Monday, February 16, 2009

Animal Pharm Science: Vitamin A Deficiency Increases Marbling

Do you want marbling in your meat? I mean, fat-infiltration of your meat-muscles...biceps, triceps, quads and gluts.

M-A-X-I-M-A-L gluteus maximus is what I'm going for! Maximization with functional exercises like squatting and digging volleyball-style which is oh-so-nice...

Not... marbled...meat!!

Looking at journals of animal farm science, studies for increasing USDA Grades of beef and Marbling Scores (MS) have yielded some interesting perspectives regarding vitamin A and its role in controlling obesity. Do Americans get enough vitamin A? The beef industry has figured out that better grades and thus higher market value can be achieved by restricting vitamin A in the food fed to commercial cows. In fact, by depleting liver stores and restricting the content in food, the grade of meat and percentage of intramuscular (IM) fat increase quite substantially. Better yield for livestock owners. Higher levels of blood glucose (BG) are also associated with lower vitamin A status and higher marbling.

HHHhhmmm... why??

Is the livestock which is raised commercially on grains clinically obese, diabetic, inflamed, cancerous (well, unlikely...they're slaughtered too young), high in MUFA, low in saturated fats, vitamin A and vitamin D deficient? With vast desaturase deficiencies?

Livestock owners may be purposefully inducing vitamin A deficiency in order produce higher USDA grade meat for the market. Should we be consuming this kind of low-quality protein?

Humans are actually not that different biochemically and physiologically from our bovine cousins. At one time, bovine insulin was used in Type 1 diabetes mellitus treatment and management. Until human recombinant insulin was developed, pork and beef-derived products were it. Porcine (pork) insulin actually produces less skin irritation and injection site adverse effects like (lipodystrophy, allergic reactions) than bovine, yet bovine filled the needs of many Type 1 diabetes individuals for decades.

One the most curious observations is how cows become very lean (and thus less profitable for ranchers) during spring and summer. This is theorized to be secondary to the increased vitamin A intake from pasturing and eating grass. Vitamin D and increased sunshine probably can be attributed to this relevation as well.

The last set of researchers link how our steroid nuclear receptors are all interrelated in controlling adiposity and the creation of fat cells (adipocytes). They propose a "model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily." PPARs have been discussed here before and their crucial role in attenuating chronic and acute diseases including CAD and cancer: Happy Cows...etc.

Who might be vitamin A deficient?
--those who don't consume a lot of wild seafood/grassfed meat (like me but I've discovered... Whole Wallet now)
--those with Hashimoto's hypothyroidism -- Hashimoto's (vitamin A supplementation improves iodine efficacy; hypothyroidism=first sign of vitamin A deficiency in chicks)
--Oprah Winfrey
--Steve Jobs
--those with other autoimmune diseases: Grave's, RA, SLE, Sjogrens, multiple sclerosis, NASH, primary biliary cirrhosis, (??!) CAD, etc
--those with cancer -- see HERE and HERE and HERE--chronically ill
--those with infections or high CRP -- see HERE, HERE and HERE
--children less than age 4 and women -- see HERE too
--those who eat 'low fat'
--those with skin conditions (again, autoimmune origin and wheat-triggered): eczema, rosacea, skin cancer, poor wound healing, atopic dermatitis, psoriasis, dermatitis herpetiformis, porphyria cutaneous tarda
--diabetic-induced rats fed vitamin A deficient lab chow
--those with gluten enteropathy, (known v. unknown) wheat/casein allergies, 'leaky gut' and a poor intestinal barrier which prevent absorption of fat and fat-soluble vitamins
--those without a gallbladder who may not produce sufficient digestive enzymes to absorb fat and fat-soluble vitamins
--those who take Orlistat/Xenical or OTC Alli (weight loss pills which block fat and thus fat-soluble vitamins ADEK1 K2)
--those on antiseizure drugs (valproic acid, carbamezepine, phenytoin which increase metabolism/elimination of vitamin A)
--those who have had gastric bypass which unnaturally cuts out a great portion of our most important absorptive surface area for fat and nutrients, the duodenum
--Inuit children with frequent lower respiratory tract infections and otitis media (who are probably no longer consuming their traditional H-G-fish Paleo diets but the S.A.D. grain-based one like Americans)
--third world countries where night-vision blindness is prevalent

What dose of Vitamin A is sufficient?

