Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[stargazer1111]

There is no such thing as zero vitamin A milk. 1% milk has almost 300 IU per litre, and 0.1% has almost 30 IU per litre. That's with cows eating at least some grass but there are almost no carotenoids in milk and the cows are supplemented so I doubt it's any different with grain-fed cows. I very much doubt it's 0 IU retinol unless they managed to make it 0.00% fat

This milk has every gram of fat removed and no vitamin A added back in. They sent me the lab results showing no detectable levels of vitamin A

 

[tallglass13]

There is no such thing as zero vitamin A milk. 1% milk has almost 300 IU per litre, and 0.1% has almost 30 IU per litre. That's with cows eating at least some grass but there are almost no carotenoids in milk and the cows are supplemented so I doubt it's any different with grain-fed cows. I very much doubt it's 0 IU retinol unless they managed to make it 0.00% fat

Actually I called organic pastures today spoke with a representative they had to call me back. Their skim milk has 0% vitamin A oh, okay actually more accurate is that it is not fortified with anything and the small minoot amounts it would be left is all that's in there.

 

[Cirion]

Interesting on that VA free milk. I'm done experimenting with dairy though, but maybe one day I'll try it again. Milk is just too high in tryptophan for my tastes

 

[Spondive]

No skin problems for 23 men after going Poison/"Vitamin A" free for 2 years!

I wonder what their diet was like

 

[stargazer1111]

Interesting on that VA free milk. I'm done experimenting with dairy though, but maybe one day I'll try it again. Milk is just too high in tryptophan for my tastes

I am concerned about the potential for it to escape the detection of the lab's assays while bound to casein, though. This could be an issue.

 

[postman]

Actually I called organic pastures today spoke with a representative they had to call me back. Their skim milk has 0% vitamin A oh, okay actually more accurate is that it is not fortified with anything and the small minoot amounts it would be left is all that's in there.

I'm sorry but it's nonsense. If it's 1% it will have almost 300 IU per litre, and if it's 0.1% it will have almost 30 iu per litre. Which is not a lot but still some, comparable to things like chicken meat, as a source of protein.

This milk has every gram of fat removed and no vitamin A added back in. They sent me the lab results showing no detectable levels of vitamin A

If it's literally 0.00% fat then yes that could be the case but I doubt that. I wonder what kind of accuracy the lab measured the VA content to, I suspect it's just yet another very low listing that they rounded down to zero, as so many of these labs seem to do. In either case the exposre would be very low anyways. I haven't looked into the casein thing though.

 

[Blossom]

I'm sorry but it's nonsense. If it's 1% it will have almost 300 IU per litre, and if it's 0.1% it will have almost 30 iu per litre. Which is not a lot but still some, comparable to things like chicken meat, as a source of protein.


If it's literally 0.00% fat then yes that could be the case but I doubt that. I wonder what kind of accuracy the lab measured the VA content to, I suspect it's just yet another very low listing that they rounded down to zero, as so many of these labs seem to do. In either case the exposre would be very low anyways. I haven't looked into the casein thing though.

There was a discussion about how when A is converted to retinoic acid by heat it no longer fluoresces. I’m sure Grant would share the science that led him to that line of thinking.

 

[Amazoniac]

Chitin and Chitosan are different.

But they have similar properties. So if you're dealing with something that has the potential to be problematic, will require a significant dose to affect, have a great risk of compromising other nutrients before making a difference on vitamin A, and still not addressing the cause of the disturbance, in my opinion it's not worth it.

This is a safer option:
- Why Ray Recommends Eating Lots Of Calcium
- Grant Genereux's Theory Of Vitamin A Toxicity (carotene thread)

Not long ago it was posted a story of a woman taking 600,000 IU daily (a few days using 1,000,000 and 2,000,000 IU) for 18 months. The only thing they did was to advise stopping supplementation. It took a few days to normalize various signs of excess and a month to stop hair loss. Reports like this makes us wonder what's actually going on in people who only get better when the avoidance is extreme. I guess most of the effort must be on understanding the underlying issue rather than coming up with new management strategies, unless you suspect it's an inevitable condition and the person is after more variety in the diet.

No skin problems for 23 men after going Poison/"Vitamin A" free for 2 years!

charlie, I know the guys that were banned from the thread did something that you judged inappropriate, but (as you know) right now there's a private conversation going on functioning as a sub-foro for the oppressed minority. It would be much more productive to have the shamans making their good points here again.

