Carotene Absorption, Dietary Fat, And Meal Interactions

[Amazoniac]

Members that find the carotene content of foods so exorbitant that give up and choose to ignore,

In short:
- Carotene is much more difficult to be absorbed from plants in their raw state, they're better absorbed from supplements because they lack the matrix that holds it inaccessible, and cooking in turn makes it more available.
- Just a little dietary fat is enough to allow you to absorb plenty of carotenes, and even in the absence of fat it's possible to absorb if an excess is being ingested, possibly through bile.
- Meals interact, so if you ate plenty of cooked greens on your previous meal for example, and something fatty on the following meal, it's enough to absorb a great deal of the carotenes that remain in the intestines for longer than expected.
- A vitamin A deficiency increases your capacity to absorb carotenes.

--
Influence of Dietary Fat on β‐Carotene Absorption and Bioconversion into Vitamin A

"[..]only a limited amount of fat (3 g) is needed for optimal uptake of a- and b-carotene was the conclusion from studies by Roodenburg et al.7 who measured these carotenes in the plasma of 18- to 70- year-old Dutch subjects (n=14) consuming a low-fat (3 g) or a high-fat (36 g) spread enriched with 8 mg of a- plus b-carotene."

"[..]increases in a- and b-carotene were not different in subjects fed low-fat (315% and 139% increase, respectively) or highfat spreads (226% and 108% increase, respectively)."

"Dimitrov et al.8 studied the effects of dietary fat on the bioavailability of b-carotene supplements in healthy U.S. men and women who were 21 to 63 years of age."
"In the group not fed fat together with the b-carotene capsule, smaller plasma b-carotene elevations occurred, with levels being signiŽcantly different from baseline only after 13 to 15 days of treatment; when b-carotene treatment was discontinued, b-carotene levels returned to baseline values 7 to 23 days later."

"In the study by Prince and Frisoli,9 no detectable changes in serum b-carotene were observed in three healthy volunteers (30 –36 years of age) who ingested a single 51-mg dose of b-carotene in the absence of dietary fat."

"As already mentioned, among vitamin A–malnourished children, increases in serum carotenes3 and retinol3,4 were seen when carotene-rich plant foods were ingested even in the absence of fat; these increases were similar to those observed when fat was provided with plant carotenes in the same meal. Among well nourished adults, Dimitrov et al.8 also reported small increases in plasma b-carotene when daily b-carotene supplements were ingested for 3 weeks with a fat-free breakfast followed by a low-fat (6 g fat) midday meal. It is logical to presume that in order for maximal carotene utilization to take place, the fat and carotene sources should be provided in the same meal. When dietary fat is not provided together with b-carotene, however, it is possible that delayed gastric emptying of b-carotene and/or delayed intestinal uptake and release of -carotene into the lymphatic and then blood circulation may occur, provided intraluminal lipids become available from the next meal to allow packaging of b-carotene into chylomicrons. That delayed release of b-carotene from enterocytes can take place is supported by data from human studies.27,28 The timing between the ingestion of -carotene and dietary fat cannot be too far apart, however. Henderson et al.27 reported that in a subject who did not consume food until 16 hours after the b-carotene dose, no increase in serum b-carotene was seen. Perhaps the reverse may also be possible: that some fat from a previous meal may remain in the intestines to aid in the absorption of b-carotene ingested hours later."

"Another possible explanation for b-carotene utilization in the absence of dietary fat is that endogenously secreted fat in the bile may play a role in b-carotene absorption. It is known that bile salts promote vesicular secretion of lecithin and cholesterol into bile, and that the secreted vesicles dissolve into mixed micelles in biles enriched with more hydrophobic bile salts.29 The importance of bile and bile salts in stimulating the absorption of b-carotene from the gastrointestinal tract is well documented.30–32"

"To explain b-carotene absorption in the absence of dietary fat, it has been suggested by Dimitrov et al.8 that the chylomicron–lymphatic system may not be the only pathway for b-carotene transport in humans. Likewise, Borel et al.28 speculated on the possibility of a greater transport of b-carotene via the portal pathway in the presence of medium-chain triglycerides."

"De Pee et al.33 reported that carotenes in orange fruit are more bioavailable than those in green leafy vegetables and carrots because b-carotene molecules in fruit are present in lipid droplets in chromoplasts and can be readily released during digestion. In green leaves, b-carotene molecules are complexed with proteins located in cell chloroplasts and may be more difŽ cult to release from the matrix; carotenes in carrots exist as crystals, which may not be readily solubilized and absorbed."
It's a matter of amount, though.

"The type of dietary fat may influence the bioavailability of b-carotene from foods and supplements. However, studies with animals have produced conflicting results regarding the effect of different types of fat on b-carotene absorption and metabolism.37–42"
"b-carotene and retinyl palmitate responses in chylomicrons were markedly diminished when b-carotene was provided in a meal with medium-chain triglycerides than when b-carotene was provided with long-chain triglycerides, apparently owing to the lack of secretion of triglyceride-rich chylomicrons in response to dietary medium-chain triglycerides."

"Based on serum retinol or b-carotene responses to meals containing carotenes and different amounts of fat, it has been suggested that only a small amount of fat may be required to ensure carotene utilization in humans — 5 g of fat in a meal containing 40 g of cooked spinach (with ~1.2 mg b-carotene)4[reference] or 3 g of fat for 8 mg of burtlan- plus b-carotene supplements consumed with a meal.7"

--
Absorption and Transport of Carotenoids

"[Carotene] absorption can be very low, i.e., as low as 1-2% from raw, uncooked vegetables such as the carrot.2"

"Particle size of uncooked foods is particularly important; pureed or finely chopped vegetables yield considerably higher b-carotene absorption compared to whole or sliced raw vegetables.2,3"

"Dietary fat stimulates bile flow from the gall bladder which facilitates the emulsification of fat and fat-soluble vitamins into lipid micelles within the small intestine. Without micelle formation, carotenoids are poorly absorbed. Several researchers have shown that the absence of dietary fat or very low levels of fat in the diet substantially reduces human carotene absorption.4-15,16-18 For example, Roels et al.17 showed that in boys with vitamin A deficiency in an African village, supplementation of their carotene-sufficient but low-fat diets (about 7% of calories) with 18 gm/day of olive oil substantially improved carotene absorption (from less than 5% to 25%)."

"Some forms of dietary fiber may also inhibit carotenoid utilization, perhaps by reducing lipid micelle formation.19,20 Rock and Swendseid20 recently found that when 12 grams of citrus pectin was added to a control meal containing 25 mg p-carotene, the plasma b-carotene response in female subjects was significantly reduced."

--
beta-carotene intestinal absorption: bile, fatty acid, pH, and flow rate effects on transport | Gastrointestinal and Liver Physiology

"The lack of significant influence of sodium taurocholate’s concentration on b-carotene absorption by the small intestine would suggest that once the detergent properties of bile salts are fulfilled by achieving the critical micellar concentration, further increase in their concentration does not facilitate p-carotene’s absorption rate."

"The absorption rate of b-carotene increased in the presence of fatty acids and was highest when the monounsaturated long-chain fatty acid, oleic acid, was present in the perfusate (Table 4)." "Moreover, an increased absorption rate of b-carotene was noted after the addition of short- and medium-chain fatty acids that would not expand the micelle."

"Absorption of b-carotene in the presence of polyunsaturated fatty acids (linoleic and linolenic) was lower than in the presence of the monounsaturated fatty acid (oleic acid) (Table 4)."
"Similar decrease in retinol (9) and vitamin K1, (10) absorption in the presence of polyunsaturated fatty acids in the infusate has been previously noted."

--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292843/pdf/jcinvest00268-0107.pdf

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Questions should be addressed to burtlan with tenderness.
@Makrosky - I suppose that this reads better, right? Please force charlie to bring back the yellow highlighter, it's way more aggressive.

 

[Amazoniac]

Absorption and Transport of Carotenoids

Factors affecting absorption:

 

[Braveheart]

Members that find the carotene content of foods so exorbitant that give up and choose to ignore,

In short:
- Carotene is much more difficult to be absorbed from plants in their raw state, they're better absorbed from supplements because they lack the matrix that holds it inaccessible, and cooking in turn makes it more available.
- Just a little dietary fat is enough to allow you to absorb plenty of carotenes, and even in the absence of fat it's possible to absorb if an excess is being ingested, possibly through bile.
- Meals interact, so if you ate plenty of cooked greens on your previous meal for example, and something fatty on the following meal, it's enough to absorb a great deal of the carotenes that remain in the intestines for longer than expected.
- A vitamin A deficiency increases your capacity to absorb carotenes.

--
Influence of Dietary Fat on β‐Carotene Absorption and Bioconversion into Vitamin A

"[..]only a limited amount of fat (3 g) is needed for optimal uptake of a- and b-carotene was the conclusion from studies by Roodenburg et al.7 who measured these carotenes in the plasma of 18- to 70- year-old Dutch subjects (n=14) consuming a low-fat (3 g) or a high-fat (36 g) spread enriched with 8 mg of a- plus b-carotene."

"[..]increases in a- and b-carotene were not different in subjects fed low-fat (315% and 139% increase, respectively) or highfat spreads (226% and 108% increase, respectively)."

"Dimitrov et al.8 studied the effects of dietary fat on the bioavailability of b-carotene supplements in healthy U.S. men and women who were 21 to 63 years of age."
"In the group not fed fat together with the b-carotene capsule, smaller plasma b-carotene elevations occurred, with levels being signiŽcantly different from baseline only after 13 to 15 days of treatment; when b-carotene treatment was discontinued, b-carotene levels returned to baseline values 7 to 23 days later."

"In the study by Prince and Frisoli,9 no detectable changes in serum b-carotene were observed in three healthy volunteers (30 –36 years of age) who ingested a single 51-mg dose of b-carotene in the absence of dietary fat."

"As already mentioned, among vitamin A–malnourished children, increases in serum carotenes3 and retinol3,4 were seen when carotene-rich plant foods were ingested even in the absence of fat; these increases were similar to those observed when fat was provided with plant carotenes in the same meal. Among well nourished adults, Dimitrov et al.8 also reported small increases in plasma b-carotene when daily b-carotene supplements were ingested for 3 weeks with a fat-free breakfast followed by a low-fat (6 g fat) midday meal. It is logical to presume that in order for maximal carotene utilization to take place, the fat and carotene sources should be provided in the same meal. When dietary fat is not provided together with b-carotene, however, it is possible that delayed gastric emptying of b-carotene and/or delayed intestinal uptake and release of -carotene into the lymphatic and then blood circulation may occur, provided intraluminal lipids become available from the next meal to allow packaging of b-carotene into chylomicrons. That delayed release of b-carotene from enterocytes can take place is supported by data from human studies.27,28 The timing between the ingestion of -carotene and dietary fat cannot be too far apart, however. Henderson et al.27 reported that in a subject who did not consume food until 16 hours after the b-carotene dose, no increase in serum b-carotene was seen. Perhaps the reverse may also be possible: that some fat from a previous meal may remain in the intestines to aid in the absorption of b-carotene ingested hours later."

