Want to Boost Hormone Production? POP Crude Cod Liver Oil or Industrial Waste: Persistent Organic Pollutants (POPs) in Crude Cod Liver Oil Modulate Steroidogenesis.

Image 1: If you are concerned
about the hormonal side(?)-effects
of persistent organic pollutants,
better make sure you buy pharma-
ceutical grade cod liver oil.

I know, what you are thinking now: "Not again, the ProfDrAndro anti-fish oil rant." Yet, this is neither about your beloved fish oil, nor is it ranting. Its an unfortunate fact that environmental poisons such as persistent organic pollutants (POPs) find their way into the food-chain of fish. The fish your shiny cod liver oil pills are made of are no exception from this rule and if the producers did not take (costly) measures to remove these toxins from the crude cod liver oil, chances are the non-dioxin-like POPs have already begun to accumulate in your adrenal coretex (Colby. 1994; Ribelin. 1984). So, even if you are a fish-oil enthusiast, give this blogpost a chance and read on...

Still ahead of print is a study by Montano and some European colleagues (Montano. 2011). In their paper which will be published in the Journal of Food and Chemical Toxicology, the authors describe the effects of crude cod liver oil, pharmaceutical grade cod liver oil and the industrial waste that is produced in the manufacturing process of the former on human adrenocortical adenome cells. The latter are considered a valid tool to model the general effects of exogenous toxins on steroidogenic key pathways in humans. They will yet not provide quantitative dose response relationships between oral intake of "contaminated" fish oils. It would thus warrant further investigations how much of the "Crude Atlantic Cod Liver Oil" that was used in the study you would have to consume to achieve the (un-)desired(?) hormonal "boost" both the crude cod liver oil and the industrial residue induced even at the lowest (dilution factor 1/10000), the pharmaceutical grade oil only at the highest concentrations (dilution factor: 2.5/1000):

‘‘Cod’’[crude cod liver oil] mixture significantly increased cortisol and P4 [progesterone] production at all concentrations tested. It also increased T [testosterone] production at 1E-3-dilution and E2 [estradiol] at the two highest concentrations. ‘‘Pharm’’ [pharmaceutical grade cod liver oil] mixture in contrast, was unable to significantly trigger changes in hormone production, with the exception of increased E2 production by the highest concentration tested (2.5E-3-dilu-tion). However, the production of E2 triggered by the highest ‘‘Pharm’’ concentration was half from that produced by the exposure to ‘‘Cod’’ and ‘‘Ind Res’’ at the same dilution. ‘‘Ind Res’’ mixture significantly induced the production of E2, P and Cort at 1E-3-dilution.

Assuming that you do not consume the industrial waste (God knows what is in all those cheap fish oil products out there, though), the data in figure 1 shows that you would still ramp up your hormone production significantly (i.e. statistically significantly), as long as you bath your steroidogenic cells in high enough concentrations of polluted crude cod liver oil.

Figure 1: Induction in hormone expression in human adrenocortical adenoma cells after incubation with crude cod liver oil (Cod) or pharmaceutical grade cod liver oil (Pharma) at doses of 1/10000 (E-4) and 1/1000 (E-3) relative to control (DMSO)
(data adapted from Montano. 2011)

These results shed a new light on some of the studies showing ergogenic / anabolic effects with fish oil supplementation - what if it was not the fish oil, but rather the pollutants in the oil that increased hormonal output and lead to small, yet statistically significant effects in terms of muscle gain, fat loss or whatever else was measured in these studies? Well, I guess if you want to take "advantage" of these toxins you just have to keep buying the cheapest fish oil out there from the most shady supplement company you can find. If, however, you insist on having fish oil as a source of supplemental n-3 PUFAs (instead of just reducing the overload of n-6 fats in your diet), these results would indicate that it may be wise to invest a few more bucks into some legitimate pharmaceutical grade fish or cod-liver oil, regardless of whether or not you believe that oral dosing would elevate tissue concentrations of POPs enough to replicate the effects observed in this in-vitro study. Afterall, with daily ingestion of polluted fish oil, tissue accumulation would certainly be an issue.

Too Much of a Good(?) Thing: When Fish Oil Starts Clogging Your Arteries and Fattening Up Your Liver.