I also understand you like Garrett for whatever reason, but he is a charlatan, and a qualified one (it took me longer than what I'm proud of to realize). It's much faster for him to make careless and mindless comments than it is to go through each in prudent and measured way. Unfortunately many of you are spreading the word without questioning what he posts, so we need more of such opposing voices around.

Without Contraries There is No Progression

If you unban them one more time I can buy you a Purely Carrot from Jamba Juice if you want. Offer valid for a limited time only.

 

[Amazoniac]

..or we can ask @Constatine: what is your opinion on all this the truth?

 

[Dobbler]

People gettin banned for going against vitamin a trend now? nice

 

[Orion]

I am concerned about the potential for it to escape the detection of the lab's assays while bound to casein, though. This could be an issue.

I asked Grant about this on his forum, and there are no studies that have directly test this, we need an actual lab to take heated milk casein and test for retinoic acid. We know that in the past before retinoic acid was discovered(1920s to 1950s), they heated the casein and retinol disappeared, so we assume it turned to RA via oxidation.

Retinol in Casein bypassing liver

Any reason you are not using rice for carbs?

We are on similar paths, I took high dose retinyl palmitate as well after reading that same study. 300K/day for few months, also two rounds of accutane in the past, different body chemistries, different reactions. Main symptoms for me were; sleep issues, cognitive decline-depression, skin worsening(acne, dandruff, oiliness, flakiness), eye site decline in left eye, continued hair shedding.

Now into my 6 months of low VA, symptoms very slowly fad, come and go, but continue in a positive direction.

 

[schultz]

Here is the funny part. While I was toxic with vitamin A, I was simultaneously almost toxic with vitamin D because I was taking 20-30,000 IU per day of the D at the same time. My D level was 189 ng/ml at the time I was in the ER. The toxic range starts at 200. I'm lucky I saw this and stopped taking so much. The D level dropped much more quickly than the vitamin A and I am now on about 8,000 IU per day which keeps it at a reasonable, non-toxic level. My serum calcium was surprisingly normal.

They didn't check PTH or anything else because the doctors were stupid. They had to wikipedia hypervitaminosis A and had no idea what to look for. I did and I requested the specific tests but they obviously didn't listen because I am only a biochemist.

That's too bad as it would have been interesting to see the other numbers. I am surprised your calcium level was normal considering that D level. The important thing is you recovered!

"When a pharmacological dose of preformed vitamin A is ingested (about 20 times the vitamin A recommended daily allowance in this study), LRAT capacities are overwhelmed, the esterification of retinol by ARAT becomes significant, and retinyl esters are produced using ingested fatty acids. This can explain the appearance of retinyl linoleate after the sunflower meal. When a high dose of preformed vitamin A is ingested together with a small amount of fatty acids, LRAT capacities are overwhelmed, and ARAT cannot esterify the excess of free retinol because of shortage of newly absorbed fatty acids. In these conditions a large fraction of retinol is incorporated in its free form in chylomicrons. This mechanism can explain why amounts and species of triacylglycerols affect the pattern of retinoids secreted in chylomicrons only when a pharmacological dose of preformed vitamin A is ingested."

This is quite fascinating. I imagine this effect would result almost entirely from using supplements of vitamin A. I posted a study in another thread regarding vitamin A, before I started posting on this thread, which was talking about how retinol in the form of liver produces a smaller and delayed rise in retinol levels whereas supplements can cause a quick spike. Here is the quote...

"Buss et al. [4] examined the serum levels of potentially teratogenic metabolites of vitamin A in 10 nonpregnant women, when consumed as dietary retinyl palmitate, both in the form of liver and as a supplement. Dietary retinol in the form of liver produced a smaller and delayed rise in serum retinol levels than vitamin A consumed as retinyl esters. This suggests that the latter form of vitamin A may have a more marked effect in producing teratogenic metabolites. Therefore, not only must pharmacokinetic properties of vitamin A metabolites be considered, but also the dietary form in which vitamin A is consumed.

