The Current StAte

The Current StAte​

A blog entry about vitamin A is a tough one for several reasons. First, the literature is heavy on the chemistry and biology, and I am neither a chemist, nor a biologist (nor a scientist of any kind). Second, because vitamin A is a fat-soluble vitamin, stored mainly in the liver, the anecdotal evidence from keepers is difficult to verify without veterinary assistance—an option that is often forgone for financial and/or bio-ethical reasons. Worse still, it is not entirely clear what would count as “normal levels,” so even if someone was willing to invest in/risk serum analysis or liver/tissue biopsy, the results would require a certain amount of guesswork. If vitamin A deficiency or excess is suspected, most vets and experienced keepers will simply adjust supplement regimes and wait for results. Third, vitamin A levels vary with the levels of the other major fat-soluble vitamins, such as D3. This means that questions about whether x amount of A is too much or too little are not merely questions about A, but questions about the complex relationship that holds between several vitamins. Last, our current state of knowledge is poor. We have a few pivotal papers on which to draw, but none are conclusive. So, like most everything else in the hobby, we are left groping in the dark. Given all this, what I hope to accomplish here is to make plain where the hobby appears to be with respect to vitamin A and its provision in supplementation.

1. Preformed A: The Retinoids

Vitamin A is actually a family of fat-soluble compounds, rather than a single compound (Higdon, Drake, Delage, Ross, & Tan, 2003). The catchall term for all these compounds is ‘retinoid’. For our purposes, I want to focus on retinol—also called preformed vitamin A, or vitamin A1. Even here, things are not simple, since it turns out that retinol is typically found in animal tissue as an ester called retinyl palmitate (Abate, Coke, Ferguson, & Reavill, 2003). The other relevant A compound is retinal, which figures centrally in eyesight (think retina). However, it turns out that most of the relevant retinoids can be converted to one another, given a particular bodily need (Higdon, Drake, Delage, Ross, & Tan, 2003). Therefore, and to the chagrin of the scientific community, I am going to fudge the chemistry here, and use ‘preformed A’ as a broad term referring to that family of compounds that includes retinol proper, retinal, retinyl palmitate, retinoic acid, etc.

Preformed A is found almost exclusively in animal tissue [1], rather than plants. In particular, useful levels of preformed A occur mainly in animals with a liver, with insects typically being poor sources (they don’t have livers). Preformed vitamin A is an essential nutritional component for chameleons for several reasons. It plays a role in the maintenance of healthy skin, the mucous membranes and the cells responsible for mucous secretion, eyesight, muscles, and teeth (Coke & Ferguson in Abate, Coke, Ferguson, & Reavill, 2003). It also contributes to reproductive health, the immune system and cell differentiation/proliferation (Ferguson and Reavill in Abate, Coke, Ferguson, & Reavill, 2003). Excess preformed A (hypervitaminosis A) causes several dangerous conditions in chameleons including enlargement of the liver, metabolic bone disease, severe weight loss, soft tissue mineralization, cracking skin and edema of the gular region (Coke in Abate, Coke, Ferguson, & Reavill, 2003). Deficiency in preformed A (hypovitaminosis A) is equally detrimental, causing slowed growth, metabolic bone disease, closed oozing eyes, edema, tail tip necrosis and muscle weakness (Ferguson, et al., 1996).

While these symptoms show the importance of preformed A in chameleon biology/nutrition, they also suggest a further fact—one that complicates the discussion. Note that in both hyper and hypovitaminosis A, edema and metabolic bone disease (and its ilk[2]) appear among the symptoms. This suggests some intimate link with calcium and/or vitamin D3[3]. Indeed, studies have shown that excessive preformed A can inhibit vitamin D3’s ability to maintain healthy calcium levels in the blood (Johansson & Melhus, 2001) (Rohde & DeLuca, 2005)[4], and contribute to the development of rickets (Stevens, V.I. & Blair, 1983). Similarly, prolonged hypervitaminosis A has been linked to abnormal bone growth, and remodelling/hardening of the soft tissues surrounding the bones (Reavill in Abate, Coke, Ferguson, & Reavill, 2003). The implication is that preformed A can have dramatic affects on calcium storage.