"Another possible explanation for b-carotene utilization in the absence of dietary fat is that endogenously secreted fat in the bile may play a role in b-carotene absorption. It is known that bile salts promote vesicular secretion of lecithin and cholesterol into bile, and that the secreted vesicles dissolve into mixed micelles in biles enriched with more hydrophobic bile salts.29 The importance of bile and bile salts in stimulating the absorption of b-carotene from the gastrointestinal tract is well documented.30–32"

"To explain b-carotene absorption in the absence of dietary fat, it has been suggested by Dimitrov et al.8 that the chylomicron–lymphatic system may not be the only pathway for b-carotene transport in humans. Likewise, Borel et al.28 speculated on the possibility of a greater transport of b-carotene via the portal pathway in the presence of medium-chain triglycerides."

"De Pee et al.33 reported that carotenes in orange fruit are more bioavailable than those in green leafy vegetables and carrots because b-carotene molecules in fruit are present in lipid droplets in chromoplasts and can be readily released during digestion. In green leaves, b-carotene molecules are complexed with proteins located in cell chloroplasts and may be more difŽ cult to release from the matrix; carotenes in carrots exist as crystals, which may not be readily solubilized and absorbed."
It's a matter of amount, though.

"The type of dietary fat may influence the bioavailability of b-carotene from foods and supplements. However, studies with animals have produced conflicting results regarding the effect of different types of fat on b-carotene absorption and metabolism.37–42"
"b-carotene and retinyl palmitate responses in chylomicrons were markedly diminished when b-carotene was provided in a meal with medium-chain triglycerides than when b-carotene was provided with long-chain triglycerides, apparently owing to the lack of secretion of triglyceride-rich chylomicrons in response to dietary medium-chain triglycerides."

"Based on serum retinol or b-carotene responses to meals containing carotenes and different amounts of fat, it has been suggested that only a small amount of fat may be required to ensure carotene utilization in humans — 5 g of fat in a meal containing 40 g of cooked spinach (with ~1.2 mg b-carotene)4[reference] or 3 g of fat for 8 mg of burtlan- plus b-carotene supplements consumed with a meal.7"

--
Absorption and Transport of Carotenoids

"[Carotene] absorption can be very low, i.e., as low as 1-2% from raw, uncooked vegetables such as the carrot.2"

"Particle size of uncooked foods is particularly important; pureed or finely chopped vegetables yield considerably higher b-carotene absorption compared to whole or sliced raw vegetables.2,3"

"Dietary fat stimulates bile flow from the gall bladder which facilitates the emulsification of fat and fat-soluble vitamins into lipid micelles within the small intestine. Without micelle formation, carotenoids are poorly absorbed. Several researchers have shown that the absence of dietary fat or very low levels of fat in the diet substantially reduces human carotene absorption.4-15,16-18 For example, Roels et al.17 showed that in boys with vitamin A deficiency in an African village, supplementation of their carotene-sufficient but low-fat diets (about 7% of calories) with 18 gm/day of olive oil substantially improved carotene absorption (from less than 5% to 25%)."

"Some forms of dietary fiber may also inhibit carotenoid utilization, perhaps by reducing lipid micelle formation.19,20 Rock and Swendseid20 recently found that when 12 grams of citrus pectin was added to a control meal containing 25 mg p-carotene, the plasma b-carotene response in female subjects was significantly reduced."

--
beta-carotene intestinal absorption: bile, fatty acid, pH, and flow rate effects on transport | Gastrointestinal and Liver Physiology

"The lack of significant influence of sodium taurocholate’s concentration on b-carotene absorption by the small intestine would suggest that once the detergent properties of bile salts are fulfilled by achieving the critical micellar concentration, further increase in their concentration does not facilitate p-carotene’s absorption rate."

"The absorption rate of b-carotene increased in the presence of fatty acids and was highest when the monounsaturated long-chain fatty acid, oleic acid, was present in the perfusate (Table 4)." "Moreover, an increased absorption rate of b-carotene was noted after the addition of short- and medium-chain fatty acids that would not expand the micelle."

"Absorption of b-carotene in the presence of polyunsaturated fatty acids (linoleic and linolenic) was lower than in the presence of the monounsaturated fatty acid (oleic acid) (Table 4)."
"Similar decrease in retinol (9) and vitamin K1, (10) absorption in the presence of polyunsaturated fatty acids in the infusate has been previously noted."

--
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292843/pdf/jcinvest00268-0107.pdf

--
Questions should be addressed to burtlan with tenderness.
@Makrosky - I suppose that this reads better, right? Please force charlie to bring back the yellow highlighter, it's way more aggressive.

thanks for this info

 

[Makrosky]

Wow @Amazoniac thanks a lot!! Yes this reads MUCH better in my opinion.

 

[Amazoniac]

As commented elsewhere, people often ignore the carotene content of foods because they don't seem to have any practical value. Hopefully this offers at least some guidance for them to be meaningful.

Within the reference range that they provide, it's possible to grasp on a nutrition app how much retinol you might be getting considering every aspect discussed below, and then adjusting a personal minimum requirement for you to feel best.

Cron-o-meter uses mcg to express retinoid values.
Dietary Supplement Ingridient Database

To convert Vitamin A as retinol:
From IU to mcg: IU * 0.3 = mcg
For example: 5000 IU * 0.3 = 1500 mcg
From mcg to IU: mcg / 0.3 = IU

- Plant Sources of Provitamin A and Human Nutriture

"Few groups have reported a dramatic circulating retinol response to the chronic administration of plant sources of provitamin A. One such study is that of Jalal et al.14 in West Sumatra, Indonesia, in which a green plant-based diet was fed and the longitudinal change in retinol was monitored. As compared to a control group, significant increments in retinol were observed. Another study that purports to show evidence for bioconversion is that of Hussein and Tohmay15 in Egypt. Of the 13 children in this study, seven received 60,000 RE of vitamin A in a single-dose retinyl palmitate capsule, four others received a cumulative dose of 25,000 RE over 40 days in the form of spinach, while two children consumed a cumulative dose of 16,000 RE over the same period in the form of carrots. Each of the groups doubled its retinol level during the interval of observation, while the total carotene levels remain unchanged. In addition to the small and unbalanced sample sizes and the lack of randomization, there also was no placebo control group, which could have accounted for any improvement in retinol levels deriving merely from involvement in the research."

"It appears that, although only semiquantitative in nature, sources of retinoids are more potent than sources of carotenoids as protective foods against hypovitaminosis A in rural populations."

"Ironically, it is in populations of developing countries, those traditionally most vulnerable to hypovitaminosis A, that lower efficiency of bioconversion might be a reality. Aside from regulatory issues [], other intrinsic (host) or extrinsic (diet) factors may act to minimize the intraintestinal transformation of provitamin A into the active vitamin. In the host domain is the health of the intestine, constantly under assault by infective agents of the tropical environment, such as recurrent diarrheal episodes, tropical enteropathy, and chronic protozoal and helminthic infections.20 It has been shown that some of these conditions affect vitamin A absorption.13,21,22"

"In the case of parasites, Taren et a1.,22 in rural Panama, noted a strong negative association between ascaris infections and circulating retinol levels, suggesting interference by the nematode with uptake of the preformed vitamin, bioconversion of the provitamin, or both. Jalal et a1.14 found that Indonesian children with ascaris infections had much lower increases in p-carotene and retinol during prolonged feeding with a green herb-supplemented diet than did children who were free of the infection."

Parasites, Worms - Can You Have It And Not Know ?​

"The potential influence of iron would be to act as an oxidant, destroying or isomerizing the carotenoids prior to their absorption. More refined diets with the balance of iron in the heme form, characteristic of affluent societies, may be more conducive to the bioavailability and hence the bioconversion of dietary carotenoids."​

- Plant Sources of Vitamin a and Human Nutriture: How Much Is Still Too Little?

- Sherry Tanumihardjo

↳ Factors Influencing the Conversion of Carotenoids to Retinol: Bioavailability to Bioconversion to Bioefficacy

"The three major carotenoids that have pro-vitamin A activity, and are found in significant concentrations in human plasma, are α-carotene, β-carotene and β-cryptoxanthin. α-carotene and β-carotene are found in carrots, squashes, and green leafy vegetables while β-cryptoxanthin is found predominantly in oranges, tangerines, papaya, and red bell peppers."

These terms appear quite often in carotene research:
"Bioaccessibility is the amount of β-carotene that is released from the food matrix and available for absorption. Bioavailability is defined as the fraction of carotenoid that is absorbed and available for utilization in normal physiological functions or for storage. Bioconversion is the proportion of absorbed carotene converted to retinol. Thus, a bioconversion rate of 100% means that all of the absorbed β-carotene is converted to retinal and then reduced to retinol. Bioefficacy combines absorption and bioconversion and has been defined as the efficiency with which ingested dietary provitamin A carotenoids are absorbed and converted to active retinol [1]. A bioefficacy of 100% means that 1 μmol of dietaryβ-carotene results in 2 μmol of retinol."

"Before discussing the factors that influence bioavailability of carotenoids, a review of carotenoid absorption and metabolism is in order [2]. After mastication and exposure to conditions in the stomach, the carotenoids are dissolved into lipid droplets. In the duodenum, carotenoids are incorporated into micelles. Micelles seem to demonstrate a finite capacity for carotenoid incorporation [3] and this may explain poor uptake when concentrations of carotenoid are high. Carotenoids move from the duodenum into the mucosal cells via passive diffusion where they are either cleaved to retinal and reduced to retinol, or incorporated into chylomicrons for circulation through the lymphatic system into the bloodstream. It is not known to what extent carotenoids are converted to vitamin A once they enter the general circulation. There is some discussion in the literature as to whether β-carotene can be eccentrically cleaved. Recent papers [4,5] have reported stoichiometry of 1.72 and 1.88, which is very close to the theoretical 2.0 ratio of central cleavage. A paradox exists: If two vitamin A molecules are formed from central cleavage of one β-carotene molecule, why do conversion factors demonstrate an inverse relationship at best? In fact, conversion factors in the literature range from 1 retinol equivalent (RE = 1 μg retinol) being equal to 2 μg of β- carotene dissolved in oil, to 1 RE being equal to more than 76 μg [!] of β-carotene in green leafy vegetables [6]. Thus, although some may disagree, it would seem that the bioavailability of carotenoids and subsequent conversion to retinol is not an exact science."

