO is better as a replacement for animal fats, but that it is still relatively unhealthy if just adding to overall fat intake. So I reduced EVOO quite dramatically and my profile improved accordingly. It's true that my case is n=1, but my case was built on information and studies I deemed reliable and convincing.

Anyway, to each their own. Back to the topic at hand:

Here are my numbers from yesterday, without trying to hit any particular targets on purpose. But I hit 100% vitamin E without almonds. I was unaware that scallions have so much vitamin E -- they are seriously up there as a wonder food :)

Now, my fat intake was still 23%, with 62% carbs (349% of recommended fiber) and 16% protein (beans and a bit of tempeh, and also the scallions are chockfull of it!). Usually mushrooms and legumes are responsible for  most of my protein calories.

But I guess my point is that it wouldn't be so difficult to get your tocopherols from veggies like sprouted broccoli seeds, scallions, asparagus, peppers, etc., without the fat.

As to the centenarians comparison with 50-something controls, all I can say is that their elevated Lp(a) levels may simply be a sign that they are more likely to die in the next few years than the 50-somethings.... :) 

Lp(a) levels vary wildly among individuals and populations (Africans have about 3x the levels of Asians, for example), but in general,  it's pretty well established that significant elevation from baseline is an predictor, independent from LDL, of higher risk for a whole bunch of calamities.

Similarly, extrapolating from 5 subjects is like extrapolating that smoking is good for us, because Jeanne Calment smoked until she was 119 :)

CORRECTION:

Just noticed that I had screwed up my scallions count and had input 11 large ones instead of 4 medium ones :(

So, scallions are great, but not enough to supply all that much vitamin E. But a couple of red bell peppers and some sprouted broccoli seed will get you over the daily recommended dose :)



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Edited by Ron Put
Correction

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Today  I ate an all-time low of 8% fats, but that just because I was out and only included 5 grams pistachios, 5 grams 85% chocolate as fatty foods. 1700 kCAl, 62%carbs, 30% protein, 8% fats. 2% RI omega3s, 19% RI omega 6, 10% tocopherols. All that protein was a lot of nonfat yogurt, I was thirsty and on the go, and that food is very digestible. Carbs mainly watermelon, honey, some weetabix, some oat bran, 3 prunes. Anyway, not a representative day and one full of deficiencies in nutrients.

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Just having some fun with cronometer and showing that a CR, VLF healthy diet is practically impossible to achieve. This because it appears impossible to hit the low fat target and at the same time satisfy both the omega-3 and the omega-6 requirements. 10% is too low. I don't know what would happen with a diet like this, maybe nothing, maybe some serious issue... 10% fats, 13% protein

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My understanding is that very low fad diets are to address very specific existing health conditions and are not aimed at the general population, or to improve longevity in healthy subjects, as CR aims to do. I've met a couple of people who are on those -- a dentist friend of a friend I met recently told me he has been on a 10% fat diet for well over a decade, but he had had some serious CV health issues before that.

Actually, the traditional Okinawan diet (non-existent today) which was well-studied, included less than 10% fat and protein, and over 80% carbohydrates (mostly from purple potatoes and greens). So, it's effectively a VLF diet.

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4 hours ago, Ron Put said:

Actually, the traditional Okinawan diet (non-existent today) which was well-studied, included less than 10% fat and protein, and over 80% carbohydrates (mostly from purple potatoes and greens). So, it's effectively a VLF diet.

Yes, but as far as I remember, many micronutrients did not reach their RDAs. It may happen nothing, it may be pretty risky in the case the individual is in the higher percentiles of requirements.

Also, now I wonder where the people who follow the 10% fat diet take their omega 6s. Everything else may be supplemented, maybe it's better to eliminate flaxseeds, supplement DHA and eat only omega6s, to approach the requirement. I also wonder how much fat there is

4 hours ago, Ron Put said:

I've met a couple of people who are on those -- a dentist friend of a friend I met recently told me he has been on a 10% fat diet for well over a decade, but he had had some serious CV health issues before that.

I also wonder if the numbers are accurate 10% maybe stands for a more realistic 15-20%. Not many people are able to eat such a fatless diet aside from fruitarians. 

 

 

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And, getting back to tocopherols, Al Pater has just posted a link on an article underlining the protective effects of such micronutrients. Since now I'm eating less fats, I'm being very careful on this now. Although probably cronometer underestimates the tocopherols contained in EVOO, with respect to the Hi-P EVOOs this community usually consumes.

