Silicon-Powered Anti-Heart Disease Sausages / High Protein Breakfast, High Satiety, No Change in Food Intake / 49% Higher Chance of Healthy Aging Depends on Moderation

Can you pump them up w/ silicon and to negate their atherosclerotic effects!? 

In today's installment of the Nutrition Research Update in the Short News, I am going to tackle three studies that deal with the surprisingly pronounced, yet practically potentially irrelevant benefits of eating a high protein breakfast, silicon... not in breasts, but sausages as a means to protect you from heart disease and the fact that calories count so much that even on a "healthy diet" only those who eat in moderation will age healthily.

That sounds interesting? Fine! I am not going to waste any more time and will fast forward to the first study...

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• Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age - In the eponymous study, Baum et al. determined whether consumption of a protein-based breakfast (PRO) increases postprandial energy metabolism and substrate oxidation, reduces hunger, and reduces food intake at lunch compared with a carbohydrate-based breakfast (CHO) in normal weight (NW) vs. overweight/obese (OW) children. Both, the normal and over-weight children participated in the same randomized, crossover protocol that arranged for all participants to be served a
  • high PRO [344 kcal, 21% protein (18 g), 52% carbohydrate, and 27% fat] or 
  • high CHO [327 kcal, 4% protein (3 g), 67% carbohydrate, and 29% fat]
  breakfast, after which the energy expenditure (EE), substrate oxidation, appetite, and blood glucose were measured over a 4 h period. To access whether the high protein intake would also affect the participants appetite, the subjects had free access to a lunch buffet and food intake was recorded.
  

  

  Figure 1: Energy expenditure, fat and carbohydrate oxidation in the 4h post breakfast (Blum. 2015).

  The results were unambiguous: After breakfast, OW children in the PRO group had higher (P < 0.0001) EEs and fat oxidation over the 4 h period than did the NW children in the CHO and PRO groups. Of these, the increase in energy expenditure was transient and didn't last for the full 4h period. The increase in fat oxidation in response to the high protein intake, on the other hand, lasted for the full 4 h period (+16%; P < 0.05) and went hand in hand with a surprisingly pronounced 32% increase in carbohydrate oxidation in the PRO vs. CHO (P < 0.01) trial.
  

  

  Table 1: Despite decreased hunger and increased fullness, the protein breakfast did not reduce the total energy intake or modify the macronutrient ratio of the foods the kids selected at the lunch buffet (Baum. 2015).

  Now, all this sounds great, but even though the subjects experienced decreased feelings of hunger (−14%; P < 0.01) and increased fullness (+32%; P < 0.05) after the PRO than the CHO breakfast, the lack of effect on the intake at the subsequent ad-libitum lunch is disappointing to say the least. This and the lack of long-term data make it very difficult to predict if a similar increase in protein during breakfast only would actually help the subjects lose weight.  
• Silicon ... not breasts, but enhanced meat may protect older individuals against atherosclerosis - That's at least what a recent rodent study by Garcimartin et al. (2015) suggests.

  "Research has shown that silicon can play an important role in protecting against degenerative diseases. Restructuring pork by partially disassembling meat would permit the incorporation of active components with potential functional effects. However, there has been no research to date on the impact that silicon, as a functional ingredient in restructured pork (RP), has on lipoprotein composition, metabolism, and oxidation" (Garcimartin. 2015).

  In order to find out whether the addition of silicon would actually have a meaningful effect, the scientists added 1.3g/kg silicon to sausages that were then fed to one group of old rodents while the rest received regular, non-enriched sausages as part of regular and pro-atherogenic cholesterol-enriched diets.
  
  The results were quite astonishing, as is partially normalized the changes induced by the high cholesterol diet. Compared with the rodents who received the regular sausages, those on the silicon sausages had lower VLDL compound concentrations (P < 0.001; e.g., 75% less VLDL cholesterol) and a significantly reduced VLDL oxidation (65% less conjugated dienes and 85% less TBARS) that went hand in hand with an increase in LDL-receptor expression (200% more).
  

  

  Figure 1: The silicon in the sausages increased the LDL receptor density to (almost) normal, the amount of cholesterol protecting AE in the blood and liver, as well as its ratio to the amount of cholesterol. The result is obvious: With as little oxidized VLDL in the blood as the control, we can safely assume that the rodents that consumed the silicon enriched sausages have a sign. lower atherosclerosis risk (Garcimartin. 2015).