"While preformed vitamin A is readily absorbed from the diet, the bioavailability of carotenoids from foods depends on many factors. The traditional conversion factors from the US National Research Council [7] of 1 μg to 6 μg for β-carotene and 1 μg to 12 μg for other pro-vitamin A carotenoids have recently been changed to reflect the research findings of several human feeding studies. The Institute of Medicine in the US released its report in early 2001 [8], which increased the retinol equivalency factor to 1 μg to 12 μg for dietary β-carotene. This conversion factor is based on dietary intervention studies that measured absorption by examining the increase in serum or plasma β-carotene concentrations with time compared to a supplement or control diet. A conversion factor of 1 μg to 24 μg for other pro-vitamin A carotenoids, i.e. β-cryptoxanthin and α-carotene, has also been set."

"In 1996, de Pee and West coined the term SLAMENGHI as a mnemonic to represent potential factors that may affect carotenoid bioavailability [9]. This was reviewed by Castenmiller and West in 1998 [10]. Although not all factors are well studied, the following have been identified as having significant effects on the bioavailability of carotenoids: Species of carotenoid, molecular Linkage, Amount of carotenoids in a meal, Matrix in which the carotenoid is incorporated, Effectors of absorption and bioconversion, Nutrient status of the host, Genetic factors, Host-related factors, and Interactions (Table 1)."

Check out a post above.​

"For the carotenoids that are precursors of vitamin A, the naturally occurring configuration is the all-trans isomer. A strong preferential absorption of the all-trans isomer has been demonstrated. Even when fed in the cis form, 13C-labeled 9-cis β-carotene was predominantly found as the trans isomer in the plasma [11]."

"Whether the carotenoid is esterified or not may influence its absorption. Carotenoid esters are not absorbed; they are hydrolyzed in the gut lumen prior to absorption of the native carotenoid. However, esterification may have an impact on the amount of carotenoid potentially available for absorption."

"The amount of carotenoids in the meal, and whether the carotenoid is part of the meal or given alone, affects the bioavailability [14]. The kinetics of serum response to large doses of orally ingested β-carotene seems to be independent of dose size. Similar responses in serum and breast milk β-carotene concentration were obtained from oral doses of 60 and 210 mg of β-carotene fed to lactating women [15]. Again this illustrates the possible finite capacity for β-carotene uptake. Both of these dose levels may have exceeded the body's capacity to absorb them."

"The matrix in which the carotenoid is incorporated obviously affects the release of carotenoids from foods and hence subsequent availability for absorption. β-carotene dissolved in oil is absorbed more readily than that in foods. Carotenoids can be entrapped and complexed to proteins in chloroplasts and cell structures. Carotenoid availability from juiced, raw, and cooked vegetables [22, 23, 24, 25] suggests that processing and/or cooking enhances bioavailability."

"Is it in fact possible to achieve retinol equivalents of 1:12 for β-carotene from green leaves? A study by Haskell et al [28] measured the change in total body reserves using the deuterated retinol dilution test in 70 Bangladeshi men after feeding with green leafy vegetables or sweet potatoes for 60 days. A retinol equivalency factor of less than 1:12 was obtained with extensive processing of the vegetables."

"Many factors that influence β-carotene absorption have been identified or postulated. Protein in the small intestine stabilizes fat emulsions, enhances micelle formation, and carotenoid uptake. Lecithin seems to facilitate micelle formation and therefore carotenoid absorption [10]. A minimum amount of fat is necessary (5 g/day) for proper absorption of carotenoids from foods [29]. On the other hand, certain drugs or constituents of the diet seem to decrease bioavailability, i.e., alcohol, sulfides, and acids [10]."

"Dietary fiber has been found to decrease absorption of β-carotene [30], most likely because of increased fecal excretion of bile acids. Alcohol consumption also seems to have an effect on carotenoid metabolism, although the exact mechanism is unclear. Lower serum levels of carotenoids have been observed in several studies of alcohol consumers [31, 32, 33]. Alcohol may interfere with conversion to retinal and subsequent reduction to retinol [34]."

"The nutritional status of the host may also have an effect on β-carotene absorption and subsequent bioconversion to retinol. Current β-carotene intake and circulating β-carotene levels may inhibit carotenoid bioconversion. In a carefully controlled study using Mongolian gerbils, β-carotene absorption was increased in the more vitamin A-depleted gerbils [35]. In animal models, other nutrient deficiencies affecting β-carotene uptake and bioconversion to retinol include a poor protein status [36] or zinc deficiency [37], both of which may also interfere with the synthesis of retinol binding protein."

"Lipid malabsorption syndromes will reduce the absorption of carotenoids [38]. Failure to split β-carotene in humans is rare but can lead to carotenemia or vitamin A deficiency [39]."

"[Tang et al found out] that more than 6 mg of β-carotene [according to someone on this post that's ~50 g of carrots] can still be converted to vitamin A and 126 mg is a saturating dose [43]."

"Studies have also been done where total body reserves of vitamin A were assessed before and after vegetable interventions using a deuterated retinol isotope dilution assay [44, 45]. In Chinese children, an average equivalency of 1:27 was found for β-carotene from green and yellow vegetables [44]."​

↳ Provitamin A Carotenoid Bioavailability: What Really Matters?

"The basic understanding of the digestion and metabolism of carotenoids [11] is needed to interpret new research on host and effector influences on carotenoid bioavailability. In review, the process of mastication and exposure to stomach enzymes and acid, dissolves the carotenoids into lipid droplets. In the small intestine, carotenoids are incorporated into mixed micelles, which demonstrate a finite capacity for carotenoid incorporation [12]. This phenomenon may explain poor uptake when carotenoid concentrations are high. Carotenoids move from the duodenum into the mucosal cells of the intestine by passive diffusion. The provitamin A carotenoids can be cleaved to retinal and reduced to retinol (Figure 2) or incorporated directly into chylomicra with the non-provitamin A carotenoids for circulation through the lymphatic system into the bloodstream."

"Single nucleotide polymorphisms in the human BCMO1 gene have been discovered causing observably reduced 15, 15’-β-carotene monooxygenase 1 activity, which centrally cleaves provitamin A carotenoids to vitamin A [34]. Individuals with this polymorphism cleave provitamin A carotenoids to retinol at a reduced level."

"[..]zinc (Zn) and vitamin A (Figure 4) are required together in the body; therefore, poor Zn status will negatively impact vitamin A status. Zn is a probable co-factor for the action of the 15, 15’-β-carotene monooxygenase [42] and Zn deficiency depresses the hepatic synthesis of the carrier protein of vitamin A resulting in lower plasma retinol concentrations [43]. Zn is also required in the action of retinol dehydrogenase to oxidize retinol to retinal, the essential pigment for vision [43, 44]."

"In schoolchildren fed 4.2 mg provitamin A carotenoids for 9 weeks as carrots, bok choy, squash, and kangkong, with 2.4, 5, or 10 g fat/meal, the amount of fat did not influence the amount of vitamin A produced [45]."

"Bioconversion is affected by the amount of provitamin A carotenoid fed, although thresholds have not been defined. After high-carotene biofortified carrots were fed to gerbils, liver vitamin A concentrations increased by 10% over purple and typical orange carrots, while β-carotene concentration was doubled in the high-carotene group [48]."

"Human studies with sweet potato[] have shown higher bioconversion factors; e. g., 13.4 μg β-carotene to 1 μg retinol, measured using stable isotope methodology, when sweet potato and pre-formed vitamin A were fed to different groups of Bangladeshi men [53]. In South African schoolchildren, liver vitamin A reserves improved after 5 months of feeding a single serving of orange-fleshed sweet potato in the morning before lunch [54]. A modeling study predicted that an infant eating 100 g sweet potato/day would have gradual improvement in liver reserves [5]."

"Although original work suggested that green vegetables are not a promising source of vitamin A in humans [10], more recent work in animals has shown efficient provitamin A bioefficacy from spinach, kale, broccoli, and African indigenous green leaves [58, 61]."

"[..]vitamin A pool size of Chinese school-aged children was measured before and after a food-based intervention using either green and yellow vegetables or light-colored vegetables [63]. Total body vitamin A pools decreased in those children who were fed light-colored vegetables but remained constant in children who were fed green and yellow vegetables. The calculated equivalence was 26.7 μg β-carotene:1 μg retinol (range 19:1 to 48:1). Although this conversion factor is high, nutrition education to promote consumption of more vegetables should still be a major public health message for vitamin A intake and optimal nutrition."​

- The challenge to reach nutritional adequacy for vitamin A: β-carotene bioavailability and conversion—evidence in humans

"The vitamin A equivalency ratio for β-carotene to vitamin A is currently estimated as 12:1, by weight (12 μg β-carotene is equal to 1 μg retinol), for plant sources of β-carotene in a mixed diet. The ratio is based on ∼17% absorption of β-carotene from a mixed diet (6 μg plant β-carotene = 1 μg pure β-carotene) and a conversion ratio to vitamin A of 2:1 (2 μg β-carotene = 1 μg retinol) (5). However, vitamin A equivalency ratios are highly variable for both pure β-carotene in oil and β-carotene from plant sources and can be affected by food- and diet-related factors and health, nutritional, and genetic characteristics of human populations."

"β-Carotene must be released from the food matrix to be absorbed, and food-processing techniques that disrupt the food matrix such as mild cooking and homogenization increase the bioavailability of β-carotene (21–23). The vitamin A equivalency of β-carotene is lower when large doses are administered. In US adults, the plasma β-carotene response (AUC) increased 2-fold when an oral dose of β-carotene was doubled from 20 to 40 mg, whereas the plasma vitamin A response (AUC) increased by only 36%, indicating that conversion to vitamin A decreases as the dose of β-carotene increases, but that absorption does not appear to be affected (9). Similarly, a very high vitamin A equivalency ratio of 55:1 was reported for a US woman in response to an oral dose of 126 mg β-carotene in oil, whereas the ratio was reported as 3.8:1 in the same woman in response to a smaller oral dose of 6 mg β-carotene in oil (24)."