Posted by al Pater:

Quote

Relationship Between Serum Alpha-Tocopherol and Overall and Cause-Specific Mortality.
Huang J, Weinstein SJ, Yu K, Männistö S, Albanes D.
Circ Res. 2019 Jun 21;125(1):29-40. doi: 10.1161/CIRCRESAHA.119.314944. Epub 2019 May 6.
PMID: 31219752
Abstract
RATIONALE:
Although there has been a long-standing interest in the human health effects of vitamin E, a comprehensive analysis of the association between circulating vitamin E and long-term mortality has not been conducted.
OBJECTIVE:
Determine whether serum α-tocopherol (the predominant form of vitamin E) is related to long-term overall and cause-specific mortality and elucidate the dose-response relationships with better quantification of the associations.
METHODS AND RESULTS:
We conducted a biochemical analysis of 29 092 participants in the ATBC Study (Alpha-Tocopherol, Beta-Carotene Cancer Prevention) that originally tested vitamin E and β-carotene supplementation. Serum α-tocopherol was measured at baseline using high-performance liquid chromatography, and during a 30-year follow-up we identified 23 787 deaths, including deaths from cardiovascular disease (9867), cancer (7687), respiratory disease (2161), diabetes mellitus (119), injuries and accidents (1255), and other causes (2698). After adjusting for major risk factors, we found that men with higher serum α-tocopherol had significantly lower all-cause mortality (hazard ratios=0.83, 0.79, 0.75, and 0.78 for quintile 2 (Q2)-Q5 versus Q1, respectively; Ptrend<0.0001), and significantly decreased mortality from cardiovascular disease, heart disease, stroke, cancer, respiratory disease, and other causes, with risk reductions from 17% to 47% for the highest versus lowest quintile. The α-tocopherol association with overall mortality was similar across subgroups of smoking intensity, years of smoking, alcohol consumption, trial supplementation, and duration of follow-up. The association was, however, significantly modified by baseline age and body mass index, with stronger inverse associations for younger men and men with a lower body mass index ( Pinteraction≤0.006).
CONCLUSIONS:
In this long-term prospective cohort study, higher baseline serum α-tocopherol biochemical status was associated with lower risk of overall mortality and mortality from all major causes. Our data support the long-term health benefits of higher serum α-tocopherol for overall and chronic disease mortality and should be replicated in other more diverse populations.
KEYWORDS:
epidemiology; mortality; multivariate analysis; risk factors; vitamin E

 

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And this is a really 1800 kcal VLF diet, fruitarian, 4% fats, which may avoid a lack of tocopherols and phylloquinone, by eating an unordinate quantity of kiwifruit: 1 kg per day. Main deficiency is amminoacids. As weird as it may seems, some people try to manage diabetes with this. To overcome amminoacid deficiency, twice the quantity would be necessary, almost 7 kg per day, 3600 kcals.

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On 6/25/2019 at 2:20 PM, mccoy said:

Yes, but as far as I remember, many micronutrients did not reach their RDAs. It may happen nothing, it may be pretty risky in the case the individual is in the higher percentiles of requirements.

...

I also wonder if the numbers are accurate 10% maybe stands for a more realistic 15-20%. Not many people are able to eat such a fatless diet aside from fruitarians. 

 

 

As far as fat intake, it was even lower that 10%.

I don't have the time to search more now (I posted an exhaustive study comparing animal protein to plant protein effects elsewhere, which discussed the Okinawan diet in some detail), but this is consistent with what I recall:

"In percentages, that’s 85 percent carbs, 9 percent protein and 6 percent fat, including 2 percent saturated fat."
https://www.msn.com/en-us/health/nutrition/okinawa-diet-what-is-it-and-what-are-its-health-benefits/ar-BBW1CuO

About 70% of the carbs came from mostly purple potatoes and the diet likely had deficiencies, especially in proteins (which recent studies suggest may promote longevity).

There is a lot of nonsense from the meat and dairy folks touting the post- mid-1960s Okinawan diet, which dramatically changed as they became wealthier and started consuming among the highest percentage of animal protein in Japan. Perhaps this change was somewhat OK for the already old geezers who had spend their lives on the old plant-based, low protein diet, and may have benefited from higher protein intake in their old age, but it didn't do much good to the younger Okinawans, who now have relatively high (for Japan) obesity and diabetes rates.

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Mccoy: Just having some fun with cronometer ...

I'm wondering how you factor in critical  absorption/bioavailability issues.  And if you don't,   how much does that detract from the usefulness of your highly detailed and precise nutrient intake calculations?