Here is where I posted that (link)

I was trying to make the case that, although I wouldn't supplement vitamin A during pregnancy, I don't think there is a need to avoid liver. For one thing 4oz of liver has only 22,000 IU and if you're eating it once a week that is not a lot compared to a 10,000IU per day supplement. You shouldn't eat it everyday though... (I am aware that vitamin A levels in liver can vary quite a bit... something else to consider)

Part of his theory is that the retinol is converted to retinoic acid by heat and is not detected by normal analysis.

I am under the impression he was talking about early chromatography (I may be wrong). New methods should be able to detect it.

 

[Blossom]

New methods should be able to detect it.

That would be great especially for people who like and tolerate milk but still feel they need to watch their A intake.

 

[Amazoniac]

The Institute of the Medicines has set 2:1 as the equivalence of purified b-carotene in oil to retinol. James Olson noted in one of his articles that it becomes less efficient as the dose increases, and he seems right. However! If the efficiency of carotene adsorption doesn't become less efficient along, it means that they'll keep getting adsorbed but without having a poisonous function, leaving the person with a disproportionate amount of these compounds in the body that can has undesirable hormone-like effects. The same problem will occur if the person is a poor converter of propoison A to poison A.

- A review of vitamin A equivalency of β-carotene in various food matrices for human consumption

"VEB ['Vitamin A equivalency of b-carotene'] may be regarded as constant as long as the consumption of b-carotene is within physiological ranges and the host is in good wealth. With pharmaceutical doses of b-carotene, serum b-carotene levels increase, and VEB can decrease when an oral dose of b-carotene increases(2,12,13). The habitual diet type determines the composition of the diet, and therefore various nutrient-to-nutrient interactions affect to a larger extent the absorption of b-carotene. For example, b-carotene absorption can be inhibited by lutein(14,15), when a minimum amount of about 5 g dietary fat is consumed simultaneously in a meal to ensure intestinal b-carotene uptake(16). Also, absorption of b-carotene is reduced when dietary fibre content increases. Fibre interacts with bile acids, resulting in decreased absorption of fats and fat-soluble substances such as b-carotene(17)."

"The current recommendation of the FAO/WHO is 3·3:1 and that of the IOM is 2:1 for VEB in oil. Fortified foods and dietary supplements are available, which contain physiological doses of b-carotene in oil(2,4) to complete an inadequate diet pattern. In four studies with unlabelled b-carotene, the IOM recommendation of 2:1 for VEB in oil has been confirmed(28,29,63,64). In seven studies with labelled compounds, a VEB in oil ranging from 3·4:1 to 9·1:1 has been reported in adults, which was less efficient than that reported by the four studies for VEB in oil of 2·0:1 to 3·2:1 in school children. As has already been established(12,65), the studies using higher amounts of ingested b-carotene resulted in higher reported VEB. By only considering the studies with amounts of ingested b-carotene that were lower than 6mg, a VEB in oil for a Western diet ranged from 2·3:1 to 5·7:1 and for a ‘prudent’ diet from 2:1 to 6·3:1. Furthermore, by only considering the studies with amounts of ingested b-carotene that were lower than 2mg, a VEB in oil for a Western diet ranged from 2·3:1 to 3·6:1 and for a [mediterranean] diet from 2:1 to 3·8:1."

"For humans consuming b-carotene dissolved in oil, a VEB between 2:1 and 4:1 is feasible in a Western diet as well as in a [mediterranean] diet. The down-regulation mechanism of the expression of BCMO1 by high doses and genetic polymorphisms in the BCMO1 gene might explain the observed variations in VEB in oil."

This is quite fascinating. I imagine this effect would result almost entirely from using supplements of vitamin A. I posted a study in another thread regarding vitamin A, before I started posting on this thread, which was talking about how retinol in the form of liver produces a smaller and delayed rise in retinol levels whereas supplements can cause a quick spike. Here is the quote...

"Buss et al. [4] examined the serum levels of potentially teratogenic metabolites of vitamin A in 10 nonpregnant women, when consumed as dietary retinyl palmitate, both in the form of liver and as a supplement. Dietary retinol in the form of liver produced a smaller and delayed rise in serum retinol levels than vitamin A consumed as retinyl esters. This suggests that the latter form of vitamin A may have a more marked effect in producing teratogenic metabolites. Therefore, not only must pharmacokinetic properties of vitamin A metabolites be considered, but also the dietary form in which vitamin A is consumed.