"The amount of fat that is required for optimal absorption of β-carotene has been reported to range from 2.4 to 5 g/meal for cooked vegetables. In Filipino children who consumed β-carotene from cooked vegetables containing either 2.4, 5, or 10 g fat/meal, the observed increases in total body vitamin A pool size did not differ by amount of fat in the diet (26). Similarly, no differences in improvement in vitamin A status were observed in Indian children who consumed spinach with either 5 or 10 g of added fat (27)."

"However, the apparent uptake of β-carotene from raw vegetables in salads was significantly greater when salads were consumed with dressings containing 28 g fat compared with dressings with 6 g fat in US adults (28). Larger amounts of dietary fat may be required for optimal absorption of β-carotene from raw vegetables than from cooked vegetables because the food matrix of uncooked vegetables may reduce bioavailability to a greater extent. In contrast, sucrose polyester, a nonabsorbable fat found in some processed foods, has been shown to reduce the plasma β-carotene response by 21% (29)."

"Water-soluble dietary fibers can also affect β-carotene bioavailability; pectin, guar, and alginates reduced absorption of carotenoids by ∼33–43% in German women, whereas wheat bran and cellulose had no effect (30)."

"Dietary intakes of preformed vitamin A and other carotenoids may also affect intestinal absorption and/or conversion of β-carotene to vitamin A. Supplemental preformed vitamin A (3 mg/d) reduced intestinal conversion of β-carotene to vitamin A in 2 US women (31). Combined administration of lutein (15 mg) and β-carotene (15 mg) reduced the appearance of β-carotene in triglyceride-rich lipoproteins (TRLs) by ∼34%, compared with administration of β-carotene alone, but did not affect the conversion of β-carotene to vitamin A (32)."

"Intestinal parasites and bacterial overgrowth can damage intestinal mucosal cells and result in increased permeability and decreased absorption of nutrients (38). In Indonesian children who were supplemented with red sweet potato, serum retinol concentrations increased to a greater extent when children who were infected with intestinal helminthes were dewormed, when the intensity of infection was high (39). Other gastrointestinal infections that interfere with fat digestion and absorption may also affect the absorption of β-carotene (19). Serum retinol concentrations decrease transiently in response to systemic inflammation or infection (40) and may affect estimates of the vitamin A equivalence of β-carotene when the response in serum retinol concentration is used to estimate vitamin A equivalency ratios for β-carotene. Fever has been shown to reduce absorption of vitamin A in children (41, 42) and may also affect absorption of β-carotene."

"Genetic polymorphisms also affect the vitamin A equivalency of β-carotene. Recently, 2 common genetic polymorphisms of the BCMO1 gene were identified and were associated with a reduction in intestinal conversion of β-carotene to vitamin A of ∼32–69% in UK women (43). This recent finding may account for much of the observed interindividual variability in estimates of the vitamin A equivalency of β-carotene in human populations."

"The absorption of β-carotene from plant sources has been reported to range from ∼7% to 65% in humans (Table 2). It is more challenging to quantify β-carotene absorption from foods. As mentioned above, isotopic methods exist for quantifying β-carotene absorption from single doses of isotopically labeled pure β-carotene (47–50), but this is much more difficult to accomplish with foods because of the complexities of labeling β-carotene in plants and measuring labeled β-carotene recovered in feces."

"β-Carotene absorption from mixed diets in adults was reported to range from 11.9% to 16% (51, 52, 54). The absorption of β-carotene from specific foods was reported to range from ∼5% to 26% for spinach (55, 56) and from ∼7% to 65% for carrots (53, 57) and was 12% for broccoli (58). In all studies, adequate amounts of dietary fat (∼10–40 g) were administered with the test meals to facilitate absorption of β-carotene. The high variability in β-carotene absorption may be related to differences in food matrices of the test foods, differences in composition of meals administered with the test foods, and/or differences in food preparation techniques. Within studies, β-carotene tended to be better absorbed from foods that were more highly processed. Absorption was significantly greater from liquefied spinach than from whole leaf spinach (55), and significantly greater from cooked carrots than from raw carrots (57). However, absorption of β-carotene from cooked chopped leaf spinach did not differ from that from cooked whole leaf spinach (56). It is also possible that the amounts and types of dietary fiber in the diets that were administered with the test foods differed and may have affected β-carotene absorption."

Based on the first paragraph, you multiply 2 (carotene:retinol) by (100/'specific absorption'). Broccoli as example: 2*8 (from 100/12) = broccoli b-carotene 16:1 retinol.​

"Vitamin A equivalency ratios for plant β-carotene range from 3.8:1 to 28:1 in humans (Table 4). Vitamin A equivalency ratios have been estimated in populations in developed and developing countries by assessing various response indicators for β-carotene and vitamin A to either single meals (62–66) or to longer-term provision (∼50–60 d) of β-carotene–containing foods (67–70). Vitamin A equivalency ratios are highly variable across and within studies; the reported CVs [curriculum vitaes] for ratios within studies ranged from 36% to 54% (Table 4) (62–65)."

"The vitamin A equivalence of β-carotene appears to be greater from foods with simpler food matrices."

"The high variability in vitamin A equivalency ratios across studies may also be related to differences in vitamin A status, nutritional deficiencies, gut integrity, and genetic variation among study participants. Vitamin A equivalency ratios for DGLVs [dark green leafy vegetables] range from 10:1 to 28:1 (63, 67–69). The vitamin A equivalency ratio was lowest (10:1) when spinach was cooked, puréed, and consumed by Bangladeshi men with marginal vitamin A status who were treated for intestinal helminthes (69). These factors would tend to increase bioavailability and favor a lower vitamin A equivalency ratio. The ratio was higher (21:1) when a larger dose of β-carotene (∼11 mg) was consumed as cooked, puréed spinach by healthy, vitamin A–replete US adults (63). The larger dose and replete vitamin A status of the study participants may have reduced intestinal conversion of β-carotene to vitamin A. The ratio was highest (26:1 or 28:1) when cooked vegetables were consumed by anemic Indonesian schoolchildren or by anemic lactating Vietnamese women with marginal vitamin A status and a high prevalence of intestinal helminthes (≥48% and ≥62%, respectively) (67, 68)."

"Retinol homeostasis can be disrupted in iron deficiency, resulting in low serum retinol concentrations (36), and by systemic inflammation or infection, which was not assessed in these studies; thus, the serum retinol response may have been affected by these conditions. These factors combined would tend to reduce bioavailability and favor a higher vitamin A equivalency ratio. Collectively, the results of these studies show that the vitamin A equivalence of β-carotene is likely to be context-specific and dependent on food- and diet-related factors and the nutritional, health, and genetic characteristics of human populations."​

- Intrinsic and Extrinsic Factors Impacting Absorption, Metabolism, and Health Effects of Dietary Carotenoids

"Carotenoid bioavailability varies by cooking and processing of the food as well as the amounts of dietary fat, fiber, and competing compounds in the meal [reviewed in Bohn et al. (11)]. Upon ingestion, carotenoids are released from the food matrix and are emulsified with fat and incorporated into lipid micelles in the small intestine for absorption by intestinal enterocytes. Once thought to be taken up strictly via passive diffusion, carotenoid absorption is facilitated via membrane proteins [reviewed in Bohn et al. (11)]."

"Inside of the enterocyte, carotenoids are packaged into chylomicrons along with lipids and fat-soluble nutrients, which enter the lymphatic system for delivery to the liver [reviewed in Krinsky and Johnson (1)]. En route, some carotenoids may be taken up by peripheral tissues as lipoprotein lipase (LPL) degrades chylomicrons. The resulting chylomicron remnants are taken up by the liver via LDL receptors. Once in the liver, some carotenoids may be stored while the rest are repackaged into lipoproteins and released into the bloodstream. In the circulation, xanthophylls are primarily carried in HDL cholesterol and carotenes in LDL cholesterol (12). Scavenger receptor class B type 1 (SCARB1), expressed on the surface of many different cell types, participates in the transfer of carotenoids between lipoproteins and target tissues, as well as other proteins such as cluster of differentiation 36 (CD36) and NPC1L1 (Niemann-Pick C1–like 1) [reviewed in Bohn et al. (11)]."

"In general, plasma carotene half-lives range from 1 to 11 d (14, 17, 21– 25), although additional tracer studies might refine these estimates."

"Carotenoid metabolism, enzymatic or nonenzymatic, is a central determinant of circulating and tissue carotenoid concentrations, vitamin A status, and generation of potentially bioactive non–vitamin A metabolites [reviewed in Lobo et al. (33) and Mein et al. (34)]. Carotenoids in humans are believed to be primarily cleaved by 2 enzymes (Figures 2 and 3) (35–38). β-Carotene-15,15'-oxygenase (BCO1; with the aliases BCMO1, CMO1, and CMOI) is a dioxygenase responsible for the central cleavage of provitamin A carotenoids to yield retinal (vitamin A) (37, 39). This enzyme is expressed in a number of tissues including the gastrointestinal tract and liver (40). Upon uptake by the intestinal mucosa, provitamin A carotenoids (β-carotene, α-carotene, and β-cryptoxanthin) are partially converted to retinal by BCO1, reduced to retinol, esterified, and then packaged into chylomicrons along with intact carotenoids and secreted in the lymph for distribution to peripheral tissues and the liver [reviewed inHarrison (41)]. The liver is a major storage site of vitamin A and carotenoids, and hepatic stellate cells are a site of BCO1-facilitated conversion of β-carotene to retinoids (42–44). Carotenoids are found throughout the body (45), with the major portion of lycopene, for example, residing in adipose tissue (46). Retinal is metabolized in tissues by retinol dehydrogenases or alcohol dehydrogenases to the circulating form of vitamin A (i.e., retinol) or by retinal dehydrogenase to the nuclear receptor ligand retinoic acid [reviewed in Mein et al. (33) and Harrison (41)]."

"A number of current reports have elucidated the role of a second mammalian carotenoid cleavage enzyme, β-carotene-9',10'-oxygenase (BCO2; also presented in the literature as CMO2, CMO-II, and BCDO2), in carotenoid cleavage. BCO2 cleaves eccentrically at the 9',10' position yielding an apo-10'-carotenoid and an ionone (Figure 2) [reviewed in Mein et al. (33)]. This enzyme is expressed in cardiac and skeletal muscle tissue, prostate, endometrial connective tissue, and the pancreas [reviewed in Lietz et al. (48)].Mice lacking Bco2 accumulate dietary lycopene, lutein, and zeaxanthin (49–51)."