Edited by Sibiriak

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Vitamin E Bioavailability: Mechanisms of Intestinal Absorption in the Spotlight

Antioxidants (Basel). 2017 Dec; 6(4): 95.
PMID: 29165370
 

 

Quote

 

3.5. Factors Modulating Vitamin E Absorption by the Intestinal Cell

As for vitamin E transfer to mixed micelles, numerous factors can influence vitamin E transport across the intestinal cell, which likely explains the important variations observed regarding vitamin E absorption efficiency. Indeed, different studies report efficiency in ranges of 10–95% [70,71,72]. However when deuterium-labeled vitamin E was used to assess absorption, this range was reduced to 10–33% [73].

The intestine does not seem to specifically discriminate between vitamin E stereoisomers [74], or between α- and γ-tocopherol [30,75]. However, a study found a higher absorption of α-tocopherol compared to γ- and δ-tocopherol in lymph-cannulated rats [76], which is consistent with the existence of a ω-hydroxylase that preferentially metabolized these two last vitamers in 3′ and 5′ carboxychromanol metabolites that can be excreted in the urine [77].

The food matrix can also influence specifically this step of vitamin E absorption. The presence of fibers did not modify vitamin E absorption in humans [78,79]. Conversely, lipids can be classified as effectors of vitamin E absorption as they can promote chylomicron formation. It is interesting to note that a minimal quantity of fat of 3 g was required for an optimal tocopherol absorption, and that increasing further this amount did not led to a better vitamin E bioavailability [80]. This was partly confirmed in another trial where α-tocopherol-acetate was almost negligible when ingested with 2.7 g fat [81]. However, these data are conflicting with other studies showing that the higher the amount of fat, the better vitamin E absorption [73,82], or conversely that dairy fat from whole milk does not increase vitamin E absorption compared to low-fat milk [83].

Mono and polyunsaturated fatty acid seem to promote vitamin E absorption compared to saturated fatty acids in cockerels [84] and in Caco-2 cells [85]. Conversely, phosphatidylcholine decreased α-tocopherol absorption efficiency in rats [86,87], an effect that was reversed by the presence of lysophosphatidylcholine [86]. Authors suggested that vitamin E was associated with phospholipids, leading to a low uptake. As we showed that the presence of phosphatidylcholine in mixed micelles was associated with a decreased binding of mixed micelles on scavenger receptor extracellular loops [52], we suggest that neutral phospholipids can also impact vitamin E absorption by modifying micellar interaction with the membrane proteins responsible for its uptake.

We showed that α-tocopherol E could compete for absorption with other lipid micronutrients such as γ-tocopherol and carotenoids [30,88], as well as vitamin A, D, and K [65] in Caco-2 cells. Except for vitamin A, these competitions are presumably due to common uptake pathways involving cholesterol transporters. Vitamin A uptake mechanisms are still unknown. However, it has been hypothesized that vitamin E was protecting vitamin A against oxidation in the intestine, leading to vitamin E degradation and reduced absorption in chickens [89]. Polyphenols such as naringenin could also reduce vitamin E uptake in Caco-2 cells [88]. The underlying mechanisms still need to be resolved, but we can suggest that polyphenols can impair (micro) nutrient absorption by interfering with membrane protein functioning, as previously shown with digestive enzymes [90]. Although this is still debated [91], a study showed that phytosterols (2.2 g per day during 1 week) could inhibit vitamin E absorption in normocholesterolemic subjects [92].

Finally, it is noteworthy that genetic factors including polymorphisms in genes coding for vitamin E and lipid intestinal metabolism such as SR-BI, CD36, ABCA1, ABCG1, or apoB have been associated with a modulation of vitamin E bioavailability in humans [93].

 

 

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The dose-response effects of the amount of oil in salad dressing on the bioavailability of carotenoids and fat-soluble vitamins in salad vegetables

Agatha Agustiana Iowa State University  Thesis 2010

https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=5084&amp;context=etd

 

Quote

The minimal amount of dietary fat necessary to optimize the bioavailability of fat-soluble nutrients from vegetables is currently controversial. Inclusion of as little as 3 g of fat was needed for optimal absorption of a carotenoid and tocopherol supplement ingested in the form of a margarine spread (Roodenburg et al., 2000). In a 12 week intervention study in Phillipino children, optimal absorption of provitamin A carotenoids from cooked carrots, squash and green leafy vegetables was achieved with only 2.4 g of fat per meal (Ribaya-Mercado et al., 2007).

Data from our study show for the first time that consumption of raw salad vegetables with as little as 2 g of oil compared with 0 g of oil is adequate to show significant increases in the absorption of α-carotene, β-carotene, α-tocopherol, γ-tocopherol, retinyl palmitate, and trans-lycopene. Compared with 0 g of added oil, phylloquinone absorption was significantly greater when 4 g of oil or more (8 g and 32 g) was added to the salad dressing. In agreement with these results, our previous salad study showed significantly greater absorption of carotenoids with full fat (28 g of canola oil) compared with reduced fat (6 g of canola oil) salad dressing.