  In spite of the fact that there are differences in the susceptibility of mouse and man to the pro-atherogenic diets of the results do - just as the authors point out - still suggest that silicon added to restructure pork can strongly counterbalanced the negative effect of high-cholesterol-ingestion and, as I would like to add, the negative effects of endogenous cholestrol (by increasing its uptake by LDL receptors and decreasing its susceptibility to oxidation) thus "functioning as an active hypocholesterolemic, hypolipemic, and antioxidant dietary ingredient" (Garcimartin. 2015).
• Healthy eating requires a controlled (not restricting) energy intake to increase one's chance of "aging healthily" by almost 50% - If you question if eating "healthy" and not eating everything in sight is even worth it, you will like the results of a recent study from the Sorbonne in Paris (Essmann. 2015).
  
  In her latest study Karen E Essmann and her colleagues analyzed the diets of a subgroup of 2769 participants of the SU.VI.MAX (SUpplémentation en Vitamines et Minéraux AntioXydants) trial. They identified subjects consuming "healthy" and those on the "standard Western diet", adjusted the data for a large number of potential confounders and the influence of high(er) and low(er) energy intakes.
  

  

  Table 2: Overview of the criteria the scientists applied to identify "healthy eating" - CES-D, Center for Epidemiologic Studies–Depression Scale; DKTMT, Delis-Kaplan version of the Trail Making Test; IADL, instrumental activities of daily living; MMSE, Mini-Mental State Examination; RI-48, 48-item cued recall test; SF-36, Medical Outcome Study Short Form 36; SPPB, Short Physical Performance Battery.

  In that, the scientists found that the association between "healthy eating" and "healthy aging" was mediated by low(er) energy intakes. Only in subjects with median or lower energy intakes, the association between "healthy eating" and "healthy aging" reached statistical significance, so that the non-gluttonous "healthy eaters" were 49% more likely to age healthily.
  
  Since we are already talking "healthy eating", let's briefly mention that scientists from the University of Eastern Finland just confirmed the obvious (Haapala. 2015): A poorer diet quality is associated with worse cognition in children. What is a bit surprising, though, is that the relationship was stronger in boys than in girls.

In contrast to Blum's study, a previous study with high fat breakfasts showed sign. reduced 24h food intakes | more

Bottom Line: So what did we learn today? I guess if you want to find a general bottom line it is as simple as "when it comes to nutrition, things are never as straight forward as it is often portrayed in the mainstream media". High protein breakfasts, for example will help you to control your energy intake (by increasing satiety and fullness) and increase your energy expenditure, but they (certainly) won't make you lose weight in a scenario where you simply eat whatever is in sight. The same goes for the link between "eating healthy" and "aging healthy" which is significant (+49%) only in those who don't overeat on their healthy diets (note: a median intake is enough, you don't have to fast!).

And if that was not complex enough, take a look at the silicon sausage study. With the right additives even something as junk-foody as sausages can have almost "medical" effects. Whether silicon supplements have the same effects in men and women, though, would require future (long-term) studies | Comment on Facebook!

References:

• Assmann, et al. "A Healthy Dietary Pattern at Midlife, Combined with a Regulated Energy Intake, Is Related to Increased Odds for Healthy Aging." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.210740
• Baum, et al. "Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age." J. Nutr. first published on 12 August 2015 doi:10.3945/jn.115.214551
• Garcimartín, et al. "Silicon-Enriched Restructured Pork Affects the Lipoprotein Profile, VLDL Oxidation, and LDL Receptor Gene Expression in Aged Rats Fed an Atherogenic Diet." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.213934
• Haapala, et al. "Associations of diet quality with cognition in children – the Physical Activity and Nutrition in Children Study." British Journal of Nutrition (2015): FirstView Article.

Virgin Coconut Oil Minimizes Weight Gain and Improves Blood Lipids (HDL⇈, LDL + VLDL ↘) to Reduce Atherogenic Index by 84% Even in Rats on Non-Atherogenic Diets

There are more than a dozen of options for virgin coconut oil on the market and there's no way the normal custumer can tell which one is actually "virgin" and which is a fraud and maybe even adulterated with palm oil - the technology to identify adulterations is there (Manaf. 2007), but I haven't heard of a label that would prove that the products were tested.