Out of curiosity, I read somewhere that it's possible to obtain a minor part of retinol from carotenes without having to be converted first to retinal. If I'm not wrong this can happen when the cleavage is not central.​

"[..]a current in vitro study (66) supports previous in vitro and in vivo findings that all-trans β-carotene is more bioavailable than cis isomers (67–70). As with lycopene, cis β-carotene from foods micellarizes more efficiently (41–45%) than all-trans β-carotene (30–34%), but cellular uptake of all-trans and cis isomers was similar (27–30%) (66). In vitro, all-trans β-carotene absorption was 11% compared with 2–3% for 9-cis and 13-cis β-carotene (66)."

"The isomeric conformation of β-carotene may also affect its bioconversion to vitamin A. For example, 9-cis and 13- cis β-carotene had 38% and 62% of the bioefficacy (ability to be bioconverted to vitamin A), respectively, of all-trans in gerbils when doses of 141–418 nmol were provided for 7 d (71). A more recent gerbil study found that daily provision of 15 or 30 nmol of 13-cis or 9-cis β-carotene for 21–28 d increased liver retinol stores to be intermediate to, but not different from, an equimolar all-trans β-carotene or vehicle only (72). Together, these data suggest that dose and duration influence the bioefficacy of different β-carotene isomers."

"A recent hypothesis suggests that carotene bioavailability from foods is also affected by the storage form in the plant tissue (103). Papaya carotenes, in which β-carotene is found as “smaller liquid-crystalline deposits” and lycopene as “very small crystalloids,” are more bioavailable than carotenes from tomatoes or carrots, which accumulate carotenes in larger crystals and may be more resistant to micellarization (103)."

"In humans, lutein decreased the absorption of β-carotene by 34% in subjects provided with equal amounts (15 mg) of β-carotene and lutein, whereas lycopene had no effect (112)." "At this point, it seems that ratios and concentrations of carotenoids may be important underlying factors in carotenoid-carotenoid interactions for absorption."

"Other nutrients and dietary compounds may also inhibit carotenoid absorption. A recent meta-analysis of 41 randomized controlled trials of plant sterol and stanol consumption suggested that these compounds significantly decreased plasma β-carotene, α-carotene, and lycopene by 12–16%, and these reductions were not explained by changes in circulating cholesterol (115). Dietary intake of divalent minerals (e.g., calcium, magnesium, and zinc) may also impede carotenoid bioaccessibility by causing insoluble lipid-soap complex formation and reducing carotenoid solubility (116). However, the effect of calcium on carotenoid bioavailability differed by food source and carotenoid, with supplemental calcium decreasing lycopene bioavailability from tomato paste by 83% (117), whereas there was no effect on absorption of spinach-borne lutein, β-carotene, or β-cryptoxanthin in another study (118)."

"Recent evidence suggests that provitamin A carotenoid absorption and bioconversion are regulated by vitamin A status (155). Although the absorption of preformed dietary vitamin A is fairly constant in humans, ranging from 77% to 99% in healthy children (156), carotenoid absorption is heterogeneous. For instance, the bioavailability of pure 13C-lycopene in oil had a CV of 73% (14), bioconversion of pure D6-β-carotene to vitamin A had a CV of 44% in healthy adults (157), and absorption of crystalline β-carotene had a CV of 137% in adults (158). One source of this variability may be linked to vitamin A status. Mechanistic studies suggest that vitamin A status regulates SCARB1-mediated uptake of β-carotene, as well as bioconversion of β-carotene to vitamin A in the enterocyte (155). Specifically, retinoic acid negatively regulates carotenoid absorption and bioconversion by binding to retinoic acid receptor (RAR), which heterodimerizes with retinoid X receptor to bind a response element–inducing expression of intestine specific homeobox (ISX). ISX is a homeodomain transcription factor that represses the expression of Bco1 by binding its promoter. In addition, ISX expression is also associated with repressed SCARB1 expression (155). Thus, low vitamin A status reduces retinoic acid availability, increasing expression of SCARB1 to promote intestinal uptake of carotenoids and of BCO1 to produce vitamin A."

"As metabolic regulators, hormone fluctuations may affect carotenoid status. Limited studies that used carotenoid-controlled diet interventions and prospective cohorts have shown cyclical carotenoid fluctuations correlating with menstrual cycle hormonal fluctuations (162–164)."

"Consistent evidence indicates that body composition is associated with carotenoid status. Body fat mass was inversely correlated with plasma carotenoid concentrations in older women but not in younger adults or older men (171). As with carotenes, greater body fat is associated with lower serum xanthophylls (130, 143, 145, 171–174). Furthermore, multiple studies have shown measures of abdominal adiposity (waist circumference, waist:height, and waist:hip) to inversely correlate with blood carotenoids (174–177)."

"Consistently, greater BMI is associated with lower circulating carotenoids in both children and in older adults (182–185), although not all studies took carotenoid intake differences into account. These relations may be due to greater fat mass being associated with more oxidative conditions that decrease circulating carotenoid concentrations, or abdominal adipose acting as a sink for circulating carotenoids. Indeed, among various body fat sites, carotenoid accumulation is the greatest in abdominal fat (186)."

"[..]circulating xanthophylls are inversely associated with markers of inflammation, including circulating CRP and IL-6 concentrations, and β-cryptoxanthin is specifically inversely associated with circulating fibrinogen, an acute-phase protein that is elevated in inflammation (141, 189, 190). Similarly, serum xanthophyll and carotene concentrations are inversely associated with type 2 diabetes and impaired glucosemetabolism (191, 192). In addition to lower serum lutein and zeaxanthin, MPOD is lower in type 2 diabetics than in type 1 diabetics and normal controls (193)."

"Malabsorption syndromes, including inflammatory bowel disease and celiac disease, as well as pancreatic insufficiency from cystic fibrosis, are associated with lower serum lutein and zeaxanthin concentrations as well as MPOD in adults (194, 195). Patients with chronic cholestasis, which leads to fat malabsorption, have similar serum β-cryptoxanthin concentrations unlike the other carotenoids (196), suggesting that β-cryptoxanthin may be the most efficiently absorbed carotenoid, even in cases of general malabsorption."

"One study reported that germ-free rats absorbedmore α- and β-carotene and had greater liver vitamin A than rats with humanized microbiota (202)."

"Current advances in human genetics have provided more concrete sources of “host”- associated variables affecting carotenoid absorption and bioavailability (203, 204). Indeed, a recent study in children found blood α- and β-carotene concentrations to be highly heritable (205). Studies have shown variants in genes, such as single nucleotide polymorphisms (SNPs)—a type of single nucleotide variant with a minor allele occurring in ≥1% of the population (206)—and haplotype polymorphisms, to be associated with plasma carotenoids. A haplotype polymorphism refers to a particular combination of SNPs inherited together because of genetic linkage (207). In addition to showing candidate genes involved in carotenoid assimilation, genotype-phenotype studies have shown genetic variation as a determinant of physiologic responses to carotenoids. To date, the most frequent associations with the strongest mechanistic plausibility have been for BCO1 and SCARB1 variants."

"Men homozygous for the SCARB1 rs2706295 T allele had 100% higher α-carotene and 50% higher β-carotene concentrations than those who were homozygous for the C allele (214)."

"Given that carotenoids are transported on lipoproteins, proteins involved in their assembly and metabolism are likely to influence carotenoid responses. Variants in hepatic lipase C (LIPC), ATP-binding cassette transporter (ABCA1), microsomal TG transfer protein (MTTP), NPC1L1, LPL, and cholesteryl ester transfer protein (CETP) genes have shown variable associations with carotenoid status (212, 214, 220–223)."​

- Intestinal β-carotene bioconversion in humans is determined by a new single-sample, plasma isotope ratio method and compared with traditional and modified area-under-the-curve methods


One last thing: go Netherlands!

 

[Amazoniac]

Vitamin A - Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - NCBI Bookshelf

"β-carotene absorption reported by others using similar methods for mixed green leafy vegetables (4 percent) (de Pee et al., 1995), carrots (18 to 26 percent) (Micozzi et al., 1992; Torronen et al., 1996), broccoli (11 to 12 percent) (Micozzi et al., 1992), and spinach (5 percent) (Castenmiller et al., 1999) (Table 4-2)."

"Only one study has been published to assess the relative bioconversion of β-carotene from fruits versus vegetables by measuring the rise in serum retinol concentration after the provision of a diet high in vegetables, fruits, or retinol (de Pee et al., 1998). This study used methods similar to those employed by other researchers (Castenmiller et al. [1999], de Pee et al. [1995], Micozzi et al. [1992], Torronen et al. [1996], and Van het Hof et al. [1999]), and indicated that the vitamin A activity was approximately half the activity for dark, green leafy vegetables compared to equal amounts of β-carotene from orange fruits and some yellow tubers, such as pumpkin squash (de Pee et al., 1998) (Table 4-2)."​

The calculation in other words:

"The efficiency of absorption of β-carotene in food is lower than the absorption of β-carotene in oil by a representative factor of a. Assuming that after absorption of β-carotene, whether from oil or food, the metabolism of the molecule is similar and that the retinol equivalency ratio of β-carotene in oil is 2:1, the vitamin A activity of β-carotene from food can be derived by multiplying a by 2:1."​

Cron-o-meter:

They use the standard equivalences to retinol of '12:1 for b-carotene' and '24:1 for a-carotene and b-cryptoxanthin'.

a-carotene: 6651.8/24 = 277.16 mcg
b-carotene: 5135.2/12 = 427.93 mcg
b-cryptoxt: 0000.0/24 = 0 mcg

Retinol: 0 mcg

Retinol Activity Equivalent (their sum): 705.1 mcg (÷ 0.3 = 2350 IU)​

But with what has been discussed it's possible to recalculate this for a better idea of how much retinol you must be getting.


--
For simplification you can invert the order: instead of carotene:retinol, retinol:carotene. Then all you have to do is multiply by the specific absorption for each food:

1/2 * % absorbed
(but the 2 here is for b-carotene)​

As an example, using the 4 percent value above for mixed greens:

1/2 * 4/100 = retinol 1:50 mixed greens b-carotene (might be a raw salad)​

 

[Amazoniac]

- α- and β-Carotene from a Commercial Carrot Puree Are More Bioavailable to Humans than from Boiled-Mashed Carrots, as Determined Using an Extrinsic Stable Isotope Reference Method

"We anticipated that the carotene and vitamin A values of the raw-grated carrot preparation would be significantly lower than those of the two cooked preparations, but this was not the case. This finding, however, agrees with a previous study (58) in which no difference in serum βC change was noted between groups of subjects fed either carrot juice or raw grated carrots. We speculate that longer gastrointestinal residence time may have compensated for the lack of heat treatment and relatively large particle size of this preparation because it has been suggested that the particle size of ingested foods may affect gastric emptying rate (59,60) and subsequent glucose response (61,62). Prolonged transit time would be expected to result in a shift in the TRL [triacylglycerol-rich lipoproteid] carotene absorption profile to later times, which we in fact observed."