Increasing the amount of oil in the salad dressings from 0 g up to 32 g resulted in dose-dependent increases in the absorption of carotenoids, tocopherols and phylloquinone from salad vegetables. In contrast, Unlu et al. (Unlu et al., 2005) reported no significant differences in carotenoid absorption from salads ingested with 12 g or 24 g of fat from avocado or avocado oil suggesting a “nonlinear” effect on carotenoid bioavailability. This might be due to the different source of fat used. Roodenberg et al. (2000) showed that different carotenoids require different amounts of fat to be optimally absorbed. Lutein esters required a higher amount of fat (36 g) for optimal absorption compared with α-carotene and β-carotene (3 g) (Roodenburg et al., 2000). 

The mechanisms by which co-ingested fat affects the bioavailability of fat-soluble nutrients have been investigated in both in vivo and in vitro studies (Huo et al., 2007). The amount, type and composition of co-ingested fat have been shown to affect a number of steps in the digestion and absorption of fat-soluble nutrients. First, lipid is necessary for the release of carotenoids and fat-soluble vitamins from plant matrices. The presence of dietary fat stimulates secretion of digestive enzymes and also solubilizes fat-soluble nutrients from the diet for absorption. Moreover, in vitro digestion showed that both amount and type of co-ingested lipid affect micellarization and chylomicron secretion (Huo et al., 2007). Micellarization refers to incorporation of fat-soluble compounds into micelles for transport across the water layer bringing them to close proximity of enterocytes for uptake (Huo et al., 2007).

A low amount of oil (0.5-1%) was needed for in vitro micellarization of α-carotene, β-carotene and lycopene (Huo et al., 2007). Addition of triacylglycerol (TAG) improved the micellarization of carotenes dependent upon fatty acid chain length, but independent of the degree of unsaturation or position of the double bond (Huo et al., 2007). The efficiency of micellarization or bioaccessibility of carotenoids was reported to be inversely proportional to their hydrophobicity (LUT+ZEA > AC and BC) (Huo et al., 2007).

Long chain fatty acids were more effective in improving micellarization compared with short chain fatty acids. Hu et al (Hu et al., 2000) showed the different effects of sunflower oil and beef tallow on postprandial plasma triacylglycerol response and in turn on the absorption of fat-soluble nutrient, β-carotene. Ingestion of β-carotene with a meal rich in sunflower oil resulted in lower appearance of β-carotene and greater appearance of triacylglycerol in triacylglycerol-rich lipoproteins compared to a meal rich in beef tallow. The high content of polyunsaturated fatty acid (PUFA) and saturated fatty acid in sunflower oil and beef tallow, respectively, may likely have contributed to the different effects.

The time progression of the emergence and the half life of triglycerol and carotenoids in chylomicrons were reported to be analogous (Erdman et al., 1993). Studies on postprandial lipid metabolism revealed the effects of co-ingested fat on blood triglycerol levels (Lairon et al., 2007). Triacylglycerol can be included to form the lipid-rich portion of the prechylomicron (Mansbach & Siddiqi, 2010). Evans et al. (Evans et al., 1998) reported that chylomicrons are pre-formed rather than newly formed before they are released into the circulation (Evans et al., 1998), which explains how an increased amount of triglyceride improves the absorption of fat-soluble nutrients perhaps via enhancing the size of chylomicron particles in enterocytes.

Moreover, the presence of lipid on the luminal side of the endoplasmic reticulum of enterocytes prevents the ubiquitin-proteasome degradation of apoB48 (Sakata et al., 1993), which is a crucial component of the chylomicron. Thus, it is reasonable to speculate that the absorption of fat-soluble nutrients and the postprandial triglycerol level share similar trends in their responses to different amounts of dietary fat in a meal.

The type of co-ingested fat may influence the bioavailability of fat-soluble nutrients by affecting the plasma triglycerol level and chylomicron formation. An in vivo study investigating the influence of different types of fat on postprandial triglyceride-rich-lipoproteins revealed an increase in apoB containing lipoproteins after short-term consumption of an olive oil-rich diet (Perez-Martinez et al., 2009; Jackson et al., 2002). ApoB48 can be used to identify, quantify and estimate the size of mature chylomicrons since each chylomicron only contains one apoB48 (Phillips et al., 1997). Monounsaturated fatty acids, the primary fatty acids in olive oil, have been reported to elicit higher postprandial lipemia compared with polyunsaturated (PUFAs) and saturated fatty acids (van Greevenbroek et al., 1996). Moreover, short and medium fatty acids are transported as membrane complexes via albumin through the portal route, whereas long fatty acids are utilized in the chylomicron formation leading to an elevated triglycerol level in the lymph and thus more efficient transport of fat-soluble nutrients.