If you are no regular visitor of the SuppVersity, I guess, you are religiously taking your (high dose?) fish oil, day in day out. So what? It probably lowers your total and low density cholesterol (LDL-C; it may reduce your triglycerides and thus improve your insulin sensitivity. Yet, in doing all those "great" things, the unmetabolized and peroxidized remainder of everyone's favorite wonder-supplement begin to clog your arteries and liver - at least, if you believe in the validity of that kind of rodent studies which suggested the usefulness of fish oil, in the first place.

Image 1: Micrograph of non-alcoholic fatty liver disease, caused by the same kind of lipid accumulations
Shirazi et al. observed in the rats receiving fish oil treatment (image by Nephron)

Shirazi et al. (Shirazi. 2011) recently published a paper reporting exactly that: "Fish oil increases atherosclerosis and hepatic steatosis, although decreases serum cholesterol in Wistar rat" - The scientists had fed two groups of pregnant rats (and, after birth, their offspring) with either a fish oil containing or a standard, soy oil based diet. Both diets had the same overall fat content of 70 g/kg (according to standard AIN93-G recommended by American Institute of Nutrition). In terms of total calories, the diets thus contained 15.9% of the total energy in form of either fish or soy oil. The overall omega-3 to omega-6 ratios of the diets were 6:10 for the fish oil and 1.1:10 for the soy bean oil groups; where omega-3 in fish oil came from EPA and DHA, while the omega-3 content in the soy bean oil diet came from alpha-linoleic acid (ALA).

Image 2: In the aorta of rats on a diet rich in fish oil, fatty streaks like that
formed in the aortae (image source www.heartsite.com)

After 70 days the rats were killed and hepatic and aortic specimen were analyzed. The results are unsettling:

[...] fatty streak in fish oil fed pups were significantly more than that in the other group. [... liver] ductular cell hyperplasia in pups fed with fish oil was significantly more than that in animals fed with standard diet. There was a positive relationship between fatty streak in aorta and ductular hyperplasia in liver (r = 0.470 and p= 0.037)

Although the animals had free access to food (ad-libitum feeding) the pathological changes cannot be a consequence of differing calorie intakes. Both groups consumed roughly 16g of the respective diet. According to Shirazi et al., a feasible explanation for these observations and their inconsistency with previous studies by Saraswathi et al. (Saraswathi. 2009), Bringhenti et al. (Bringhenti. 2010), Zampolli et al. (Zampolli. 2006),and Casós et al. (Casos. 2008) would be the lower total amount of dietary fish oil, different (more varied) overall fat compositions of the diets and shorter study periods, respectively:

One possible explanation for this discrepancy is that in our study animals faced higher amounts of dietary fish oil; Saraswathi et al. used 209 g/kg of mixed oils (including coconut oil, olive oil, corn oil and soy bean oil) plus 60 g/kg fish oil, while we used 70 g/kg fish oil which was the only dietary fat source. The dosage of fish oil used in Zampolli et al. and Casós et al. studies were 1% and 5%, respectively, which was lower than 15.9% used in the present study. In the study performed by Bringhenti et al. animals were fed with fish oil containing diet from weaning till puberty which is a shorter period comparing to ours.

On the other hand, the results of this study stand in line with those of Ritskes-Hoitinga et al. (Ritskes-Hoitinga. 1998), Verschuren et al. (Verschuren. 1998) and Brenner et al. (Brenner. 1990), which, in parts (e.g. Ritskes-Hoitinga) observed even more severe  aortic atherosclerosis and hepatic steatosis than Shirazi and his colleagues. [ Something to think about: Isn't it telling that all those studies have been published before the fish oil craze? And before GlaxoSmithKline started making big bucks by selling is "pharmaceutical grade fish oil" Lovaza. Add to that the fact that Shirazi et al. obviously did not find an American publisher for their study and make up your own thoughts. ]

So what? In essence these results only confirm what I have been saying before. Supplementation with reasonable amounts of fish oil (~2g) may make sense, especially if your diet is naturally low in omega-3 fatty acids in general and DHA, in particular. Mega-dosing on the other hand, or trying to compensate for fatphobia by overconsumption of fish oil, i.e. consuming a low- to no-fat diet, while supplementing huge amounts of fish oil >5g), falsely believing that you would do your body a favor by providing him exclusively with the "good essential fatty acids", will do more harm than good. After all, the "best" (do we really think low total cholesterol is good) serum cholesterol and triglyceride levels are useless, if you die from clogged arteries and a liver defect.