Here is where I posted that (link)

I was trying to make the case that, although I wouldn't supplement vitamin A during pregnancy, I don't think there is a need to avoid liver. For one thing 4oz of liver has only 22,000 IU and if you're eating it once a week that is not a lot compared to a 10,000IU per day supplement. You shouldn't eat it everyday though... (I am aware that vitamin A levels in liver can vary quite a bit... something else to consider)

Poisonyl [] esters in foods are complexed with proteins, so their digestion is more elaborate and this can help to prevent overwhelming how much the intestine can process at a time.

People gettin banned for going against vitamin a trend now? nice

Has you asked both sides what happened before leaving the comment? The most convincing and communicative is the one that's right.

 

[Amazoniac]

- Carotenoid - Wikipedia

• "Carotenoids with molecules containing oxygen, such as lutein and zeaxanthin, are known as xanthophylls."
• "The unoxygenated (oxygen free) carotenoids such as α-carotene, β-carotene, and lycopene, are known as carotenes. Carotenes typically contain only carbon and hydrogen (i.e., are hydrocarbons), and are in the subclass of unsaturated hydrocarbons."

This is curious. Poison -ol, -al, -oic acid are all oxygenated. To make carotenes useful as frank poisons they require the carotenoid oxygenases (such as BCMO1 that was just mentioned above).


--
- Attractive Skin Coloration: Harnessing Sexual Selection to Improve Diet and Health (link from the Wikipedia page)

"Removal of parasites via antihelmintic treatment increases the redness and size of carotenoid-based combs in red grouse (Lagopus lagopus) (Mougeot et al., 2010). Further, male greenfinches (Carduelis chloris) with larger carotenoid-based plumage patches are less susceptible to, and exhibit faster clearance of, viral infection (Lindstrom and Lundstrom, 2000)."

"[An] hypothesis proposes that carotenoid coloration may reflect actual condition due to the toxicity of carotenoid breakdown products (Vinkler and Albrecht, 2010). The carotenoid maintenance handicap hypothesis postulates that the toxic by-products of carotenoid oxidation are more likely to be formed when systemic antioxidant reserves are low (Vinkler and Albrecht, 2010). This theory also postulates that the relationship between oxidative stress and carotenoid pigmentation is linked to testosterone, which increases carotenoid bioavailability (Blas, Perez-Rodriguez, Bortolotti, Vinuela, and Marchant, 2006), but simultaneously increases oxidative stress (Wikelski, Lynn, Breuner, Wingfield, and Kenagy, 1999). [?] The honesty of carotenoid ornamentation is preserved as only the individuals with competent antioxidant systems may exhibit intense carotenoid coloration; the oxidation challenge posed by testosterone cannot be endured by individuals with inadequate antioxidant resources (Vinkler and Albrecht, 2010)."

"Carotenoid pigments are present in all layers of human skin (Lademann, Meinke, Sterry, and Darvin, 2011) and as in some animal species these pigments, alongside melanin and hemoglobin, impart coloration to human integument, predominantly contributing to normal skin yellowness (Alaluf, Heinrich, Stahl, Tronnier, and Wiseman, 2002). The abundance of carotenoids in the skin is contingent on dietary intake of carotenoid and antioxidant-rich foods. Fruit and vegetable consumption in particular is associated with dermal carotenoid concentrations, as measured in vivo via Raman spectroscopy (Darvin et al., 2008; Rerksuppaphol and Rerksuppaphol, 2006) and in biopsy samples via high-performance liquid chromatography (Mayne et al., 2010). Consequently, skin color is partially contingent on diet; across individuals, daily intake of fruit and vegetables is correlated with skin yellowness (Stephen, Coetzee, and Perrett, 2011). Within-person changes in fruit and vegetable consumption are also associated with skin yellowness and redness changes over a six-week period (Whitehead, Re, Xiao, Ozakinci, and Perrett, 2012c)."

"Carotenoid pigmentation of human skin is perceived as healthy and has recently been suggested to be a more important cue of condition for attractiveness than commonly investigated facial morphology cues (e.g., masculinity, Scott, Pound, Stephen, Clark, and Penton-Voak, 2010; Stephen et al., 2012). When observers are able to manipulate facial skin coloration along a yellowness axis, images are reliably increased in yellowness to optimize apparent healthiness. This holds across black South African, Asian and Caucasian facial stimuli for observers of each of these ethnicities (Stephen, et al., 2011; Stephen, et al., 2012; Stephen, Smith, Stirrat, and Perrett, 2009; Whitehead, Coetzee, Ozakinci, and Perrett, 2012a), suggesting that this cue of health generalizes across cultures."