You are probably as fed-up with the hype around coconut oil as I am, right? Coconut oil here, coconut oil there. For this, for that and "did you know that coconut oil will also ..." Yes, you can even argue that a new branch of broscientists and snake oil vendors is dealing with little else than coconut oil.

In spite of that, I consider it at least remotely possible that the data from a recent rodent study that was published in the UK Journal of Pharmaceutical and Biosciences (Sharig. 2015) will catch your attention. I am sure you won't catch fire, though, but maybe at least some sparks, when you read that a relatively low dose of virgin coconut oil slowed down the weight gain, even if the oil was added to a non-obesogenic diet. Not excited? Well what about its triglyceride and total cholesterol lowering prowess and it's ability to keep LDL and VLDL in check while increasing HDL significantly - that's at least news-worthy isn't it?

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But first things first - here's what the scientists did: The scientists bought a bunch of 2 months old rats. After 2 weeks of acclimatization, they randomly assigned them to one of the following diets:

• Group 1 was fed the normal pellet diet (control),
• Group 2 was administered normal diet with VCO (1 ml/day),
• Group 3 named as HCD received bread with pellet,
• Group 4  animals received HCD bread and pellet with VCO (1 ml/day),
• Group 5 called as HLD animals received cheese with pellet,
• Group 6 named HLD animals received cheese and pellet with VCO (1 ml/day)

All groups had free access to diets and water ad libitum for 10 weeks. To make sure the virgin coconut oil was actually consumed, the VCO was administered by oral gavage at a dose of 1.42 ml/kg. That's the rodent equivalent of ~3 tablespoons of coconut oil which is what Fife recommends in "Coconut Cures" (2005) you should take everyday to - as the title of the book says - prevent and treat common health problems with coconut (not all of the claims made in the book can be considered scientifically proven, btw).

How much virgin coconut oil is that? And does it have to be virgin? For most people the approximate equivalent dose you'd have to consume are 3 tablespoons or equal to 45 ml/day. That was the easy part. Whether it has to be virgin coconut oil is a bit harder to explain, but in view of the significant correlation Marina et al. found between the total phenolic content of virgin coconut oil and its scavenging activity (r=0.91), and between the total phenolic content and its reducing power (r=0.96), I would be surprised if the phenol-depleted regular coconut oil would have the same beneficial effects on your atherosclerosis risk.

The rodents remained on their respective diets for 8 weeks before... no, not before they were sacrificed, but before the scientists from the Managemant and Science University in Malaysia used a spectrophotometer and commercial enzymatic kits to determine the lipid parameters by enzymatic endpoint method, as well as the plasma total cholesterol (TC), triglyceride (TG) and high-density lipoprotein (HDL) levels were measured using commercial enzymatic kits.

Figure 1: Effect of Virgin coconut oil on plasma lipid profile of albino Wistar rats after 8 weeks (Shariq. 2015).

A brief glimpse at the data in Figure 1 shows that the addition of virgin coconut oil did in fact have a not exactly life-saving, but still health-relevant effect on the lipid metabolism of the rodents. What I personally consider most intriguing is that this was the case for all diets, including the normal one.

he effect of virgin coconut oil on weight (WT), Atherogenic index (AI) and % of protection in diet-induced atheroscle-rosis after 8 weeks (Shariq. 2015).

So what's the bottom line? If we assume that the effects translate to human beings (this can be assumed, since the use of coconut oil predicts a beneficial lipid profile in pre-menopausal women in the Philippines | Feranil. 2011), virgin coconut oil could in fact exert health-relevant lipid modulating effects of which the data in Table 1 shows that it has a significant anti-atherosclerotic effect even if you consume a normal (=rel. healthy diet). But even though that's impressive, it does not warrant the claim that virgin coconut oil was a "cure-it-all" that would battle cancer, Parkinson's, multiple-sclerosis and what-not. So, if you hear about any of these miracle cures, please remain skeptical: VCO is not the cure for everything.