Cod Liver Oil vs. URTI. 2x Higher Fat Oxidation W/ Optimal Workout Timing, Aggressive Diabesity Control, Seaweed & Breast Cancer and NO Supplements Superior to Sugar

Self-proclaimed experts will say: "No cod liver! It's poison! It has way too much vitamin A... you better pop a kg of vitamin D pills if you want to do something for your health." Really? How do you explain the results of the Robertson study, then?

"Grandma was right" - That's if you will the statement of the week - a statement that is verified by the SuppVersity Figure of the Week which is p = 0.04 and describes the probability that the association between the consumption of cod liver oil and a decreased occurrence of upper respiratory tract infects (URTI) Swedish researchers observed in a cohort of 6350 middle-aged and elderly participants in the Tromsø Study 6, of which Robertsen et al. had actually expected that it would finally confirm the protective effects of high(er) vitamin D levels / intake against respiratory disease. As it turned out, however, neither vitamin D (25-OHD), nor the intake of fish, n-3 capsules or vitamin and/or mineral supplements were significantly associated. Shamed be he who thinks of vitamin A now ;-)

• 2-Fold Increase in Fat Oxidation W/ Correct Workout Timing (Darvakh. 2013) -- If we assume that you want to burn the maximal amount of fat during a workout, timing could be a more important factor than previously thought.

  

  Figure 1: Maximal fat oxidation, intensity necessary to achieve the maximal fatty acid oxidation and total fat oxidation per minute; all values expressed relative to absolute mean in each category (Darvakh. 2013)

  In a recent study from the Department of Physical Education and Sport Sciences at the Shahid Chamran University of Ahvaz in Iran the maximal rate of fatty acid oxidation in healthy, but untrained subjects was 2x higher in the afternoon compared to both the morning and evening conditions.
  
  What's likewise interesting to observe is the fact that the exercise intensity that was required to achieve maximal fatty acid oxidation was higher in the morning. No wonder that the total fatty acid oxidation per minute in all three trials was the highest, when the participants worked out in the morning!

  ---

  Bottom line: It's not just the missing dietary control, but also the mere idea that "burning fat for fuel" during a workout would have beneficial effects on long-term weight loss - let alone help you shed weight, when you are not in a caloric deficit that renders the results of the study at hand interesting, but more or less irrelevant. My personal advice would thus be: Work out, whenever you can muster the time and whenever you got the choice, base your decision on when to work out on performance measures, not results from studies like these (learn more about planning your workouts here).

• Is the time ripe for aggressive diabesity cures?! (Belsare. 2010) -- Everyone who has listened to the Wednesday episode of Super Human Radio, when Carl Lanore interviewed the Indian researcher Milind G. Watve, co-author of the paper at hand, will already be familar with the concept:
  

  

  Table 1: Molecules that affect aggressive behavior as well as insulin resistance (Belsare. 2010)

  Physical aggression is known to increase secretion of epidermal growth factor (EGF) in anticipation of injuries and EGF is important in pancreatic beta cell regeneration too. In anticipation of injuries aggression related hormones also facilitate angiogenesis and angiogenesis dysfunction is the root cause of a number of co-morbidities of insulin resistance syndrome.
  
  Reduced injury proneness typical of ‘diplomat’ life style would also reorient the immune system resulting into delayed wound healing on the one hand and increased systemic inflammation on the other. Diabetes is negatively associated with physically aggressive behaviour."

  These and the unquestionably striking associations the researchers collected in the tabular overview I used as a basis for table 1 to the right of this post (you read it a follows: arrows indicate up-/down-regulation or pos-/neg. correlation; "A"/"B" causation / reverse causation shown in A1/B1 = mutant or knockout experiment; A2/B2 = pharmacological/physiological exp. based on infusion or use of agonists/antagonists); C indicates only statistical association w/out direct evidence for causality), would unquestionably justify the hypothesis:
  

  "[...]that suppression of physical aggression is the major behavioural cue for the development of metabolic syndrome."