"Similar results are found when participants are asked to manipulate facial skin color along empirically-derived carotenoid pigment and diet-linked color axes. For instance, Stephen et al. (2011) supplemented participants’ diets with β-carotene and quantified the impact on skin lightness, redness and yellowness. Observers chose to increase the level of β-carotene pigment coloration (predominantly yellowness) in facial skin to optimize healthy appearance. Participants also preferred β-carotene skin coloration to melanin coloration when these pigments were simultaneously able to be manipulated. Further, in a psychophysical study, observers were able to detect skin color differences associated with modest increases in fruit and vegetable consumption (two portions per day, Whitehead et al., 2012c) suggesting that humans are sensitive at discriminating subtle differences in skin carotenoid pigmentation. These studies have also found that diet-related changes in the spectral reflectance of skin occur selectively at wavelengths associated with peak absorption of light energy by carotenoids (Stephen, et al., 2011). Hence carotenoids, rather than melanin are presumed to be responsible for dietary effects on skin color (Stamatas, Zmudzka, Kollias, and Beer, 2004)."

Spoiler: Melatonin × Carotenoids

 

[InChristAlone]

- Carotenoid - Wikipedia

• "Carotenoids with molecules containing oxygen, such as lutein and zeaxanthin, are known as xanthophylls."
• "The unoxygenated (oxygen free) carotenoids such as α-carotene, β-carotene, and lycopene, are known as carotenes. Carotenes typically contain only carbon and hydrogen (i.e., are hydrocarbons), and are in the subclass of unsaturated hydrocarbons."

This is curious. Poison -ol, -al, -oic acid are all oxygenated. To make carotenes useful as frank poisons they require the carotenoid oxygenases (such as BCMO1 that was just mentioned above).


--
- Attractive Skin Coloration: Harnessing Sexual Selection to Improve Diet and Health (link from the Wikipedia page)

"Removal of parasites via antihelmintic treatment increases the redness and size of carotenoid-based combs in red grouse (Lagopus lagopus) (Mougeot et al., 2010). Further, male greenfinches (Carduelis chloris) with larger carotenoid-based plumage patches are less susceptible to, and exhibit faster clearance of, viral infection (Lindstrom and Lundstrom, 2000)."

"[An] hypothesis proposes that carotenoid coloration may reflect actual condition due to the toxicity of carotenoid breakdown products (Vinkler and Albrecht, 2010). The carotenoid maintenance handicap hypothesis postulates that the toxic by-products of carotenoid oxidation are more likely to be formed when systemic antioxidant reserves are low (Vinkler and Albrecht, 2010). This theory also postulates that the relationship between oxidative stress and carotenoid pigmentation is linked to testosterone, which increases carotenoid bioavailability (Blas, Perez-Rodriguez, Bortolotti, Vinuela, and Marchant, 2006), but simultaneously increases oxidative stress (Wikelski, Lynn, Breuner, Wingfield, and Kenagy, 1999). [?] The honesty of carotenoid ornamentation is preserved as only the individuals with competent antioxidant systems may exhibit intense carotenoid coloration; the oxidation challenge posed by testosterone cannot be endured by individuals with inadequate antioxidant resources (Vinkler and Albrecht, 2010)."

"Carotenoid pigments are present in all layers of human skin (Lademann, Meinke, Sterry, and Darvin, 2011) and as in some animal species these pigments, alongside melanin and hemoglobin, impart coloration to human integument, predominantly contributing to normal skin yellowness (Alaluf, Heinrich, Stahl, Tronnier, and Wiseman, 2002). The abundance of carotenoids in the skin is contingent on dietary intake of carotenoid and antioxidant-rich foods. Fruit and vegetable consumption in particular is associated with dermal carotenoid concentrations, as measured in vivo via Raman spectroscopy (Darvin et al., 2008; Rerksuppaphol and Rerksuppaphol, 2006) and in biopsy samples via high-performance liquid chromatography (Mayne et al., 2010). Consequently, skin color is partially contingent on diet; across individuals, daily intake of fruit and vegetables is correlated with skin yellowness (Stephen, Coetzee, and Perrett, 2011). Within-person changes in fruit and vegetable consumption are also associated with skin yellowness and redness changes over a six-week period (Whitehead, Re, Xiao, Ozakinci, and Perrett, 2012c)."