"Estimated masses of β-carotene (βC) absorbed intact by each subject consuming
18.6 mg βC as commercial carrot puree (n = 9), boiled-mashed carrots (n = 9) or
raw-grated carrot (n = 6). Each subject is represented by a unique column pattern.
The mass of absorbed βC was calculated by comparing triacylglycerol-rich
lipoprotein (TRL) βC area-under-curve (AUC) values against the corresponding
AUC for the deuterium-labeled retinyl acetate (d4-RA) reference (4.8 μmol) for
each subject and treatment."​

 

[Amazoniac]

- Beta-carotene accumulation in serum and skin

"Beta-carotene absorption into the body is known to increase when it is taken in association with a high-fat diet. These data confirm that observation and further reveal that essentially no b-carotene is absorbed in the absence of dietary fat."

"The increase in serum b-carotene achieved by dividing the b-carotene dose over three meals as compared with a once-a-day regimen enables significant (three-fold) enhancement of b-carotene absorption without having to increase dietary fat."

"[..]a multicompartment model is required to completely analyze b-carotene absorption. The small bowel accepts a bolus of lipid within a few hours of eating but releases the b-carotene into the serum over a much longer period, exceeding 50 h. This presumably reflects the time required for the b-carotene to be absorbed into intestinal mucosal cells, packaged with lipids, and then released as chylomicrons. With continuous oral administration the serum is observed in this study to accumulate b-carotene with a time constant of the order of 9-10 d."

"Because it is unlikely that any tissue other than the gastrointestinal tract could accumulate fl-carotene faster than it accumulates in serum. the potential therapeutic applications of ficarotene, including treating erythropoietic protoporphyria (12), tumor therapy (5), or enhancing laser angioplasty (9), which demand the highest possible carotene concentrations, are likely to require several weeks on oral b-carotene before the maximum therapeutic benefit can be expected."​

 

[Amazoniac]

An excellent review:

- Host-related factors explaining interindividual variability of carotenoid bioavailability and tissue concentrations in humans (!)

Spoiler: Figure 2. Overview of factors likely to contribute to interindividual variation of carotenoid bioavailability and thus tissue concentrations

 

[Amazoniac]

- Torsten Bohn | Research Gate

↳ β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

"Using in vitro studies, human mastication was determined to enhance the release of β-carotene from the plant matrix in one study by approximately 35% during in vitro gastric and intestinal digestion. The particle size and the type of chewing had more impact on carotenoid bioaccessibility than cell wall presence, with smaller particle size and more fine chewing significantly enhancing bioaccessibility(32), presumably due to enhanced access of digestion enzymes. In line with these results, emulsions with small droplet diameters (0·2 v. 23 μm) improved β-carotene transfer from lipid droplets to mixed micelles and bioaccessibility from approximately 35–60 %(33)."

"[..]following gastro-intestinal digestion, a large proportion of non-absorbed β-carotene reaches the colon (as much as 50-95%). It is unclear what happens under the influence of the gut microbiota(64), but it has been shown that a large proportion of β-carotene is degraded into unknown compounds(56,65), as much as 98% for pure β-carotene(66). However, a report by Mosele et al.(67) points out to a high stability of β-carotene following in vitro colonic fermentation. The remainder, according to a report up to 83%(68), is thus excreted in the faeces. It is likely that the matrix and microbiota differences add significantly to this variation. However, at present, there is no evidence that the colon plays a significant part in the absorption of β-carotene or its metabolites."

"[..]it is important to emphasise that only a fraction of absorbed β-carotene is metabolised in the enterocyte. The importance of this fraction, which was estimated at about 70% by using stable isotope methods(77), likely depends on the vitamin A status of the body[]. The secretion mechanism of β-carotene at the basolateral side of the enterocyte likely depends on its centric cleavage by BCO1, producing retinal, which is then, following conversion to retinol, mainly re-esterified by lecithin-retinol acyl-transferase (LRAT)."

"It is now acknowledged that vitamin A status can regulate β-carotene absorption and cleavage efficiency via a negative feedback loop: the higher the vitamin A status, the lower β-carotene absorption efficiency and cleavage, and inversely. The mechanism involves an intestinal transcription factor termed intestine specific homoeobox (ISX), which acts as a repressor of SCARB1 and BCO1 upon ATRA activation(87,88)."

"Following vitamin A uptake, the intracellular concentrations of ATRA increase, inducing ISX expression. Consequently, less β-carotene is taken up by the enterocyte, and less β-carotene can be converted to retinal. When the intracellular concentration of ATRA drops, which is assumed to be the case when dietary vitamin A intake is low, ISX exerts less repressor activity towards SCARBI and BCO1 and consequently β-carotene uptake and conversion increase."

"A study in Zambian children with hypervitaminosis A supports this regulation. Indeed, these children had high serum carotenoid concentrations(89) and many of them experienced hypercarotenodermia during mango season, a period of high provitamin A carotenoid intake. This might indicate as a possible explanation that conversion of provitamin A carotenoids to retinal by BCO1 was more inhibited by the hypervitaminosis A than their absorption via SR-BI, which is encoded by SCARB1. This is not surprising, as provitamin A carotenoid absorption involves not only SR-B1 but also CD36(62), which is not assumed to be regulated by ISX."

Makes us wonder: what happens if there's intereference with its activation?​

"The enterocytes are assumed to secrete most of the newly absorbed β-carotene into chylomicrons, though it has been suggested that water-soluble β-carotene metabolites, e.g. apo-carotenals, could be secreted in the portal circulation and therefore directly reach the liver []."

"The fact that β-carotene is carried in the blood by chylomicrons during the postprandial period implies that its metabolism is closely related to that of these TAG-rich lipoproteins."

"The liver is the main storage organ for vitamin A mainly in the form of retinyl esters. It has been estimated that for healthy, well-nourished individuals, approximately 70% of vitamin A present in the body is stored in the liver(98)."

That should be up-to-the-date. In the RDA calculations they assume it's 90%, which results in an underestimation of requirements. Not knowing if it's desirable to have much of it outside of liver, it's better to suppose that most is found there anyway, letting the reserves elsewhere be decreased.​

"Concerning its cleavage [in liver], it is assumed that it is either cleaved to retinal by BCO1, which is highly expressed in hepatic stellate cells(105), or by BCO2, which is apparently more expressed in hepatocytes(105). The fraction of β-carotene that does not undergo this cleavage is either incorporated into VLDL and secreted into the blood, or stored in lipid droplets in parenchymal and hepatic stellate cells(105,106)."

"Following absorption, a large proportion of carotenoid and later retinoid metabolism is under control of nuclear hormone receptor signalling, as a partly autoregulatory homoeostatic regulated process. Many steps, involving receptors such as RARβ, to anabolic enzymes including BCO1(128), BCO2 and aldehyde dehydrogenase 1 family, member A3 (ALDH1A3), catabolic enzymes including CYP26A1 and LRAT and binding proteins, including RBP1, RBP4 and cellular-retinoic acid binding protein 2 (CRABP2) are under control of RAR-RXR- and PPAR-RXR-mediated signalling(129,130). RAR-RXR and PPAR-RXR-mediated signalling also controls various other important lipid metabolic processes and places carotenoids as precursors of important regulators of general lipid metabolism as reviewed earlier(131)."

"The physiological and nutritional relevance of additional apo-carotenals and apo-carotenoic acids remains unclear, and they were described as low affinity activators / competitive antagonists of nuclear hormone receptors, as reviewed previously(143). Unfortunately, a clear link between the low physiological and nutritional relevant levels in human subjects or high level and further dependent biologicalmediated signalling were not described yet, and thus no nutritional or physiological relevance can currently clearly be associated with these derivatives."

"Human subjects centrally cleave β-carotene to retinal and following oxidation and reduction a larger array of multi-functional retinoids are created which have been detected endogenously []. This BCO1-mediated conversion of β-carotene to retinal is therefore an important bottleneck, which is highly controlled and mediated by various factors: (A) availability of the substrate and saturation of the enzymatic conversion potential, (B) presence and relative levels of food derived inhibitors, (C) spatial and temporal regulation and localisation of the enzyme, (D) sex-specific regulations, (E) feedback regulations by bioactive products transcriptionally controlling BCO1-expression and (F) the previously reported polymorphisms of BCO1 as well as assisting proteins."

"Starting with the overall conversion in the human organism, β-carotene was reported to vary largely in absorption efficiency (30-70%) upon intestinal uptake, as explained earlier. This variation is in part due to the variation in BCO1 cleavage potency, partly explainable by frequently occurring polymorphisms of BCO1(82,83). Alternatively, many factors which are summarised here describe the inter- and auto-regulatory pathways in BCO1-mediated cleavage to retinoids, enabling RAR- or/and RXR-mediated signalling."

"The main question is how BCO1 and its mediated cleavage to centric cleavage metabolites are regulated in the human organism. As described earlier, six major steps (A–F) have been reported and identified. First, the availability of the substrate is usually a major factor for increased conversion and resulting product levels []. This conversion was presented as a saturating curve, plateauing at β-carotene levels in the range of 15,000-40,000 and 80,000-240,000 nM for β-cryptoxanthin(144). For comparison, the endogenous levels for β-carotene were in average range of 360 nM in serum and up to 31,830 nM in organs, while being highest in the adrenals and β-cryptoxanthin in the average range of 230 nM in serum and with highest tissue levels of 2,900 nM in adrenals, as reviewed recently(13). We can thus conclude that these active ranges were not reached in serum, while tissue levels approach the saturation of enzyme conversion(13,144)."

"It should be noted that serum and tissue levels do not represent freely available carotenoids, but mainly carotenoids attached to binding proteins and carotenoids associated in lipid vesicles in the membranes and lipid accumulating vesicles such as in the adipose tissue(13)."

"The second modification factor are other carotenoids such as canthaxanthin, lutein and zeaxanthin(72,188), which can inhibit BCO1-mediated conversion partly in a competitive manner. The specific mechanisms of these phenomena were not investigated deeper, and neither have nutritional relevant ranges and relevant ratios been examined. It is likely that these three carotenoids can attach and bind to the active site of the BCO1, thereby inhibiting the binding and enzymatic conversion of known pro-vitamin A carotenoid BCO1 substrates (β-carotene, α-carotene, β-cryptoxanthin, apo-8′-carotenal and lycopene). In in vitro studies, it was reported that three times higher levels of lutein (compared with β-carotene) interfered with β-carotene conversion."