Now that we are already speaking about healthy skepticism, it may be worth mentioning that it is certainly no coincidence that all the beneficial "coconut research" comes from Malaysia or the Philippines, where people have a vested interest in selling the locally produced VCO at the highest possible prices. For the study at hand, though, no sponsoring or conflict of interest was declared, since there's no funding information that does yet mean very little. Furthermore, in spite of preliminary human studies showing similar effects (e.g. Liau. 2011 | discussed previously), there's no tightly controlled human trial out there that would confirm similar or even identical effects occur in humans | Comment on Facebook!

References:

• Feranil, Alan B., et al. "Coconut oil predicts a beneficial lipid profile in pre-menopausal women in the Philippines." Asia Pacific journal of clinical nutrition 20.2 (2011): 190.
• Liau, Kai Ming, et al. "An open-label pilot study to assess the efficacy and safety of virgin coconut oil in reducing visceral adiposity." ISRN pharmacology 2011 (2011).
• Manaf, Marina Abdul, et al. "Analysis of adulteration of virgin coconut oil by palm kernel olein using Fourier transform infrared spectroscopy." Journal of Food Lipids 14.2 (2007): 111-121.
• Shariq, B., et al. "Evaluation of Anti-Atherosclerotic Activity of Virgin Coconut Oil in Male Wistar Rats Against High Lipid and High Carbohydrate Diet Induced Atherosclerosis."

If Buttered (Bulletproof) Coffee Increased Your Cholesterol & Triglycerides, You May Have Forgotten the Coffee Filter

Bulletproof coffee is a bogus fad, but is it also bad for your blood lipids?

You will probably have heard about the (over-)hyped "bulletproof coffee" (=coffee with butter in it) triggering measurable (and in some cases) significant increases in total and LDL cholesterol in bulletproof addicts (case studies + Toklu. 2015).

Now, the most obvious trigger of the cholesterol increase is the butter you put into the coffee to make it "bulletproof". Another possible reason for the increase in cholesterol is yet the coffee itself. A reason that people apparently forgot about ever since van Dusseldorp, Marijke, et al. published their 1991 paper called the "Cholesterol-raising factor from boiled coffee does not pass a paper filter."

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In their study the scientists wanted to test whether filtered coffee would trigger a similarly pronounced increase in serum cholesterol, as it has previously been observed for coffee that was prepared "Scandinavian-style" by boiling ground coffee with water and decanting the fluid into a cup (Arnesen. 1984; Førde. 1985; Aro. 1987).

To test whether the same mess would happen with filtered coffee, the scientists from the University of Nijmegen prepared their coffee as follows:

• Boiled-type coffee was prepared by pouring 0.5l of boiling water onto 25 g of coarsely ground coffee (Roodmerk, Douwe Egberts, Utrecht, The Netherlands) in an 0.5l Thermos flask. Ten minutes later, the liquid was decanted into a second Thermos flask, from which the coffee beverage was poured out into a cup or beaker just before consumption. One batch provided three cups of 0.15 l (5 fl. oz.), prepared with 8 g of ground coffee per cup. The contents of one bottle were usually consumed within half a day, after which another bottle was prepared. Most of the coffee grounds stayed behind in the first and second Thermos bottles. Those grounds that made their way into the cup were discarded by the study subjects. 
• Boiled and filtered coffee was prepared like the boiled coffee, but instead the liquid was poured into the second Thermos flask through a white paper filter (Melitta Nederland, Veenendaal, The Netherlands, 1x4, No. 4006508 200016) held in a conical plastic filter holder" (van Dusseldorp. 1991).

Subjects in both groups were allowed to dilute the brew in the second Thermos bottle with hot water if they found it too strong for their taste.

Can you do something to mitigate the effects? No, you don't have to take statins. A promising candidate would be to take 6g of taurine per day. Only 3g which is much less than the equivalent in pertinent rodent studies reduced the artherogenic index (-16% | AI is a measure that's based on the ratio of trigs to HDL) significantly and lead to slight improvements in total cholesterol levels (LDL wasn't measured | Zhang. 2004). In a rodent study, Park et al. observed a 38% reduction of LDL - significantly more than the increase that was seen in any "bulletproof coffee" case report or the boiled coffee study at hand.

The caffeine content, measured by reversed phase high-performance liquid chromatography, was 860 mg/1 for the boiled and 887 mg/1 for the boiled and filtered coffee - a difference that is way too small to explain why the 0.9 l or six cups of coffee brew the subjects were instructed to prepare and drink a day had drastically different effects on the cholesterol levels of the apparently healthy, non-smoking, non-medicated, non-dieting 33 male and 33 female habitual coffee drinker (four to seven cups of regular drip-filtered coffee per day) who participated in van Dusseldorp's study.