"Carotenoid pigmentation of human skin is perceived as healthy and has recently been suggested to be a more important cue of condition for attractiveness than commonly investigated facial morphology cues (e.g., masculinity, Scott, Pound, Stephen, Clark, and Penton-Voak, 2010; Stephen et al., 2012). When observers are able to manipulate facial skin coloration along a yellowness axis, images are reliably increased in yellowness to optimize apparent healthiness. This holds across black South African, Asian and Caucasian facial stimuli for observers of each of these ethnicities (Stephen, et al., 2011; Stephen, et al., 2012; Stephen, Smith, Stirrat, and Perrett, 2009; Whitehead, Coetzee, Ozakinci, and Perrett, 2012a), suggesting that this cue of health generalizes across cultures."

"Similar results are found when participants are asked to manipulate facial skin color along empirically-derived carotenoid pigment and diet-linked color axes. For instance, Stephen et al. (2011) supplemented participants’ diets with β-carotene and quantified the impact on skin lightness, redness and yellowness. Observers chose to increase the level of β-carotene pigment coloration (predominantly yellowness) in facial skin to optimize healthy appearance. Participants also preferred β-carotene skin coloration to melanin coloration when these pigments were simultaneously able to be manipulated. Further, in a psychophysical study, observers were able to detect skin color differences associated with modest increases in fruit and vegetable consumption (two portions per day, Whitehead et al., 2012c) suggesting that humans are sensitive at discriminating subtle differences in skin carotenoid pigmentation. These studies have also found that diet-related changes in the spectral reflectance of skin occur selectively at wavelengths associated with peak absorption of light energy by carotenoids (Stephen, et al., 2011). Hence carotenoids, rather than melanin are presumed to be responsible for dietary effects on skin color (Stamatas, Zmudzka, Kollias, and Beer, 2004)."

Spoiler: Melatonin × Carotenoids

View attachment 12711

That is crazy, none of the faces look attractive, so they picked the less crazy one, the more tan color. That might be cultural. You know back hundreds of years ago paleness was sought after because it was a sign of wealth it meant you didn't have to work the fields.

 

[schultz]

That is crazy, none of the faces look attractive, so they picked the less crazy one, the more tan color. That might be cultural. You know back hundreds of years ago paleness was sought after because it was a sign of wealth it meant you didn't have to work the fields.

Yah all the faces sort of look weird, but I can't tell if it's because they are all beside each other so the differences are very noticeable.

The idea of carotene contributing (or not) to attractiveness is very fascinating. It's not something I've ever considered.

 

[Blossom]

I’m just going with how I feel these days because science is really disappointing me time and again. I’m not sure which scientific research is accurate and which is phony. We’ve talked about this issue on the forum before but here’s a recent news story about more lies, greed and corruption in science.
Duke University to pay $112 million to US government after accusations of faking research for grants
@stargazer1111, if you learn anything on the A/casein issue would you mind posting it or sending me a PM? Thanks

 

[Tarmander]

- Carotenoid - Wikipedia

• "Carotenoids with molecules containing oxygen, such as lutein and zeaxanthin, are known as xanthophylls."
• "The unoxygenated (oxygen free) carotenoids such as α-carotene, β-carotene, and lycopene, are known as carotenes. Carotenes typically contain only carbon and hydrogen (i.e., are hydrocarbons), and are in the subclass of unsaturated hydrocarbons."

This is curious. Poison -ol, -al, -oic acid are all oxygenated. To make carotenes useful as frank poisons they require the carotenoid oxygenases (such as BCMO1 that was just mentioned above).


--
- Attractive Skin Coloration: Harnessing Sexual Selection to Improve Diet and Health (link from the Wikipedia page)

"Removal of parasites via antihelmintic treatment increases the redness and size of carotenoid-based combs in red grouse (Lagopus lagopus) (Mougeot et al., 2010). Further, male greenfinches (Carduelis chloris) with larger carotenoid-based plumage patches are less susceptible to, and exhibit faster clearance of, viral infection (Lindstrom and Lundstrom, 2000)."