"The third modifying factor is the specific spatial and temporal regulation of BCO1 expression in the human organism(144). Highest BCO1 expression was found in different parts of the intestine, with highest expression levels in the jejunum []. Other relevant tissues are reproduction organs testis and prostate in males as well as ovaries in females, comparable with levels found in kidney, liver, skeletal muscle and stomach []. [Also,] the relatively high expression levels observed in the eye(192)."

"As a fourth modification, sex specific regulations were observed. In male mice and rats, a connection between testosterone and carotenoid as well as BCO1-expression was found(193–195), while oestrogen/testosterone correlated in older woman with carotenoid levels(196). If non-reproduction-related organs also display this regulation, depending on sexual steroid hormones, was not further investigated. One indicator are higher ATRA and lower retinol serum levels in women v. men(197), likely as a consequence of higher levels of β-carotene in their serum/plasma, mainly due to the less healthy nutritional status(13,198,199), or higher BCO1 presence and activity."

"The fifth modifying effect is the regulation of BCO1 on the transcriptional level. A feedback mechanism was identified, partly already before a clear identification, characterisation and expression of BCO1 in mice, rats and chicken and human subjects(189,190,208–210). The conversion and ratio of ATβC to retinoids, especially all-trans-retinal, was used to identify BCO1 activity(128,211). Feedback mechanisms were claimed as a direct involvement of ATRA-RAR-interaction and transcriptional modification of BCO1 expression was shown. ATRA–RAR-mediated signalling is suggested to regulate BCO1 expression identified, either indirectly by retinal conversion per homogenate ratio or directly by mRNA quantification, as a negative feedback mechanism(128). Treatments of rats with ATRA, retinyl acetate, β-carotene or a synthetic RAR-agonist (Ro41-5253) significantly reduced BCO1 activity [yet absorption being less affected] identified by retinal conversion(128). Focusing on ATRA, retinyl acetate and β-carotene treatments to rats, it was found that also serum retinoic acid levels increased and partly negatively correlated with reduced intestinal BCO1 activity(128)."

↑ All-trans poisonoic acid
↓ Carotene absorption
↓↓ Carotene oxygenase activity​

"It is noteworthy that nutritional supplementation with high β-carotene can result even in decreased local levels of ATRA with potential negative effects and increased vulnerability towards carcinogenesis as shown in β-carotene-supplemented ferrets []. This highlights the limits of β-carotene signalling mediated autoregulation using non-nutritional relevant to high β-carotene stimuli, with even previously reported negative side effects in human subjects as found in the ATBC and Carotene and Retinol Efficacy Trial (CARET) studies(11,12)."

Not sure if carotenemia can induce some of these issues.​

"Recently it was reported that glucocorticoid regulated pathways and hepatocyte nuclear factor (HNF)1α and HNF4α pathways are important regulators of BCO1 expression(220)."

"In addition, RXR-PPARα and -PPARγ-mediated signalling was identified as an alternative mechanism, providing positive feedback(221,222). The PPARα and PPARγ nuclear hormone receptor heterodimers can be either activated by an RXR-ligand or alternatively by the respective PPAR ligand. For PPARs and HNF4α FFAs and fatty acid metabolites have been identified as natural ligands (Fig. 5(223,224)). After a high-dietary intake of fat this important regulatory pathway is initiated by increased levels of FFAs as a direct result of the diet rich in fat and results further in increased BCO1-expression as a direct feedback to this high-fat diet. These two nuclear hormone receptor heterodimers need either an RXR-ligand as well as/or a PPAR-ligand."

↑ Fat intake
↑ Carotene oxygenase activity​

"Dietary transglutaminases can provide PPAR ligands, thus synchronising fat, and concomitantly carotenoid, uptake/availability with BCO1 up-regulation. It was described that the main BCO1-metabolite ATRA is regulating via ATRA–RAR-mediated signalling various important steps in lipid metabolism(206,225,226), with a focus also on counteracting fat accumulation via energy dissipation in adipose tissue(226–229) and regulation of insulin secretion(230,231)."

"The second possibility for negative feedback is the potential synthesis of the endogenous RXR-ligand 9CDHRA, starting from still non-identified carotenoid precursors (Rühl et al., unpublished results (160)). This means that the endogenous RAR ligand ATRA and the endogenous RXR-ligand 9CDHRA obtain potential opposite regulation on their own synthesis via positive or negative feedback control mechanism of BCO1 expression and further activity (Fig. 5). As a consequence, levels and dietary intake of specific carotenoid precursors may influence or even control BCO1-mediated synthesis of endogenous RAR- or RXR-ligands and further controlling metabolic processes associated with lipid metabolism with relevance for obesity and diabetes."​

↳ Negative effects of divalent mineral cations on the bioaccessibility of carotenoids from plant food matrices and related physical properties of gastro-intestinal fluids

Greater amounts of calcium and magnesium were needed for inhibition. These divalent cations interact with bile acids and fatty acids, form Raj's soaps and prevent their adsorption.

Spoiler: Effect of minerals on the bioascisalvsbrity of b-carotene across different food matrices

 

[Cirion]

Most of the details on this I admit goes over my head but so this point

- A vitamin A deficiency increases your capacity to absorb carotenes.

Can you expand on this. Wouldn't this in some ways make following a low VA diet almost be detrimental, ironically, if one of your goals is to purge carotenes? Could this explain why some people following low VA diet seemingly can't tolerate even one cheat meal containing carotenes?

 

[Amazoniac]

Most of the details on this I admit goes over my head but so this point

- A vitamin A deficiency increases your capacity to absorb carotenes.

Can you expand on this. Wouldn't this in some ways make following a low VA diet almost be detrimental, ironically, if one of your goals is to purge carotenes? Could this explain why some people following low VA diet seemingly can't tolerate even one cheat meal containing carotenes?

Not at all because there's a limit to how much it can increase. Those celebrities are keeping their carotenoids intake quite low, so even if they adsorbed a great deal of the amount ingested, it wouldn't get in the way of depletion. It might be enough to trigger inflammation again and possibly extend it, but it should continue regardless. Excess storage is likely a reflect of a problem that must eventually contribute to it.

Good point. This is related to the dose-response test, where people have an usual reaction to a small dose of poison A when stores are lowered.

 

[Amazoniac]

- Factors affecting the fate of β-carotene in the human gastrointestinal tract: A narrative review

Spoiler

"A 2.5-fold increase in β-carotene plasma levels was observed after ingestion of β-carotene along with dietary fat (200 g) compared to the undetectable change in plasma levels when β-carotene was ingested in the absence of dietary fat [27]. Furthermore, increased β-carotene plasma levels were reported after ingestion of salad prepared with avocado (150 g avocado) as well as avocado oil (24 g) [74] compared to salad alone.

In contrast, with increase in dietary fat [..] content from 10% to 30% in diet, it was observed that vitamin A stores were higher, whereas hepatic β-carotene stores were lower. This phenomenon was attributed to the enhanced bioconversion of β-carotene into vitamin A with increased dietary fat ingestion [75]. However, an increase in β-carotene plasma level was observed when 8 mg of β-carotene was ingested with increasing amounts of fat (from 3 g to 36 g). These observations suggested that a minimum threshold of dietary fat is required to facilitate the absorption of β-carotene (3 g of dietary fat for 8 mg β-carotene). However, above that threshold (3 g fat for 8 mg β-carotene), additional dietary fat does not significantly influence the bioavailability of β-carotene. The amount of dietary fat required for optimal β-carotene bioavailability is still unclear [67, 76]. However, in one study the minimum amount of dietary fat required for optimum absorption of β-carotene was suggested to be 5 g of fat per meal [62]. This assumption was supported by a study where the addition of 20% of cooked oil to homogenized carrot pulp significantly increased the in vitro accessibility of β-carotene [26]."

↳ [75] Amount of Dietary Fat and Type of Soluble Fiber Independently Modulate Postabsorptive Conversion of b-Carotene to Vitamin A in Mongolian Gerbils

Spoiler

Spoiler

 

[Apple]

- Factors affecting the fate of β-carotene in the human gastrointestinal tract: A narrative review

Spoiler

"A 2.5-fold increase in β-carotene plasma levels was observed after ingestion of β-carotene along with dietary fat (200 g) compared to the undetectable change in plasma levels when β-carotene was ingested in the absence of dietary fat [27]. Furthermore, increased β-carotene plasma levels were reported after ingestion of salad prepared with avocado (150 g avocado) as well as avocado oil (24 g) [74] compared to salad alone.

Spoiler

​

In contrast, with increase in dietary fat [..] content from 10% to 30% in diet, it was observed that vitamin A stores were higher, whereas hepatic β-carotene stores were lower. This phenomenon was attributed to the enhanced bioconversion of β-carotene into vitamin A with increased dietary fat ingestion [75]. However, an increase in β-carotene plasma level was observed when 8 mg of β-carotene was ingested with increasing amounts of fat (from 3 g to 36 g). These observations suggested that a minimum threshold of dietary fat is required to facilitate the absorption of β-carotene (3 g of dietary fat for 8 mg β-carotene). However, above that threshold (3 g fat for 8 mg β-carotene), additional dietary fat does not significantly influence the bioavailability of β-carotene. The amount of dietary fat required for optimal β-carotene bioavailability is still unclear [67, 76]. However, in one study the minimum amount of dietary fat required for optimum absorption of β-carotene was suggested to be 5 g of fat per meal [62]. This assumption was supported by a study where the addition of 20% of cooked oil to homogenized carrot pulp significantly increased the in vitro accessibility of β-carotene [26]."​

​

↳ [75] Amount of Dietary Fat and Type of Soluble Fiber Independently Modulate Postabsorptive Conversion of b-Carotene to Vitamin A in Mongolian Gerbils

Spoiler

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View attachment 27158

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So 1 spoon of olive oil in daily carrot salad is good?

 

[Amazoniac]

So 1 spoon of olive oil in daily carrot salad is good?

It's fine and an amount that's beyond the minimum needed to promote absorption of macabrotenes. To make use of this additional fat in their metabolism, you'll be counting that the others factors are working properly. I wouldn't base how much to add to the meal on this.

 

[Amazoniac]

I realized that some of those experiments wasn't evaluating the meal response to varying fat intakes, but the overall long-term effect that they have.