Table 1: Effects of Consuming Boiled Coffee, Boiled and Filtered Coffee, and No Coffee on Fasting Serum Lipid and LJpoprotein Levels (van Dusseldorp. 1991).

With three exception, the subjects who had been randomly assigned to the boiled, filtered or no coffee groups, showed an excellent compliance to the coffee regimen and didn't change their diets (this was actually assessed) significantly over the 12-week study period. The changes you see in Table 1 are thus not a result of increased cholesterol intake as it would occur if you consume extra butter in your coffee (in fact, the subjects in the boiled coffee group consumed 4.2g cholesterol/MJ energy less during the trial, so it's not the increase in dietary cholesterol from butter). 

So what's causing the cholesterol increase, then? Rather than any cholesterol you put in form of butter into the coffee, van Dusseldorp et al. speculated back in the 1990s that it is the naturally occurring fats in boiled unfiltered coffee that are responsible for the cholesterol "boosting" effects. In contrast to the filtered coffee which is virtually fat fee (0.02 g/l), the boiled unfiltered coffee contains 1g/l "coffee fats". Fats of which the researchers have previously shown that they are also present in the lipid-rich supernatant of boiled coffee you can obtained after centrifugation. The same supernatant Dusseldorp et al found to trigger a 23% (!) increase in serum cholesterol (this went hand in hand with 55% increases in triglycerides).

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Now, since dietary triglycerides and phospholipids do not raise serum cholesterol when eaten in amounts of 1 g/day, the authors speculate that the cholesterol-raising factor makes up part of the sterol-rich fraction of the lipid. Since both, the markers of the endogenous production and absorption of cholesterol remained the same, these lipids must - in one way or another - decrease the clearance of LDL cholesterol, but as the authors rightly point out the parameters (lathosterol and campesterol) they measured are insufficient to exclude effects of boiled coffee on lipoprotein synthesis and turnover.

Their findings are sufficient, however, to put a "?" behind the significance of the butter, when it comes to the ill effects of bulletproof coffee on your blood lipids... What we would have to know now, is whether the people who report increased cholesterol levels have either started to drink coffee now or increased their coffee intake from capsule machines or other methods of preparation that don't run the coffee through a filter | Comment on Facebook!

References:

• Arnesen, Egil, Olav H. Førde, and Dag S. Thelle. "Coffee and serum cholesterol." British medical journal (Clinical research ed.) 288.6435 (1984): 1960-1960.
• Aro, Antti, et al. "Bioled coffee increases serum low density lipoprotein concentration." Metabolism 36.11 (1987): 1027-1030.
• Førde, Olav Helge, et al. "The Tromsø heart study: coffee consumption and serum lipid concentrations in men with hypercholesterolaemia: an randomised intervention study." BMJ 290.6472 (1985): 893-895.
• Park, Taesun, Kyungshin Lee, and Youngsook Um. "Dietary taurine supplementation reduces plasma and liver cholesterol and triglyceride concentrations in rats fed a high-cholesterol diet." Nutrition research 18.9 (1998): 1559-1571.
• van Dusseldorp, Marijke, et al. "Cholesterol-raising factor from boiled coffee does not pass a paper filter." Arteriosclerosis, Thrombosis, and Vascular Biology 11.3 (1991): 586-593.
• Toklu et al. "Rise in Serum Lipids After Dietary Incorporation of 'Bulletproof Coffee'." Journal of Clinical Lipidology 9.3 (2015): 462.
• Zhang, M., et al. "Beneficial effects of taurine on serum lipids in overweight or obese non-diabetic subjects." Amino acids 26.3 (2004): 267-271.

Retinol (Vitamin A) - A Re-Discovered Weapon in the Battle Against Atherosclerosis: Reduced Progression in Patients, Protection For Healthy Subjects From 25,000IU/Day Retinol

No it's not fish oil that's going to save your a** from dying of heart attack. It's vitamin A! 25,000IU/day for those who are already suffering from atherosclerotic lesions and heard disease could do the trick.