  However, despite the fact that "preliminary trials of behavioural intervention indicate that games and exercises involving physical aggression reduce systemic inflammation and improve glycemic control" - the same is true for "unagressive" types of exercise, so that I can't but vouch my doubts about the causative nature of aggression in this game of convenient laziness.

  ---

  

  Sugg. Podcast: Doves, Diplomats & Diabetes: A Darwinian Interpretation Of the Obesity Epidemic (listen)

  Bottom line: Irrespective of the causative or correlative nature of the lack of aggression or its presence in the etiology and resolution of the obesity epidemic.
  
  In the end, I am with Dr. Watve and his Indian colleagues: the non-pharmacological and in my humble opinion only viable solution to our problem are lifestyle changes - and as far as the "aggressiveness" is concerned, I guess, we'd just have to enforce these more aggressively. At least as aggressively as the Australians are leading their "war against" cigarette smoking - maybe a "war against" and not as a quest for revenue-generating pharmacological solutions to behavioral problems as we are still doing it by now.

• The breast cancer protective effects of seaweed - proof of principle (Teas. 2013) -- Researchers from the South Carolina Cancer Center at the University of South Carolina state in their recently published paper in the Journal of Applied Physiology that the consumption of seaweed (Undaria) in the form of a capped supplement (5g/day, total) decreases the urinary human urokinase-type plasminogen activator receptor (uPAR) concentrations in15 healthy postmenopausal women (5 had no history of breast cancer, 5 were breast cancer surivors) during a 3-month single-blinded placebo controlled clinical trial.

  ---

  What to make of these results? With the well-established increase in uPAR in post-menopausal and it's highly significant correlation with unfavorable breast cancer outcomes. The scientists argue that this controlled experiment would provide the hitherto missing "proof of principle" to confirm the epidemiologically observed anti-breast cancer effects of seaweed.

• Pre- & Post-workout supplementation with VPX' flagship products NO Shotgun & Synthesize promote fat free gains more than pure sugar (Ormsbee. 2013) -- Actually I did not even want to post this study, but it's so hilariously funny that I could not resist informing you about the marginal edge the provision of the VPX pre- & post-workout supplements NO Shotgun & NO Synthesize had in a sponsored study from the Florida State University that's been published in provisional form on Friday afternoon.
  
  When the researchers analyzed the effects the provision of the said supplements before and after each of the workouts the 29 healthy resistance trained men had compared to a maltodextrin [yeah, that's protein, BCAA, creatine, caffeine, beta alanine & more in the "multi-ingredient performance supplements (MIPS) vs. plain sugar as "control" placebo)] they found

  • 

    Figure 2: Body composition of previously resistance trained subjects after 6 weeks of standardized thrice weekly progressive strength training in participants ingesting one serving of NO Shotgun and Synthesize (MIPS) vs. 2x17g maltodextrin (placebo) pre / post workout; values expressed relative to group baseline (Ormsbee. 2013)

    no group time  interaction  for  HR,  BP,  blood  glucose,  lipids,  NOx,  hs-CRP,
    cortisol  concentrations  or  body  fat
  • significant decrease in body fat in both groups (mean ± SD; MIPS: -1.2 ± 1.2%; Placebo: -0.9  ± 1.1%), android fat (MIPS: -1.8 ± 2.1%; Placebo: -1.6 ± 2.0%), and gynoid fat (MIPS: -1.3 ± 1 .6%; Placebo: -1.0 ± 1.4%) and *drum rolls please* 
  • a  group × time interaction  for the increases in fat-free mass which were significantly  higher (4.2% vs. 1.9%) after the ingestion of the kitchen sink supplements compared to the 21g of pure maltodextrin
  What? Yeah, I know that VPX has had a very similar study done in the past (read up on the details, here) and obviously nobody read my comment back in the days that it's nice to spend some money to prove that your supplements works, but basically useless if the study protocol is designed in a way that ensures that your product will come as the more or, as in this case, rather less glorious winner.
  

  ---

  Bottom line: I wonder when the first supplement company dares doing a study comparing their product to a basic comination of creatine + whey and a cup of coffee before the workouts... what? Oh, you suspect that this could hamper their sales? Well, I guess you could be right.

