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)
--vegans
--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!

CLICK ON CITATION TO VIEW (below)
"...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.