Like Vitamin D, we need adequate amounts Vitamin A for optimal health -- the desired amount is dependent on various factors: inflammation, growth, reproductive state, hormone state, etc. Vitamin A is not the same as beta-carotene, which is the precursor of Vitamin A. Beta-carotene is the common form found in multi-vitamins.

The current RDA for Vitamin A is 5,000 to 10,000 IU daily (take in AM -- may cause insomnia). Converting from RE mcg to IU see HERE.

Here are other benefits of Vitamin A discussed here: Synergy of Vitamin D and Its Co-factor Vitamin A
Consideration for Vitamin A supplementation is necessary if diet (wild seafood, grassfed meat, organ meats) are insufficient to meet daily requirements.

Ck out Vitamin A...for your healthwise b-o-t-t-o-m . . . line. I'll be watching it for you. *wink*

Hey Gibby -- this post is per your request!

"...long vitamin A restriction (LR) specifically increased fat deposition in the i.m. depot, without promoting an increase in the overall fatness of the animal. We conclude that feeding low-vitamin A diets may be a feasible and economical strategy to affect the site of fat deposition within the beef carcass. Pyatt and Berger (2005) hypothesized that the observed
seasonal decline in carcass grade during the fall may be associated with previous high-vitamin A intake during spring and summer. Additionally, typical feedlot diets are formulated to provide 2 to 3 times NRC (1996) vitamin A recommendations (Galyean and Gleghorn, 2002). Thus, feedlot cattle in the United States are fed vitamin A in excess of their requirements. Results of
this experiment provide evidence that the vitamin A level of the diet affects the site of fat deposition in feedlot cattle.

We recently reported that feeding low-vitamin A diets to beef steers appears to increase adipocyte differentiation in the i.m. depot without affecting s.c. adipocytes. This was accompanied by numerical in- creases in marbling scores and USDA carcass quality grades, with no effects on backfat deposition and USDA yield grades (YG; Gorocica-Buenfil et al., 2007). Marbling scores also were increased when low-vitamin A diets were fed to Japanese Black cattle (Adachi et al., 1999). The duration of vitamin A restriction required to improve i.m. fat deposition remains unknown. It is likely that to affect the vitamin A status of the animal, hepatic vitamin A stores need to be depleted. However, research in this area is negligible.

The effect of feeding low-vitamin A diets on beef fatty acid composition remains unclear. The enzymatic activity of stearoyl coA desaturase (SCD), required for the endogenous synthesis of CLA in ruminants, may be reduced by retinol (Alam and Alam, 1985). However, a numerical trend (P > 0.10) was observed in marbling score and the percentage of carcasses grading USDA Choice or above (from 28% in control to 50% in LR steers). If this effect were real, it would be economically important because most formulas used in the market to determine carcass value include a premium for
carcasses ≥ Cho (USDA Agricultural Marketing Service, 2006). The numerical increase in the percentage of highly marbled carcasses is in agreement with our previous experiment (Gorocica-Buenfil et al., 2007) where we reported a 7% increase in the marbling scores when low-vitamin A diets were fed to Angus-based steers."
Effect of dietary vitamin A restriction on marbling and conjugated linoleic acid content in Holstein steers. (PDF) Loerch SC et al. J Anim Sci. 2007 Sep;85(9):2243-55.Relationship between serum biochemical values and marbling scores in Japanese Black steers. Ohwada K et al. J Vet Med Sci. 1999 Aug;61(8):961-4.

"Slight changes in the fatty acid profile of s.c. fat of the steers were detected. A greater proportion of MUFA (LOW = 41.7 vs. HIGH = 39.9%, P = 0.03) and fewer SFA (LOW = 47.1 vs. 48.7, P = 0.03) were observed in vitamin A-restricted steers. This suggests that vitamin A restriction may affect the activity of desaturase enzyme (desaturase activity index, LOW = 46.9 vs. HIGH = 44.9, P = 0.01)."
Effect of vitamin A restriction on carcass characteristics and immune status of beef steers. Loerch SC et al. J Anim Sci. 2008 Jul;86(7):1609-16.