---

That's it for this installment of "On Short Notice"!  If you still have to kill some time before you start into the weekend, I suggest you take a peek at one of the following Facebook news:

• 

  I hope you did not already forget that. The isoleucine-containing peptides in hydro-whey can also ramp up GLUT-4 expression and increase skeletal muscle glucose uptake - a true repartitioning effect (learn more)

  Endurance boosting effects of hydro whey -- Whey protein hydrolysate aka "low molecular weight whey" has superior effects on the endurance of rodents compared to regular whey isolate (read more)
• Influenza: marketing vaccine by marketing disease -- Young Harvard scientists speaks out about the hilariousness of the flu vaccine (learn more)
• Further evidence androgens program fat-cells-to-be to become bone, not fat -- "[O]ur results suggest androgens promote an osteogenic gene program at the expense of adipocyte differentiation." (read more)
• Metabolic IN-flexibility is a characteristic feature of PCOS in women -- That's corroborated by both insulin resistance and androgen excess (learn more)
  

If that's still not enough to satisfy your cravings, just "like" the SuppVersity on Facebook and keep on par with the latest news of which I am sure there will be more to come before the next full article is going to be published tomorrow.

References:

• Belsare PV, Watve MG, Ghaskadbi SS, Bhat DS, Yajnik CS, Jog M. Metabolic syndrome: aggression control mechanisms gone out of control. Med Hypotheses. 2010 Mar;74(3):578-89.
• Darvakh H, Nikbakht M, Shakerian S, Mousavian AS.  Effect of Circadian Rhythm on Peak of Maximal Fat Oxidation on Non-Athletic. Zahedan J Res Med Sci. 2013; 15 [epub ahead of print].
• Ormsbee MJ, Thomas DD, Mandler WK, Ward EG, Kinsey AW, Panton LB, Scheett TP, Hooshmand S, Simonavice E, Kim JS. The effects of pre- and post-exercise consumption of multi-ingredient performance supplements on cardiovascular health and body fat in trained men after six weeks of resistance training: a stratified, randomized, double-blind study. Nutr Metab (Lond). 2013 May 16;10(1):39.
• Robertsen S, Grimnes G, Melbye H. Association between serum 25-hydroxyvitamin D concentration and symptoms of respiratory tract infection in a Norwegian population: the Tromsø Study. Public Health Nutr. 2013 May 9:1-7.  
• Teas J, Vena S, Cone DL, Irhimeh M. The consumption of seaweed as a protective factor in the etiology of breast cancer: proof of principle. J Appl Phycol. 2013 Jun;25(3):771-779.

Science Round-Up Seconds: DHA, Algae Oil, Fish Protein, Insulin Sensitivity, Fat Loss & Muscle Gain. Plus: Night Shifts & BPA = Pro-Carcinogenic From Breast to Prostate

It's somewhat ironic that Nurse's are one of the three high risk groups for breast cancer, because they work night shifts to help others. Who the other two groups are? Female military personnel and flight attendants on international flights.

If you did already listen to yesterday's installment of the Science Round-Up, you should actually be able to connect the dots between both, the first and second course of today's installment of the Science Round-Up Seconds, and the studies on the effects of DHA on fatty acid metabolism, as well as the fallacies of insufficient, interrupted, or irregular sleep Carl and I have been addressing, yesterday.

If all that does not ring a bell, I suspect you missed the show and have not had a chance to listen to the podcast (as usual the Science Round-Up starts in the 2nd hour of the show), yet. In this unfortunate case, I'd suggest you do at least start downloading the file while you take the first bite of today's two course menu ;-)

More things fishy from proteins with funky names to DHA and fish protein

Pollachius virens (Photo: Tino Strauss) is king, when it comes to the n:3/n:6 ratio, but with <1% of fat you will still be hard pressed to get tons of omega-3s from eating pollock... but is more really better, let alone necessary? Learn how to make the right fish choices here.