Different types of fat also influence the size of micelles, which in turn affects the absorption of fat-soluble nutrients. This may account for the discrepancies in the amount of fat necessary for optimum bioavailability of fat-soluble nutrients across studies that used different types of fat. In addition, the size of fat-soluble components in the emulsion affects the diffusion rate through enterocytes. Linoleic or eicosapentanoic acid form larger micelles resulting in reduced β-carotene absorption compared with oleic acid (Raju et al., 2006).

Oil rich in oleic acid, such as olive oil, was shown to enhance the bioavailability of lutein by promoting incorporation into micelles (Laksminarayana et al., 2006). Released fatty acids from hydrolysis of dietary triglycerides play a significant role in emulsifying carotenoids and other fat-soluble nutrients for intestinal uptake  (Borel  et  al.,  1996).  Moreover,  the  composition  of  free  fatty  acids  has  an  effect  on chylomicron  secretion  (van  Greevenbroek  et  al.,  1996).    Ingestion  of  a  meal  with  medium-chain   fatty   acids   did   not   promote   chylomicron   secretion   (Borel   et al,   1998),   while unsaturated  fatty  acids,  especially  oleic  acids  facilitated  the  formation  of  lipoproteins (Jackson  et  al.,  2002;  van  Greevenbroek  et  al.,  1996). 

The  comparison  among  different  fat types  was  not  the  focus  of  this  study.  Soybean  oil  as  the  only  fat  type  used  in  this  study  is rich in polyunsaturated fatty acids.  Collection of blood samples at different time points (immediately before consumption of the test salad, and then 2, 3.5, 5, 7, and 9.5 h after salad consumption) allows monitoring of  the  postprandial  fluctuation  of  fat-soluble  nutrients  levels  in  postprandial  chylomicrons. Previous  studies  showed  predictable  elevations  in  the  appearance  of  fat-soluble  nutrients  in chylomicrons;  a  moderate  increase  2-3  h  after  test  meal  consumption  and  a  substantial increase at 5 h (Gartner et al., 1997; O’Neill et al., 1998; Brown et al., 2004). 

In this study, absorption  of α-carotene, β-carotene, α-tocopherol, γ-tocopherol,  lutein,  retinyl  palmitate, phylloquinone,  13-cis-lycopene,  and trans-lycopene  increased  over  time  and  reached  a maximum at 3.5 to 5 h.  At the 9.5 h time point, the fat-soluble nutrients in the chylomicron fraction returned to the baseline level. This trend was not observed when 0 g of oil was added to the salads. Negligible absorption of fat-soluble micronutrients was observed after ingestion of  the  test  salad  with  0  g  of  added  oil  highlighting  the  importance  of  co-ingested  fat  for carotenoids  and  phylloquinone  absorption. 

 

Edited by Sibiriak

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On 7/3/2019 at 3:23 PM, Sibiriak said:

I'm wondering how you factor in critical  absorption/bioavailability issues.  And if you don't,   how much does that detract from the usefulness of your highly detailed and precise nutrient intake calculations?

Sibiriak, as we know daily requirement of a determined nutrient is a random variable. Nutrition science factors that in a semi-probablistic way, or point-estimate, or suggesting a cautious (abundant) value such that it is enough to satisfy the individual need of 97.5% of the population.

So we are reasoning in terms of the classic RDI, or AI , which are cautious amounts of the nutrient. All cronometer nutrient figures are averages and the % refer to the % to the cautious estimate which portects most people.

So the detailed calculation suffer inevitably of such a drawback. But the result has the same conceptual validity. That is, those potential deficiences underlined by cronometer so precisely  in VLF diets are significant in the limited part of the population which suffers absorption problems, genetic polymorphisms and so on.

The articles you posted, especially the second one are extremely intersting. The latter gives a scientific base to the practice of dressing vegetables with oils. A VLF diet risks to  bring about disastrous results if done in some individuals with genetic propensity to malabsorption of tocopherols , carotenoids, phylloquinone,  at least if no oils are present naturally in the food matrix, like it happens in salads.

Last, I'll have to ask the cronometer forum how tocopherols and carotenoids are chemically analyzed. If the oils in the food matrix may be an index of their availability or absorption in the human GI tract. But some epidemiological studies also correlate the reccomended intakes to the population averages, so it may all fall back into the statistical aspect implied in cronometer.

 

Edited by mccoy

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