"It is well documented that grain feeding stimulates adipogenesis in beef cattle, whereas pasture feeding depresses the development of adipose tissues, including intramuscular (i.m.) adipose tissue. Additionally, production practices that depress adipocyte differentiation also limit the synthesis of monounsaturated fatty acids (MUFA). Marbling scores and MUFA increase in parallel, indicating that stearoyl-CoA desaturase (SCD) gene expression is closely associated with and(or) necessary for differentiation of marbling adipocytes. Similarly, marbling scores and fatty acid indices of SCD activity are depressed in response to dietary vitamin A restriction. In bovine preadipocytes, vitamins A and D both decrease glycerol-3-phosphate dehydrogenase (GPDH) activity, an index of adipocyte differentiation..."Cellular regulation of bovine intramuscular adipose tissue development and composition. Sawyer JE et al. J Anim Sci. 2008 Nov 7.

"The study aimed to systematically examine the effects of fat soluble vitamins and their analogs on terminal differentiation of adipocytes on the cellular and molecular aspects. It is well known that fat soluble vitamins especially vitamins A and D inhibit the differentiation of adipocytes in cultured cells. Furthermore, it has been revealed that the low level of dietary fat soluble vitamins, especially vitamin A and carotenoid actively stimulate the development of adipose tissue, namely bovine marbling in vivo. We have shown that the expression of retinoic acid receptor (RAR) alpha and gamma, retinoid X receptor (RXR) alpha and beta, and vitamin D receptor (VDR) mRNA were abundant in rat adipose tissue and 3T3-L1 cells. The autoregulated amplification and reduction of RAR, RXR and VDR mRNA by their own ligands, were observed in 3T3-L1 cells. Finally, we proposed the model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily."
The possibility of active form of vitamins A and D as suppressors on adipocyte development via ligand-dependent transcriptional regulators. Sugimoto E et al. Int J Obes Relat Metab Disord. 1996 Mar;20 Suppl 3:S52-7. Review.


Anonymous said...

Wow, is that picture 'schwingtastic' or what? I'm blushing over here ... Thanks for the info! As always, very informative with a side fun! So a question: is there a test for vit A as there is for vit D to determine toxicity? - Marisa

mess talker said...

I know that's gotta be your butt!
have you checked out
grassland beef. mmmm. pemmican. all grassfed. it's all frozen and not very cheap. but cheaper than whole foods' grass fed beef. plus all the offal you need. we get livers, hearts, steaks shipped overnight. the pemmican bars are amazing snacks. not true to indian recipe (close) but very good. plus people are fascinated by others chewing on meat sticks in public

Anonymous said...

Here's a great site for organic coconut oil and organic meats - I just ordered their organic, grass-fed bison and it's supposed to arrive in 4 days!!! The authored a VERY informative book on coconut oil - very anti-USDA/ADA/AHA info.

- M

Dr. B G said...


Sorry -- blushing here is not allowed... J/k!

I'm still figuring out the testing myself -- vitamin A is a legitimate test but unfortunately vitamin A is bound up by 'retinol binding protein' (RBP) much like estrogen and testosterone are bound by SHBG (sex-hormone-binding-globulin). The vitamin A blood test is not that accurate. RBP is actually considered a good surrogate marker for vitamin A status -- but again I don't know how validated it is.

I wish it were more clear! Maybe someone will write a book and we'll have it all figured out for us :)


Dr. B G said...


You're too hilarious...Of course that's my b*tt... *sarcarstic grin*!!

Believe me, I'd post my b*hind before my picture... and don't try to dissect that comment -- I have no idea what I meant by that :)

Thanks for the links!! HHhhhmmm...sounds YYYUUMM. if I ever chew a meat stick in public, I'll make sure I post a pict here first. Guaranteed.

*haaa ha*


Dr. B G said...

M --

We're talking a lot about the benefits of coconut oil (unrefined) and MCT oil at the TYP forum lately. Triggered perhaps by Dr. Davis new coconut on his blog!

Love coconut oil!! Thanks for the info dear!!


Anonymous said...

That's great info. I was wondering, ever since I started taking Vitamin A 10,000IU a day, my muscles seems to have shrinked. Is that related to the marbling? or is it just a coincidence?

Dr. B G said...


You're wonderful -- what a great BLOG! You are definitely NOT pharmaceutically challenged.

Most Americans who consume meat or seafood generally do not have vitamin A deficiency. So Vit A 10,000 IU daily maybe a bit much for your biological system. As you are aware, vit A is fat soluble and definitely accumulates if excessive. In fact, I've had toxicity when I consumed a large slab of delicious duck truffle pate (~ 1/4lb worth) -- UUGGGGhhh then I experienced a HUGE disulfiram-reaction (flushing, headache, nausea) after only a few sips of beer. Apparently, I suspect, I had transient liver toxicity from all the vitamin A.