What does all this mean? First, recall that preformed A is fat-soluble. This means that—unlike water-soluble compounds that are flushed out of the system regularly—preformed A can build up in the fatty tissues of animals. This is problematic because even low-level excess can—given sufficient time—lead to problems. And while the data patently supports the essential role preformed A plays in the health of our chameleons, it also highlights the dangers associated with an over or under supply. Additionally, it speaks to the interconnected nature of vitamin A to other important fat-soluble vitamins like D3[5], and essential minerals such as calcium. This last point gives pretty important status to preformed A in discussions of MBD—something that belies the marginal attention vitamin A garners in many threads about MBD.

So, in addition to all the other serious side effects that come along with an over/under supply of preformed A, there is a looming worry about how preformed A might figure importantly in MBD. In particular, there is a big concern about how much preformed A, relative to vitamin D3, is optimal. Luckily, there appears to be a magic solution here, a chameleon golden ratio of sorts, that several supplement manufacturers have adopted. The ratio is 10 parts preformed A to 1 part D3. Repashy and Reptivite have both adopted this, as evidenced by the their respective labels. Whether or not this has been the result of years of research into chameleon husbandry, chemistry, or just an inference from what we humans seem to require is, so far as I can tell, unclear. However, I stand to be corrected here; and for our purposes, it is unimportant. This is because, in addition to using supplements that provide preformed A and D3 in this ratio, most of us also use a good source of UVB. So, the question becomes a) whether this 10:1 ratio is based on the assumption that our captive chameleons will receive x amount of UVB exposure, or b) whether the ratio assumes no other source of D3[6]. My intuitions are that the magic ratio was not first devised with either option in mind, but was instead the result of trial and error. In other words, this 10:1 ratio does not represent the pinnacle of supplementation, but a rough guess based on what doesn’t seem to kill our chameleons.

The danger here is that our chameleons are in fact receiving UVB exposure, and we don’t know how much D3 they are producing themselves versus how much they are getting in their diet—something that obviously throws off the ratio. However, things aren’t hopeless. Several mechanisms whereby D3 levels in chameleons are naturally regulated have been noted. One view has it that a chameleon will just stop producing D3 when levels are sufficient[7]. Similarly, research appears to support the view that some chameleons regulate their own UVB exposure in response to D3 levels in their systems (Karsten, Ferguson, Chen, & Holick, 2009). Interestingly, there is also evidence that sunlight itself limits D3 production by causing photodegredation of D3 precursors in the skin (Webb, DeCosta, & Holick, 1989)(Baines, Goetz, & Chattell, 2016). In any case, there are natural mechanisms to prevent D3 overdose from ultraviolet exposure.

What would be great is if there was an analogue for preformed A—some natural mechanism whereby the amount of preformed A is limited according to an individual’s need….

2. Proformed Vitamin A: The Carotenoids

We have so far been focused on preformed A, the fat-soluble retinoid involved in a number of important bodily functions that becomes problematic when over/under supplied. There is, however, a group of compounds, the carotenoids, that are naturally occurring pre-cursors to preformed vitamin A. Called provitamin A, carotenoids play an important role in animal nutrition. For our purposes, the most relevant feature of carotenoids is that, once ingested, many animals have the ability to transform them into preformed A. Equally important, carotenoids occur in abundance in many plants as color pigments, and this puts them firmly in the food chain that stretches from plant to insect to chameleon.

While there is a multitude of research on carotenoids and their use in nutrition, a few points will be useful for us. First, there are over a thousand known carotenoids, and the nutritional benefits of relatively few have been studied. Of central interest for humans are the carotenes (alpha, beta), and beta-cryptoxanthin. These three appear to be the most important proformed A carotenoids, and some sources suggest they are the only carotenoids that can be converted into preformed A by humans (Higdon, Drake, Delage, Ross, & Tan, 2003)[8].Even more to the point, animals appear to have a built-in mechanism to limit the amount of carotenoid that is converted to preformed A according to need (Lobo, et al., 2010).

While promising, there are several challenges here. First, several researchers have expressed concerns about the efficiency of carotenoids as sources of vitamin A (Scott & Rodriquez-Amaya, 2000). Though all sides agree that some animals do indeed produce preformed A from carotenoids, research indicates the efficiency with which this function is carried out varies widely across individuals, and according to how the provitamin-containing food is prepared. Likewise, extreme variation in available carotenoids has been noted in certain vegetable crops according to soil conditions, light exposure and season of harvest (Scott & Rodriquez-Amaya, 2000). Despite this evidence, it should be noted that most of the skeptics here are concerned about the efficacy of carotenoids, as apposed to retinoids, to remedy certain human populations that appear to have chronic and widespread vitamin A deficiencies. The fact that some animals do convert some carotenoids into pre-formed A, and have internal systems in place to regulate that production is undisputed.