(Lane. 2013; Vikøren. 2013) -- Actually I wanted to title this one "Some Things Fishy", but then I remembered that there is already a SuppVersity post with this title, one I am still not able to make head or fin... ah, pardon tail of, by the way, because it clearly suggest that the consumption of oxidized fish oil is not a problem. Be that as it may, these are the SuppVersity Science Round Up Seconds, so the "more" does not refer to the said SuppVersity post on oxidized fish oil, but rather to the 70x* increase in the expression of a protein called Angiopoietin-like 4, which controls the availability of fatty acids for fuel I mentioned during the podcast (*the differential response for DHA was elucidated in a separate study on isolated rat hepatic cells, the general effect was however observed in a human trial, where all tested fatty acids, not just DHA, produced 11-12x ANGPTL-4 increases).

In view of the more of less undisputed benefits of having reasonable amounts of DHA (400mg) in your diet, it would obviously be nice if we could increase our intake of this relatively scarce omega-3 fatty acid in our diet, without having to resort  to fish and fish oil caps. A recently published overview of vegetarian dietary sources of omega-3 fatty acids by Katie Lane and her colleagues does however confirm what you've heard both Carl and me say on previous episodes of the SuppVersity Science Round Up, already.

The conversion of alpha linolic acid (ALA, the short-chain version of omega-3) from nuts (walnut) and seeds (flaxseed, echium) to DHA is literally zero. 

According to he researchers' review of the literature, only the ingestion of oils that were derived from micro-algae provide some, albeit preliminary evidence to support their usefulness as dietary source of DHA. The number of studies is yet relatively limited and "further research is necessary to evaluate optimal doses" (Lane. 2013) of respective supplements and/or food additives for "functional foods" (how I hate this word)

Micro-algae oils are not fish, though, and thus you would once more be missing out on the unique synergy only real foods have to offer: The fish proteins!

If you are not one of the many new visitors who have found their way to the SuppVersity only recently, the keyword "fish protein" should actually ring a bell... exactly! That's the stuff that has previously been shown to have astonishingly pronounced effects on glucose metabolism. Effect that have initially been observed in rodent studies and are not being replicated in human trials. Trials such as the one by Vikøren and his colleagues from the University of Bergen who report in their latest paper that was February issue of the British Journal of Nutrition that the provision of 3 g/d of a cabbed fish protein supplements for the first 4 weeks and 6 g/d for the last 4 weeks of a 2 months placebo controlled intervention study effectively and significantly

• 

  Table 1: Amino acid composition of fish, whey and casein protein (Hall. 2003; Vikøren. 2013)

  lowered the values of fasting glucose
• 2 h postprandial glucose and glucose-area under the curve,

• increased the important early insulin and 
• decreased the detrimental late insulin response to glucose ingestion 

• reduced the amount of  LDL-cholesterol (P< 0·05) and

• led to increases in lean (+0.8%) and decreases in fat mass  (-1.6%)

compared to the calorie-free placebo. Pretty impressive results, right? That's particularly true in view of the fact that neither the food intake nor the physical activity levels changed in the course of the 8-week intervention period.

What's that: Fish protein + fish oil? (Almost) whole fish, right!

Fish happens to be a way better source of taurine than the sperm of this Belgian Blue. There is in fact so little taurine bull sperm that it is "supplemented" with this amino acid in order to keep it fresh and stable and have it survive refrigeration. Apropos, you do remember that taurine can boost testosterone levels up to 250% - at least in rodents?

The obvious question therefore is: How does that work? The scientists don't provide a satisfactory explanation and to be honest, I have nothing more than a couple of half-assed hypotheses either. My best bet, and I am suggesting that despite the fact that a recent post of mine was entitled "Don't Judge a Protein By Its Amino Acid Content", would in fact be the amino acid content. If you take a look at table 1 it is obvious that the cod protein the scientists used in the study contained one amino acid you as a SuppVersity reader should by now be familiar with and neither whey, nor casein or any of the other standard proteins has to offer: Taurine!

Yet despite the fact that taurine has the potential to boost testosterone levels, increases insulin sensitivity and has in fact been shown to actively reduce body weight in a 2003 human study by Zhang et al. (Zhang. 2003), I am not sold on the idea that the relatively minor total quantity of taurine in the already low amount of fish protein (I mean 8g?) is the only reason for the non-negligible health benefits the scientists observed in their 10 male and 10 female participants (BMI 31-37kg/m²). Maybe it's another of those funky di-peptides you've read about in the context of the nutrient repartitioning effect of whey protein hydrolysate, only lately.