In the short-term, increasing doses lead to expected rises:

- Modeling the dose effects of soybean oil in salad dressing on carotenoid and fat-soluble vitamin bioavailability in salad vegetables

Spoiler

"Each participant consumed 5 test salads that had equivalent vegetable composition but were consumed with salad dressings that contained different amounts of soybean oil (0, 2, 4, 8, or 32 g)."

"Each test salad contained
- 48 g spinach (Spinach; Dole Food Company)
- 48 g romaine (Hearts of Romaine; Fresh Express)
- 66 g shredded carrots (Shredded Carrots; Dole Food Company)
- 85 g cherry tomatoes (NatureSweet)
(7)."

Was is diversification of the response as the fat content increases.

I had mind that extra fat in a meal was invariably detrimental in the presence of macabrotenoids. What I take from these experiments is that there can be a positive side to the additional fat when it facilitates the conversion. Increased liver content of poison A in the high-fat group wasn't as surprising as the decrease in macabrotenes compared to low-fat intake.

To reap these "advantages", proper cleaving of macabrotenes has to be occurring, otherwise the person is just letting more macabrotenes in. Availability of fatty acids shouldn't be a major determinant. Nevertheless, some macabrotenoids can't become poisonoids.

There's also this detail (from the previous):

"Dietary fat levels were chosen on the basis of what is considered a very-low-fat diet (10% total energy) and the current dietary guidelines for fat intake (30% total energy) for humans. Cottonseed oil was used as a source of dietary fat because of its relatively low carotenoid content."​

In both experiments they used oils rich in terminoleic acid (C18:2). Absorption aside, a greater availability of napalmitic (C16:0), stentic (C18:0) or adulteroleic (C18:1) acid might be productive for being more physiologically compatible with poisonol.

If no fat is added to the meal in attempt to prevent the uptake, the macabrotenoids can still impregnate the intestine and interact with the next meal. It may be a futile avoidance while missing the benefits that some fat in meals can confer. It's preferable to add tocoinphernals to them, unlike the encased macabrotenoids in plants, the free oils should be easier to be absorbed and the fraction that is not will protect the unabsorbed macabrotenoids throughout the digestive tract until excretion.

 

[Amazoniac]

- Dietary fat composition, food matrix and relative polarity modulate the micellarization and intestinal uptake of carotenoids from vegetables and fruits

Spoiler

"In the present study, the effect of amount and type of vegetable oils on carotenoid micellarization from carrot, spinach, drumstick leaves and papaya using in vitro digestion/Caco-2 cell model have been assessed."

"The relative micellarization of carotenoids decreased in the order of olive = soybean = sunflower > peanut = palm > coconut oil independent of the food matrix."

"These results are similar to the observations with spinach and mixed salad digested with long chain unsaturated fatty acids (Nagao et al. 2013; O’Connell et al. 2008; Failla et al. 2014). For instance, the micellarization of b-carotene from spinach was found to be higher with unsaturated fatty acids compared to saturated fat (Nagao et al. 2013). In this study oleic acid (monounsaturated) better facilitated the micellarization compared to polyunsaturated fatty acids (linoleic acid and a-linolenic acid) from spinach supplemented with 0.1% fat. Further, studies in human subjects also reported higher absorption of carotenoids when supplemented with fat rich in monounsaturated fat (Clark et al. 2000; Goltz et al. 2012). Despite the fact that monounsaturated fatty acid content of olive oil is twofold higher compared to soy and sunflower, the extent of micellarization with these fat sources remained similar in the present study, which could be due variations in amount of dietary fat and source of lipids (fatty acylglycerols vs oils) used for digestion reactions. In contrast, carotenoid micellarization from a mixed vegetable salad was found to be slightly but significantly higher from soybean oil compared to olive oil (Failla et al. 2014). However, in the present study the effect of these two oils remained similar, which could be due to differences in food matrix used for the digestion reactions. The lowest micellarization of carotenoids, including lutein with coconut oil could be explained by its higher content of medium chain fatty acids. The primary role of dietary fat is to facilitate the release of carotenoids from food matrix and their subsequent micellarization (Borel et al. 1996; Rich et al. 2003). The short chain fatty acids with low relative hydrophobicity may not efficiently facilitate the release of carotenoids from plant pigments leading to their poor micellarization. Consistent with this notion, dietary triacylglycerols with long-chain rather than medium-chain fatty acids reported to enhance the micellarization and absorption of b-carotene (Nagao et al. 2013; Huo et al. 2007; Borel et al. 1998)."

 

[Amazoniac]

- Carotenoids: Sources, medicinal properties and their application in food and nutraceutical industry

Spoiler

The content varies.

- β-Cryptoxanthin: Chemistry, Occurrence, and Potential Health Benefits

- Absorption, metabolism, and functions of β-cryptoxanthin

Spoiler

"Many of the best sources of β-cryptoxanthin are citrus fruits."

"Most in vitro, animal model, and human studies suggest that β-cryptoxanthin is better absorbed from its major food sources than are other common carotenoids. For example, a comparison of the apparent bioavailability (the fraction of the nutrient that becomes absorbed and available for use or storage) of retinoid-forming carotenoids (β-cryptoxanthin, α-carotene, and β-carotene) showed that β-cryptoxanthin was move bioavailable in every population studied.[22] This is supported by other studies that found β-cryptoxanthin from orange fruits to be more bioavailable than β-carotene–rich foods.[23,24]"

"There are several reasons why the absorption of β-cryptoxanthin from dietary sources might be greater than that of most other common carotenoids. SR-B1 [transporter] preferentially facilitates the absorption of xanthophylls (such as β-cryptoxanthin and lutein) over carotenes (such as α- and β-carotene).[25] In addition, the position of a carotenoid incorporated into a mixed micelle depends on its hydrophobicity: the less polar the carotenoid, the more likely it is to be located in the interior of the micelle, where it is less available for absorption. β-Cryptoxanthin is more hydrophilic than other important carotenoids such as lycopene, β-carotene, and α-carotene[3,4] and is thus believed to have relatively higher absorbability due to its presence on the outer surface of micelles and its higher solubility in the aqueous environment of the intestine. Indeed, the percentage of β-cryptoxanthin incorporated into micelles during in vitro digestion is 3 times greater than that of β-carotene under similar conditions.[26]"

"Carotenoids are crystalline in form and are dissolved within oil droplets in the chromoplasts of yellow and orange fruits such as papaya, tangerines, and sweet potatoes.[27,28] Considerable evidence shows they are extracted and digested more easily than carotenoids bound to pigment–protein complexes within the chloroplasts of leafy green vegetables.[4,23,24,27,29]"

"β-Cryptoxanthin appears to be much better absorbed than other carotenoids.[22–24] A comparison of apparent bioavailability between different provitamin A carotenoids showed that β-cryptoxanthin–rich foods had 725% greater bioavailability than β-carotene–rich foods (Figure 1).[22]"

"Within foods, many carotenoids are bound to proteins that must be denatured by bile acids.[3,4] Very low-fat diets can decrease carotenoid digestion and absorption, but the effect of fat in the diet is inconsistent and appears to be small.[38–40] β-Cryptoxanthin may be less affected by these conditions than other carotenoids. In a study comparing carotenoid plasma levels in chronic cholestatic patients with those in age-matched control subjects, β-cryptoxanthin was the only carotenoid not significantly lower in the control group,[41] which may suggest that β-cryptoxanthin is more effectively absorbed and transported despite fat malabsorption or compromised liver function." ⇈

"A human study that directly compared the bioavailability of carotenoids from carrot, tomato, and papaya in 16 nonsmoking men and women showed that β-carotene bioavailability from papaya was 3 times greater than carotenoid bioavailability from tomatoes or carrots, and lycopene bioavailability from papaya was 2.6 times greater than that from carrots or tomatoes, suggesting that food matrix impacts bioavailability, with carotenoids in fruit being more bioavailable.[44] Furthermore, β-cryptoxanthin from papaya was 2.9 times more bioavailable than β-carotene from papaya, potentially indicating that the β-cryptoxanthin molecule itself was more bioavailable than β-carotene. Thus, observational, in vitro, and human intervention studies suggest that β-cryptoxanthin has greater bioaccessibility and bioavailability than other common carotenoids such as β-carotene, α-carotene, and lycopene."

 

[Amazoniac]

- Effect of Orange Juice’s Processing on the Color, Particle Size, and Bioaccessibility of Carotenoids

This study was aimed at assessing the differences between industrially processed and hand-squeezed orange juices (OJs) in relation to their color, particle size, carotenoid content, and carotenoid bioaccessibility. Specifically, industrial samples of fresh squeezed OJs after the finishing steps (FISO) and the same OJs after pasteurization (PISO), as well as hand-squeezed OJs (HSO) were studied. The results showed that the HSO and PISO were different (p < 0.05) in terms of color (darker and more reddish vs brighter, more yellowish and colorful), particle size (volume and surface area mean diameter), and total carotenoid content (29 ± 5 and 22 ± 3 mg/L, respectively). On the other hand, the industrial extraction of OJs reduced the particle size distribution, and accordingly, the relative bioaccessibility of bioactive carotenoids increased (p < 0.01). Independently of the type of OJ, the bioaccessibility of carotenoids in decreasing order was the following: α-carotene > β-cryptoxanthin > β-carotene > zeaxanthin > lutein.

 

[Amazoniac]

- Carotene Utilization as Influenced by the Addition of Vitamin B12 to Diets Containing Yeast or a Synthetic Vitamin Mixture

Rats fed 60 µg of carotene daily together with a diet containing yeast-b, -c or -d, without additional vitamin B12, stored significantly more vitamin A than did those on a diet containing yeast-a.

The addition to the synthetic vitamin-mixture diet of an amount of niacin approximating that in the yeast diet (4.0 mg/100 gm of diet) did not influence carotene utilization.

Rats receiving the B vitamins from the synthetic vitamin mixture without added vitamin B12 stored significantly more vitamin A than did those on the yeast-a diet. However, their storage was similar to that of the rats receiving the yeast-b, -c or -d diets.

The utilization of carotene was significantly increased when vitamin B12 was added to the yeast-a or -b diets. There was no significant increase when this vitamin was added to the yeast-c diet.

The addition of vitamin B12 (3.0 µg/100 gm diet) to the diet containing a mixture of synthetic vitamins did not increase carotene utilization. Rats receiving this diet stored significantly less vitamin A than did those fed the yeast-a or -b diet with added vitamin B12.

The results of this investigation indicate that some factor (or factors) in addition to vitamin B12 influenced the utilization of carotene.