Unfortunately, there is a rather more serious stumbling block for anyone holding out for a carotenoid solution to the risks associated with supplementing preformed A. In 1992, John Annis, the editor (at the time) of the Chameleon Information Network, disseminated some information (via the CIN) warning against the dangers of supplementing with preformed A (Annis, 1992). This appears to have snowballed into somewhat of a panic, and breeders and hobbyist alike eschewed preformed A in favour of beta-carotene. According to Ardith Abate(Abate, Coke, Ferguson, & Reavill, 2003)—who took over editorship from Annis in 1994—an increase in cases of hypovitaminosis consequently ensued [9]. A study in the early 2000’s suggested a possible explanation.

In a seminal (to us, anyways) paper, Dierenfeld et al. examined the concentrations of carotenoids, vitamin A and E in developing eggs of Furcifer pardalis in the hopes of evaluating carotenoid and vitamin A metabolism in panther chameleons (Dierenfeld, Norkus, Carroll, & Ferguson, 2002). Besides the fascinating data about the rate at which certain elements are used during egg development, Dierenfeld et al. noted that the levels of the carotenoids beta-carotene and beta cryptoxanthin were very high at the beginning of incubation. This is significant when we consider this data in light of, say, poultry eggs, which have very little of either at the time of laying. Poultry eggs receive very little in the way of beta-carotene and beta-cryptoxanthin from their mothers because their mothers are very efficient at converting said carotenoids into preformed A. And since panther chameleon eggs had high quantities of both carotenoids, one might infer that panther chameleon mothers are very poor at converting these carotenoids to preformed A (Dierenfeld, Norkus, Carroll, & Ferguson, 2002). That inference lands the theory that carotenoids could replace preformed A in hot water.

For clarity’s sake, we have these two data points that appear to be strikes against the hope that carotenoids could be a safe substitute for preformed A:
  • After the initial preformed A scare (1992), when the hobby went the beta-carotene route, an upswing in hypovitaminosis is reported.
  • On one reasonable interpretation of Dierenfeld’s (et al.) 2002 study, panther chameleons are poor at converting Beta-carotene and Beta-cryptoxanthin to preformed A.
Indeed, taken together, the latter seems to explain the former. However, Dierenfeld herself admits that there is an alternative explanation for the high levels of carotenoids present in newly deposited eggs: During gestation, there might have been an abundance of carotenoids in the diet of the mothers relative to the mothers’ requirements. That is, the females were eating bugs whose gut contents provided them with such an abundance of these carotenoids that they did not need to convert them. And, as it turns out, most animals do not convert carotenoids into preformed A until liver stores reach a certain level of depletion (Lobo, et al., 2010), (Dierenfeld, Norkus, Carroll, & Ferguson, 2002). It is thus perfectly possible that the females had sufficient liver stores such that the conversion wasn’t necessary. This last consideration brings up another interesting datum from the study. In all cases, the mother panther chameleon passed on levels of preformed A to the eggs in relatively high quantities, given their insectivore diet—quantities similar to other lizards.

This raises the question: Where exactly are the female panthers getting their preformed A from, given their insect-based diet? Other vertebrate-eating lizards get it from the animal tissue they consume, but insects are a poor source of preformed A. Several theories have been suggested to explain how chameleons get their preformed A. If they cannot convert carotenoids, then perhaps gravid females are prompted to take vertebrate prey such as small geckos, rodents or birds. This would certainly supply them with sufficient levels of preformed A to pass on to their young. And since many wild chameleons do not live past a year or two, this amount might be enough to carry them through their lives. Something like this occurs in chicks: They are provided enough preformed A in the egg to keep them through an extended period of food items devoid of the nutrient (Dierenfeld, Norkus, Carroll, & Ferguson, 2002). So it could turn out that we are, in fact, faced with having to supplement our captives with preformed A, if we expect them to live beyond a year or two. Similarly, maybe some longer-lived chameleon species, including some panthers, regularly take vertebrate prey as above. It should be noted, however, that this explanation does not appear to work for small chameleon species.