Caution with vitamin A is necessary, esp in light of any vitamin D deficiency -- which I probably had since age 17 yo. Now my vit D is fine 60-80 ng/ml so I don'w worry about vitamin A toxicity now.

Winter is a time for hibernation (more melatonin -- if you're young and still make it) and slowed metabolism -- these are deep ancient cycles of hormones we are probably used to. If vitamin A was only a recent addition, could the muscle wasting be secondary to other things?
--less exercise?
--stagnation of workouts (need to HIIT it intensely and shake it up every 2-4wks)?
--more carb intake?

Good luck! I'd love to hear how it shakes out!


Dana Seilhan said...

Thank you, thank you, thank you. I suspected this might be a national problem and you've provided more data in that direction. It dawned on me the other day when I realized that there is no vitamin A in plant foods, but what are we told to eat to get "enough" A? Plant foods with beta carotene in them. With fat-free salad dressing.

That vitamin A content they claim on the label, when there is one? It's how much A you would get if you converted all the beta carotene.

How many of us do a full conversion of beta carotene? Nobody really knows.

I've started supplementing with vitamin A. I'm trying to find ways to get more of it into my daughter too, as the children's multi she takes derives its "vitamin A" from--you guessed it--beta carotene! She's four!


I'm about this close to wanting to pursue a medical career, just so I can legally warn people about this stuff without being accused of practicing medicine without a license. Honestly.

Dr. B G said...


UR hilarious -- where is your blog?? I'd love to read it...

I've wondered the same things as you...(I don't eat as much meat either)

I have to be careful about the vitamin A though -- it's easy to get toxic since it is fat soluble -- and we certainly don't require apparently as much as Vitamin D (I think).


mathman said...

Dr. B G -

You mentioned taking Vit. A in the morning due to problems with sleeplessness and I have heard the same thing about Vit. D. I have also heard that you should not take supplements for D and A at the same time because they somehow compete/block each other out. If this is true, then which should I take at night?

Dr. B G said...


That's curious, I haven't heard of a contraindication or vitamin-vitamin interactions between vitamin A and D. Vitamin D appears to come from sunlight mainly for populations living near the equator. Of course, trad'l Inuit and other cultures obtain vitamin D from organ/sweet meats and adipose tissues as well as bones/soups. Vitamin A is also found richly in these foods so in fact A and D are commonly consumed together at the same meal (same as Vitamin E (nuts/fatty tissues/organs) and vitamin K2 (fermented foods, organs, meat/fish). Generally we also eat during daytime/sunlight hours the same time as vit D conversion in the skin. Interesting I was just reading how HEAT generates some degree of conversion of vitamin D in certain cells. Yes -- work that heat! You'll get more vitamin D released activated at the cellular level. Many other benefits to the generation of internal HEAT are apparent now! (have you heard how good our heat-shock- and cold-shock proteins are for longevity??) It's good it is warming up here in Northern Cal -- indoor sports isn't sufficient for me...*ha haa*


Anonymous said...


What about the recent st
Dear Dr. Cannell:

Can you quote from the paper, telling us why so many experts condemned cod liver oil?

Robert, California

Dear Robert:

I don't know if copyright laws allow the author to do that, but I will take the chance. The crux of the problem is that a form of vitamin A, retinoic acid, weakly activates the vitamin D response element on the gene and perhaps blocks vitamin D's more robust activation. The first paper below is free to download. As the authors say, "there is a profound inhibition of vitamin D-activated . . . gene expression by retinoic acid."

MacDonald PN, et al. Retinoid X receptors stimulate and 9-cis retinoic acid inhibits 1,25-dihydroxyvitamin D3-activated expression of the rat osteocalcin gene. Mol Cell Biol. 1993 Sep;13(9):5907-17.

Thompson PD, et al. Heterodimeric DNA binding by the vitamin D receptor and retinoid X receptors is enhanced by 1,25-dihydroxyvitamin D3 and inhibited by 9-cis-retinoic acid. Evidence for allosteric receptor interactions. J Biol Chem. 1998 Apr 3;273(14):8483-91.