600,000 people die of heart disease in the United States every year–that’s 1 in every 4 deaths; and at least some could have been prevented, if vitamin A had not been demonized as bone-dissolving kidney and liver killer for decades. That's at least what the results of a recent study from the Shahid Beheshti University of Medical Sciences in the - at least in terms of medical paradigms - open-minded Iran (Mottaghi. 2014). Unlike their Western colleagues who would probably considered the provision of 25,000IU of retinyl palmitate per day an act of personal injury, Azadeh Mottaghi and his colleagues dared administering the said amount of pre-formed vitamin A to 31 atherosclerotic patients and 15 healthy controls for 4 full months; and the results were... Impressive!

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In the atherosclerotic patients, the provision of extra vitamin A supplementation resulted in significant decrease in IL-17 gene expression (-47%) in fresh cell, 18% in PHA activated cells and 35% in ox-LDL activated cells (p<0.05 for all).

RORc gene expression (indicative of the progression of atherosclerosis) in fresh cells as well as ox-LDL activated cells decreased significantly after vitamin A supplementation in atherosclerotic patients (p=0.0001 for both).

Figure 1: IL-17 & RORc levels in LDL- and PHA activated cells relative to baseline (Mottaghi. 2014)

No wonder, I mean, most people tend to be so high on vitamin D (figuratively) that they totally forget about Vitamin A and its crucial roles in mediating immune responses (Winoto. 2002). Retinoic acid and its metabolits and analogues are capable of ameliorating various models of autoimmune diseases such as rheumatoid arthritis (Miyagawa. 2002), type 1 diabetes (Zunino. 2007) and ulceratative colitis (Bai. 2009). A strong suppressive effect of retinoids on pro inflammatory Th17 cells function via down regulation of RORc, as it was observed in the study at hand, has been demonstrated in vitro, before. Retinoids have  can also suppress Th17 function via interactions with the retinoid alpha receptor right on the cell surface.

In vivo, it has been demonstrated that retinoic acid (RA) enhances TGF-β and Foxp3 expression and will thus decrease the differentiation of the rampant Th17 cells and downregulate their IL-17 production (Mucida. 2007) The exact underlying mechanism is not that important in this context, what is important though, is the fact that it worked in fresh cells (see above) and in phytohemagglutinin (PHA) activated cells, i.e. immune cells on a rampage that have been activated by the bean-lectin phytohemagglutinin (the reason you should never eat raw beans).

Apropos rampage, it's worth noticing that the provision of extra vitamin A led to a significant reduction in RORc gene activity and thus atherosclerotic potential in both, the already active, and activated Th-17 cells of the atherosclerotic subjects, and the PHA- and LDL-activated Th-17 cells of the healthy subjects - in conjunction with the increase in RORc in the placebo group (see Figure 1), this observation provides convincing evidence that vitamin A can also protect healthy individuals from developing atherosclerosis.

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Bottom line: It's unrealistic to assume that the provision of extra vitamin A alone would be enough to send the atherosclerosic lesions into remission. It is, however, very realistic to assume, just as the authors do it, that "vitamin A supplementation may be an effective approach to slow progression of atherosclerosis" - a marginal effect, maybe, but a significant effect for every 4th man and woman in the US who would otherwise die in 2014 due to cardiovascular disease and may now live to see another new year's fireworks. Not too bad for a "dangerous" fat soluble vitamin that cannot be patented, right?

References:

• Bai, Aiping, et al. "All-trans retinoic acid down-regulates inflammatory responses by shifting the Treg/Th17 profile in human ulcerative and murine colitis." Journal of leukocyte biology 86.4 (2009): 959-969.
• Miyagawa, Naoki, et al. "Effect of synthetic retinoid, TAC-101, on experimental autoimmune disease." Pharmacology 67.1 (2002): 21-31.
• Mottaghi, Azadeh, et al. "Vitamin A supplementation reduces IL‐17 and RORc gene expression in atherosclerotic patients." Scandinavian Journal of Immunology (2014).
• Winoto, Astar, and Dan R. Littman. "Nuclear hormone receptors in T lymphocytes." Cell 109.2 (2002): S57-S66.
• Zunino, Susan J., David H. Storms, and Charles B. Stephensen. "Diets rich in polyphenols and vitamin A inhibit the development of type I autoimmune diabetes in nonobese diabetic mice." The Journal of nutrition 137.5 (2007): 1216-1221.