On the other hand, it could turn out that they can convert some carotenoids, and as mentioned above, the wild insectivore diet is sufficiently rich in carotenoids that constant conversion is unnecessary. It could also turn out that although beta-carotene and cryptoxanthin are not effectively converted to preformed A, some other carotenoid (there are over a thousand) does play this role. This would certainly explain why moving to a beta-carotene only regime of A supplementation led to an increase in hypovitaminosis (see above in Abate, Coke, Ferguson, & Reavill, 2003). If beta-carotene is not the right carotenoid, then of course chameleons are going to be A-deficient on a beta-carotene only diet. And while it was suggested (Higdon, Drake, Delage, Ross, & Tan, 2003)that only the carotenes and cryptoxanthin can be converted into preformed A by humans; is this true for reptiles, lizards, chameleons? Unfortunately, my lack of a chemistry background is going to be a stumbling block here: I’m sure there is a chemical explanation as to whether it is, or is not possible for, say, lutein or zeaxanthin to be converted into preformed A. Significantly, levels of these two carotenoids were relatively low compared to chicken and tortoise eggs in the relevant study (Dierenfeld, Norkus, Carroll, & Ferguson, 2002). At any rate, it is perfectly possible that some other carotenoid is doing the heavy lifting with respect to vitamin A conversion.

3. The Current StAte of A

Here’s a quick summary of what we know and how we got here: Preformed vitamin A exists only in animal tissue—primarily the liver—and insects are poor sources of preformed A. We know that preformed A is a necessary part of chameleon nutrition. However, there are dangers associated with both excess and deficiency; and we aren’t really sure how much is too much and how much is not enough. In any case, testing for it is problematic. Besides the host of other health risks associated with too much or not enough, there is the associated risk of vitamin A’s interaction with vitamin D3. In particular, there is evidence to show that higher levels of A can interfere with D3’s role in the regulation of calcium absorption. The current trend to rely less on dietary D3 and more on a chameleon’s natural ability to safely produce and regulate its D3 levels via exposure to UVB led us to inquire whether such an option existed for vitamin A. We found that many animals do indeed have the ability to regulate their preformed A levels. The rub here was that this is typically accomplished by controlling the conversion of carotenoid precursors to preformed vitamin A. We learned that, for humans, the main carotenoids used for vitamin A conversion are the carotenes and cryptoxanthin. After a scare about the dangers of preformed A in the 90’s, the subsequent pendulum swing towards beta-carotene appears to have caused an increase in cases of vitamin A deficiency; and a paper in 2002 seemed like a possible explanation. Panther chameleons might not be able to convert some carotenoids into preformed A. So, here’s where we stand:

The case for supplementing with preformed vitamin A is as follows:
  • Chameleons need it
  • Insects don’t have it (they have a little, but not much)
  • It seems like the move to beta-carotene in the 90’s may be implicated in the rise in cases of vitamin A deficiency.
  • On one very reasonable interpretation of the data provided by Dierenfeld et al., panther chameleons appear not to be able to convert beta-carotene and cryptoxanthin to vitamin A.
  • Relatedly, for humans, the above two carotenoids are some of the only carotenoids that can be effectively converted into preformed A.
  • It is not at all unreasonable to think that some chameleon species do in fact get preformed vitamin A by ingesting vertebrate prey such as small geckos, birds or rodents.
  • It could turn out that although supplementing with preformed A is not natural for wild chameleons because they are born with enough to get them through their relatively short lives, we have to do it in captivity if we want them to live past 2 years.
  • In all the important papers dealing explicitly with chameleons and vitamin A supplementation, the experts almost unanimously suggest the most prudent route is to use both preformed A and carotenoids…just to be safe (Abate, Coke, Ferguson, & Reavill, 2003) (Dierenfeld, Norkus, Carroll, & Ferguson, 2002) (Ferguson, et al., 1996).
The case for reliance on proformed A is as follows:
  • We don’t know how much preformed A is too much, and an excess has serious consequences, including potential problems with calcium absorption.
  • Relatedly, preformed vitamin A is a fat-soluble vitamin that can build up in the body even with chronic low-level excess.
  • There is no mechanism that can regulate the absorption of dietary preformed A--there's no tap to turn off when we give it as preformed.
  • Properly fed insects are high in carotenoids, and this is the most likely natural source of carotenoids for chameleons.
  • Using carotenoids as the sole means of supplementing vitamin A has a built-in safety net. Evidence supports that internal mechanisms regulate the conversion of carotenoids to preformed A based on the body’s requirements.
  • The evidence about the conversion of some carotenoids admits of multiple reasonable interpretations: chameleons might be perfectly able to convert beta-carotene to preformed A, it’s just that the ones involved in the experiments were already “on full”, so to speak.
  • The notion that we can generalize from humans to chameleons regarding which carotenoids can be effectively converted into preformed A is tenuous. There are over a thousand different carotenoids, and it is entirely plausible that one or more could fit the requisite role.
  • We now have supplements that boast hundreds of different carotenoids, and our gut loading ingredients have also evolved to incorporate more carotenoid rich items.
  • While not previously mentioned, a number of keepers have raised clutches to adulthood and old age on a diet completely free of preformed A—relying instead on gut loading with carotenoid rich food items.
There are probably more reasons on either side of this quagmire, but I think I’ve presented fair arguments/evidence in an unbiased way. Though most veterans will find much of this to be old news, having clear facts laid out is, I hope, beneficial to the newcomer. In the unlikely event that anybody reads this, they will have the benefit of being able to make an informed decision about vitamin A supplementation.