The key is having the proper ratio of vitamin D to vitamin A in your body. To obtain this proper D/A ratio, you must make a choice. (1) Either obtain the D/A ratio Nature and God intended, that is, the ratio the human genome evolved on, or (2) think you know everything, intervene in a closed system, bypass the controls in the intestine and inject active A directly into your blood by taking vitamin A or cod liver oil. Vitamin A production is tightly controlled in the body, the source (substrate) being carotenoids from vegetables in your intestine. The body uses these carotenoid substrates to make exactly the right amount of retinol for your body. That is, it is a closed, tightly regulated, system, one designed to perfection by God and Nature. When you take vitamin A as retinol, such as in cod liver oil, you intervene in this closed system and bypass the controls. Proceed at your peril.

Vitamin D is also a closed controlled system and I don't recommend intervening in that system either. Vitamin D is a substrate, like carotenoids, it is not the active substance. Taking vitamin A as retinol is like taking activated vitamin D, calcitriol. Doing so bypasses controls and I have never recommended anyone take activated vitamin D except patients with renal failure under the care of a nephrologist. As long as your vitamin D dose is not excessive, you are not intervening in a closed system, you are simply providing the vitamin D substrate. The body, if and when it has enough vitamin D substrate, will use what it needs and dispose or store the rest.

Thus the goal is to provide all the vitamin A and vitamin D substrate the body would have obtained in a natural state, so the body can regulate both systems naturally. This is best done by eating colorful vegetables and by exposing your naked skin to equatorial sun every day. Since most of us can't do the later, and won't do the former, we have to take the same amount of vitamin D substrate we would have gotten if we lived 100,000 years ago, and may want to take beta-carotene substrate in a multivitamin. As far as I know, low doses of beta-carotene (1,000 to 2,000 IU per day) will not do too much harm. The best way to get vitamin D substrate, as far as I can tell, is to take about 1,000 IU of vitamin D3 per every 25 pounds of body weight in the winter and stop all vitamin D in the summer and sunbathe. Alternatively, use a tanning bed when the sun is to low on the horizon to sunbathe. Remember, when you are outside, if your shadow is longer than you are, you are not making any vitamin D.

Below are passages from our paper, the heart of the reasoning the 16 experts used to issue the warning about vitamin A and cod liver oil, that is, the words in italics below are the advice of the 16 experts listed above, not just me:

"Although activated vitamin D and vitamin A signal through common cofactors, they compete for each others function. Retinoic acid antagonizes the action of vitamin D and its active metabolite. In humans, even the vitamin A in a single serving of liver impairs vitamin Ds rapid intestinal calcium response. In a dietary intake study, Oh et al found that a high retinol intake completely thwarted vitamin Ds otherwise protective effect on distal colorectal adenoma, and they found a clear relationship between vitamin D and vitamin A intakes, as the women in the highest quintile of vitamin D intake also ingested around 10,000 IU/d of retinol.

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Furthermore, the consumption of preformed retinol  even in amounts consumed by many Americans in both multivitamins and cod liver oil  may cause bone toxicity in individuals with inadequate vitamin D status. Women in the highest quintile of total vitamin A intake have a 1.5-times elevated risk of hip fracture.

Feskanich D, Singh V, Willett WC, Colditz GA. Vitamin A intake and hip fractures among postmenopausal women. JAMA 2002;287:47-54.

Indeed, a recent Cochrane Review found that vitamin A supplements increased total mortality rate by 16%, perhaps through antagonism of vitamin D.

Bjelakovic G, et al. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev 2008 Apr 16;(2):CD007176.

Another recent Cochrane meta-analysis concluded that although vitamin A significantly reduced the incidence of acute lower respiratory tract infections in children with low intake of retinol, as occurs in the Third World, it appears to increase the risk and/or worsen the clinical course in children in developed countries.

Chen H, Zhuo Q, Yuan W, Wang J, Wu T. Vitamin A for preventing acute lower respiratory tract infections in children up to seven years of age. Cochrane Database Syst Rev 2008

As early as 1933, Alfred Hess, who discovered that sunlight both prevented and cured rickets (this 1921 paper is also free) warned about vitamin A consumption, concluding, to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.(p 662)

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hesss prophecy of a passing fad proved premature and Americans continue consuming multivitamins and/or cod liver oil containing small amounts of vitamin D but undesirable quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinol (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, most of which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinol (5,000 to 15,000 IU or, in some cases, 30,000 IU).