"[An] hypothesis proposes that carotenoid coloration may reflect actual condition due to the toxicity of carotenoid breakdown products (Vinkler and Albrecht, 2010). The carotenoid maintenance handicap hypothesis postulates that the toxic by-products of carotenoid oxidation are more likely to be formed when systemic antioxidant reserves are low (Vinkler and Albrecht, 2010). This theory also postulates that the relationship between oxidative stress and carotenoid pigmentation is linked to testosterone, which increases carotenoid bioavailability (Blas, Perez-Rodriguez, Bortolotti, Vinuela, and Marchant, 2006), but simultaneously increases oxidative stress (Wikelski, Lynn, Breuner, Wingfield, and Kenagy, 1999). [?] The honesty of carotenoid ornamentation is preserved as only the individuals with competent antioxidant systems may exhibit intense carotenoid coloration; the oxidation challenge posed by testosterone cannot be endured by individuals with inadequate antioxidant resources (Vinkler and Albrecht, 2010)."

"Carotenoid pigments are present in all layers of human skin (Lademann, Meinke, Sterry, and Darvin, 2011) and as in some animal species these pigments, alongside melanin and hemoglobin, impart coloration to human integument, predominantly contributing to normal skin yellowness (Alaluf, Heinrich, Stahl, Tronnier, and Wiseman, 2002). The abundance of carotenoids in the skin is contingent on dietary intake of carotenoid and antioxidant-rich foods. Fruit and vegetable consumption in particular is associated with dermal carotenoid concentrations, as measured in vivo via Raman spectroscopy (Darvin et al., 2008; Rerksuppaphol and Rerksuppaphol, 2006) and in biopsy samples via high-performance liquid chromatography (Mayne et al., 2010). Consequently, skin color is partially contingent on diet; across individuals, daily intake of fruit and vegetables is correlated with skin yellowness (Stephen, Coetzee, and Perrett, 2011). Within-person changes in fruit and vegetable consumption are also associated with skin yellowness and redness changes over a six-week period (Whitehead, Re, Xiao, Ozakinci, and Perrett, 2012c)."

"Carotenoid pigmentation of human skin is perceived as healthy and has recently been suggested to be a more important cue of condition for attractiveness than commonly investigated facial morphology cues (e.g., masculinity, Scott, Pound, Stephen, Clark, and Penton-Voak, 2010; Stephen et al., 2012). When observers are able to manipulate facial skin coloration along a yellowness axis, images are reliably increased in yellowness to optimize apparent healthiness. This holds across black South African, Asian and Caucasian facial stimuli for observers of each of these ethnicities (Stephen, et al., 2011; Stephen, et al., 2012; Stephen, Smith, Stirrat, and Perrett, 2009; Whitehead, Coetzee, Ozakinci, and Perrett, 2012a), suggesting that this cue of health generalizes across cultures."

"Similar results are found when participants are asked to manipulate facial skin color along empirically-derived carotenoid pigment and diet-linked color axes. For instance, Stephen et al. (2011) supplemented participants’ diets with β-carotene and quantified the impact on skin lightness, redness and yellowness. Observers chose to increase the level of β-carotene pigment coloration (predominantly yellowness) in facial skin to optimize healthy appearance. Participants also preferred β-carotene skin coloration to melanin coloration when these pigments were simultaneously able to be manipulated. Further, in a psychophysical study, observers were able to detect skin color differences associated with modest increases in fruit and vegetable consumption (two portions per day, Whitehead et al., 2012c) suggesting that humans are sensitive at discriminating subtle differences in skin carotenoid pigmentation. These studies have also found that diet-related changes in the spectral reflectance of skin occur selectively at wavelengths associated with peak absorption of light energy by carotenoids (Stephen, et al., 2011). Hence carotenoids, rather than melanin are presumed to be responsible for dietary effects on skin color (Stamatas, Zmudzka, Kollias, and Beer, 2004)."

Spoiler: Melatonin × Carotenoids

View attachment 12711

So basically eat carrots to become attractive...hmm

 

[InChristAlone]

I personally don't want to be orange. My feet have absolutely no tinge of orange. I'd like all the people claiming they do well with carotene to post a pick of the bottom of their feet.