Foot notes
(1) I have read that some forms of fungus produce retinol.
(2) E.g. fibrous osteodystrophy, osteomalacia, secondary nutritional hyperparathyroidism
(3) Among other nutrients, e.g. E, and K
[4]For transparency’s sake: The abovementioned studies were conducted on rats and humans. In my defense, there don’t appear to be any studies that have this data on Chameleons.
[5]It also appears that excess vitamin E can interfere/inhibit preformed A (Frigg & Broz, 1984), but thankfully we have a magic ratio for that too…LOL
[6]If b), then any ratio will either be skewed for a chameleon receiving UVB exposure (because s/he is producing D3 naturally), or else render UVB exposure unecessary (because there is no natural production of D3, since the body doesn’t require any more). That is, if our supplements give us the right ratio of nutrients, then UVB becomes immaterial. If our supplements are balanced, then the only question is how much of them we need to fulfill the nutrient requirements of our captive chameleons. This effectively ends not only our need for UVB, but also any further enquiry into supplements and husbandry as far as preformed A and D3 are concerned: if the only question is how much powder to use, then we’d have figured out supplementation decades ago. To be clear, our problem is not merely how much vitamin powder to provide, but also how much, and in what proportion, each ingredient needs to be provided—e.g. how much A relative to D, how much E relative to K, etc…Option a) appears even more precarious. How can a supplement that touts balancetake into account the entire community’s UVB setup? Even if there is some tacit, implied assumption that all our captive chams see UVI levels of 3 for x number of hours/day or week, none of the major supplement brands say so. The closest I’ve seen is the caveat that the product is to be used in conjunction with a good UVB system. This latter supplement being one with no fat soluble vitamins anyways. For clarity’s sake: if the 10:1 ratio is the right balance of preformed A to D3, then by exposing our chameleons to UVB—whereby they make their own D3—we are throwing the ratio off.
[7]Unfortunately I do not have a verified source here, but personal correspondence with respected members of the community have suggested that this is taken as given by scientists and experts alike.
[8]That is not to say that other carotenoids do not have some nutritional benfit. Several have been shown to have anti-oxidant properties, and many are essential elements in the eye pigment of many species.
[9]To be clear, I am merely reporting what the sources say. Whether Annis’ articles caused the mass exodus from a preformed A husbandry routine, and whether a pandemic of hypovitaminosis A ensued, is something I can’t comment on from personal experience.

Works Cited
Abate, A., Coke, R., Ferguson, G., & Reavill, D. (2003). Chameleons and vitamin A. 13, pp. 23-31. JOURNAL OF HERPETOLOGICAL MEDICINE AND SURGERY.

Annis, J. (1992). Hypervitaminosis A in Chameleons, are ae unknowingly overdosing our animal with vitamin A? CIN CHAMELEON INFORMATION NETWORK, 9, 18-25.

Baines, F., Goetz, M., & Chattell, J. (2016). How much UV-B does my reptile need? The UV-Tool, a guide to the selection of UV lighting for reptiles and amphibians in captivity. JOURNAL OF ZOO AND AQUARIUM RESEARCH, 4(1), 42-63.

Dierenfeld, E., Norkus, E., Carroll, K., & Ferguson, G. (2002). Carotenoids, Vitamin A, and Vitamin E Concentrations During Egg Development in Panther Chameleons (Furcifer pardalis). ZOO BIOLOGY, 21, 295-303.

Dorr, P., & Balloun, S. (1976). Effect of dietary vitamin A, ascorbic acid and their interaction on turkey bone mineralization. BRITISH JOURNAL OF POULTRY SCIENCE, 17, 581-599.