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Clinical lore holds that Vitamin A is an anti-infective. We suggest that lore exists because of old cod liver oil studies. Semba reviewed early literature on vitamin A, usually given as cod or halibut liver oil, as a successful anti-infective. For reasons that are not entirely clear, fish liver oils of the time contained much higher amounts of vitamin D then does modern cod liver oil, perhaps because modern processing removes the vitamin D during distillation and then replace it at lower doses. Furthermore, a meta-analysis concluded that vitamin A, when given alone, increases the incidence of respiratory tract infections. If vitamin A increases the risk of respiratory infections, its high content in modern cod liver oils will only mask the full benefit of adequate vitamin D nutrition.

Semba RD. Vitamin A as "anti-infective" therapy, 1920-1940. J Nutr 1999;129:783-791.

Grotto I, Mimouni M, Gdalevich M, Mimouni D. Vitamin A supplementation and childhood morbidity from diarrhea and respiratory infections: a meta-analysis. J Pediatr 2003;142:297-304.

As the prevalence of vitamin A deficiency in the United States is apparently much lower than the prevalence of subclinical vitamin A toxicity, we cannot recommend cod liver oil for either adults or children. (We exclude fish body oil from our warning, as it contains no vitamin A  or vitamin D  but is a very important source of omega-3 fatty acids.) For example, in a recent assessment of serum retinyl esters in a group of obese individuals, four percent had levels >10% of total retinol which usually indicates hypervitaminosis A. Instead, a diet rich in carrots, sweet potatoes, cantaloupe, and other orange fruits and vegetables will supply all the carotenoids the body needs to make retinol without the potential for hypervitaminosis A, especially when additional preformed retinol already exists in dairy products, eggs, and fortified cereal. We wish our diet were as rich in vitamin D. With the exception of infants on formula or toddlers drinking large amounts of milk or fortified juice, adequate amounts of vitamin D are virtually impossible to obtain from diet."

Hathcock JN, Hattan DG, Jenkins MY, McDonald JT, Sundaresan PR, Wilkening VL. Evaluation of vitamin A toxicity. Am J Clin Nutr. 1990;52:183-202.

Mills JP, Furr HC, Tanumihardjo SA. Retinol to retinol binding protein (RBP) is low in obese adults due to elevated apo-RBP. Exp Bio Med. In press.

Tanumihardjo SA. Food-based approaches for ensuring adequate vitamin A nutrition. Comp Rev Food Sci Food Safety. In press.

And so ends the excerpt from the 16 experts. Long story short, don't take cod liver oil or vitamin A as a retinol. Below, I add some evidence that I did not include in the paper

The above is from Dr. Cannell's newsletter re: Vit D council.

I am going to have a Vit A level, serum, run in the near future. Will be interesting to see what it shows and hopefully it will be accurate.


Dr. B G said...

Hi Marilyn (from TYP right?),

I'm looking forward to hearing your vitamin A report :) Thanks in advance -- you're AWESOME, as usual.

My personal suspicion is that Dr. Cannell is examining the data with very narrowly focused lens/vision. Yes, vitamin A appears to cause harm in certain circumstances (in the presence of extreme vitamin D deficiency, eg, no VDRs are present (vitamin D receptors). In the DeLuca article he cited -- this is the case -- the mice were raised indoors (UVB devoid) and fed lab chow that contained no vitamin D on purpose. This occurred in most of the humans studies presented also.

I liken this is the current situation where single-parents raise the family. It's not the ideal situation and it works sometimes. Vitamin D and A work synergistically together in a similar fashion. If you have one overbearing single parent and no balancing spouse, the kids unfortunately are toast. Right? Both vitamin A and D can work independently and indeed several studies show they may even fill in for each other to a certain extent. Yet, ideally -- both are present in optimal proportions for optimum health, vitality, longevity, skin, organs, heart, lungs, etc.

I do agree with Cannell where vitamin A should be prudently avoided if no vitamin D is present/supplemented. Cod liver oil should be ok -- as long as 25(OH)D is 60-80 ng/ml. I know certain brands of CLO may have more vitamin A than others and maybe these should be avoided until the serum vitamin D is at optimal concentrations. I've actually cut back on supplemental vitamin A since I've added more seafood and grassfed meat/organs to our diet.

As I'm learning more about vitamin A and D -- they are very VERY important in their complementary roles in reproduction, growth and control of proliferation (like plaque, cancer, warts, skin tags), etc. Like all things, they need to be balanced.