Ferguson, G., Jones, J., Gehrmann, W., Hammack, S., Talent, L., Hudson, R., et al. (1996). Indoor Husbandry of the Panther Chameleon Chamaeleo [Furcier] pardalis: Effects of Dietary Vitamins A and D and Ultraviolet Irradiation on Pathology and Life-History Traits. ZOO BIOLOGY, 15, 279-299.

Finke, M. (2003). Gut Loading to Enhance the nutrient Content of Insects As Food for Reptiles: A Mathematical Approach. ZOO BIOLOGY, 22, 147-162.

Frigg, M., & Broz, J. (1984). Relations between vitamin A and vitamin E in the chick. INTERNATIONAL JOURNAL OF VITAMIN AND NUTRITIONAL RESEARCH, 54, 125-134.

Frye, F. (1991). Biomedical and Surgical Aspects of Captive Reptile Husbandry(2nd ed., Vol. 1&2). Melbar, FL, USA: Krieger Publications.

Higdon, J., Drake, V., Delage, B., Ross, C., & Tan, L. (2003, Jan). Micronutrient Information Center. Retrieved Feb 4, 2020, from Linus Pauling Institute, Oregon State University:

Johansson, S., & Melhus, H. (2001). Vitamin A Antagonizes Calcium Response to Vitamin D in Man. JOURNAL OR BONE AND MINERAL RESEARCH, 16(10), 1899-1905.

Karsten, K., Ferguson, G., Chen, T., & Holick, M. (2009). Panther Chameleons, Furcifer pardalis, Behaviorally Regulate Optimal Exposure to UV Depending on Dietary Vitamin D3 Status. PHYSIOLOGICAL AND BIOCHEMICAL ZOOLOGY: ECOLOGICAL AND EVOLUTIONAL APPROACHES, 82(3), 218-225.

Lobo, G., Amengual, J., Palczewski, G., Babino, D., & von Lintig, J. (2012). Mammalian Carotenoid-oxygenases:Key Players for carotenoid functions and homeostasis. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 1821(1), 78-87.

Lobo, G., Hessel, S., Eichinger, A., Amengual, J., zongaro, S., Nay, N., et al. (2010). ISX is a retinoic acid sensitive gatekeeper that controls intestinal lipid absorption. FEDERATION OF AMERICAN SOCIETIES FOR EXPERIMENTAL BIOLOGY, 6, 1656-1666.

Rohde, C., & DeLuca, H. (2005). All-trans Retinoic Acid Antagonizes the Actions of Calciferol and Its Active Metabolite, 1,25-Dihydroxycholecalciferol, in Rats. THE JOURNAL OR NUTRITION, 135(7), 1647-1652.

Scott, K., & Rodriquez-Amaya, D. (2000). Pro-vitamin A carotenoid conversion factors: retinol equivalents--fact of fiction? FOOD CHEMISTRY, 69(2), 125-127.

Stevens, V.I., & Blair, R. (1983). Dietary Levels of fat, Calcium, and Vitamins A and D3 as Contributory Factors to Ricekts in Poults. POULTRY SCIENCE, 62(10), 2073-2082.

Webb, A., DeCosta, B., & Holick, M. (1989). Sunlight regulates the cutaneous production of D3 by causing its photodegredation. JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM, 68, 882-887.

@kinyonga @DeremensisBlue @Decadancin . You guys are probably the only people who will read this, and that sucks since you all probably know all of this already. But maybe some newer hobbyist, in the midst of a supplementation crisis, will find it useful. Happy reading!
  • IMG_2.jpg
    313.8 KB · Views: 193


Geesh...there's no way to give you any like/love etc on this post either....why is that missing? Come on @decadancing figure it out eh? :)
Thanks to all three of you for reading this. @kinyonga, I am still thinking hard about leptin. Why don’t you write a research blog about it?
There are too many holes in my theory yet....and I think vitamin D3 and vitamin A are going to be involved. :(

Make it an ongoing thing then. If you present your hypothesis, and are transparent about where more work needs to be done, then perhaps we could all pick a hole and explore. Science’ll catch up to
This is an absolutely fantastic summary of information and sources. Thank you very much.
Very good, I hope you do not mind if I post in my library on my site. Or a pdf version that has your name on it. I want you to have full credit as this is a good read and done right.

Blog entry information

Last update

More entries in General

More entries from Kaizen

Share this entry

Top Bottom