Regardless of what exactly it may be that facilitated the improvements in blood glucose management and the minor, but significant improvements in body composition, the health benefits you can derive from the consumption of cod protein make the notion of fish oil, let alone micro-algae oil supplementation appear even more retarded, when eating fish once or twice a week offers a way more natural and unquestionably more tasty solution to satisfy your DHA requirement.

Night shifts and breast, BPA and prostate cancer

There are two clockworks operating parallel in your body. The one in the brain has to be hacked by light exposure (learn more about "Sunlight a la Carte"), the one in your liver and other peripheral organs, on the other hand, can be (re-)set by specific feeding strategies, like Intermittent Fasting (learn more)

I simply assume that you have by now downloaded and listened to the podcast and are thus aware of what I said about the importance of rythmicity (if you did not really get the notion, I suggest you read up on the posts in the SuppVersity Circadian Rhythm Series to get a better grasp of the different clocks that are ticking in your body ;-) Exactly this kind of rhythmicity is continuously disturbed when you are either switching back and forth from day- to night-shifts or work the night-shift continuously and dare having a social life that's simply not compatible with sleeping all day and waking all night.

That the life of a nurse, for example takes it's toll on your health and precipitates not just the development of breast cancer (+36% after 30 years of rotating night shifts; Schernhammer. 2001), but colorectal cacers (+35% after 15 years of rotating night shifts; Schernhammer. 2003) and endometrial cancer (+47% after 20+ years and even +109% in obese women; Viswanathan. 2007), as well, has been debated ever since the early years of the 21st century.

With the recent publication of two meta-analyses the debate probably will not be over; and that despite the fact that even the less unsettling analysis by Kamdar et al. reports increases in breast cancer risk of +21% for women "with ever night-shift work exposure" (Kamdar. 2013).

"Subgroup analyses suggested that flight attendants with international or overnight work exposure and nurses working night-shifts long-term were at increased risk of breast cancer." (my emphases in Kamdar. 2013)

While the Kamdar study also included observational data, this 2nd meta-analysis, which was likewise published less than a week ago, included only case-control and cohort-studies yielding risk increases of +32% and +8%, respectively (Jia. 2013). Somethin else thatg may be worth mentioning is the fact that both, the studies the scientists ranked as "high quality" research, as well as the only existing study involving female military personnel observed even higher risk increases of +40%.

Despite methodological differences and slightly different outcomes of the two meta-analyses, both research groups do reach very similar conclusions stating that the evidence is still "weak", but does "support previous reports that night-shift work is associated with increased breast cancer risk" (Kamar. 2013) and that "large-scale epidemiological studies are needed" (Jia. 2013).

From breasts to prostates ;-)

Figure 1: Effects of 4-days of BPA injections at different dosages on systemic hormone levels (Castro. 2013)

I know the subheading sounds somewhat gross, but there are certain parallels. For one, there is the same need for large-scale epidemiological studies on the connection between BPA exposure and the development and malignancy of prostate cancer as it is the case with breast cancer and night shifts. On the other hand, BPS of which a recent study was now able to show that it messes with the aromatase and 5-alpha reductase activity in the prostate and can thus precipitate prostate cancer even in adulthood (Castro. 2013), is unquestionably relevant for the development of breast cancer, as well.

What's more, the reductions in 5α-R1 and 5α-R2 Castro et al. observed in their previously healthy, adult rodents after only 4-days of BPA injections at doses of 25, 50, 300, or 600 µg/kg per day and the concommitant increase in the expression of the third isoform of 5-α reductase (5α-R3) does not only precipitate cancerous growth, it's also a recently proposed as a biomarker of cancer malignancy. In conjunction with the quasi-reversal of hormones (see figure 1), the results of this study, which happens to be the first one to demonstrate such profound detrimental effects on mature mammals, should remind us of the fact gestation and early childhood are not the only time-points in our lives, we have to beware of endocrine disruptors.

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That's it for the Seconds and in case you are missing the information about fruits and vegetables, I will serve those tomorrow as part of the as of in fact short, but way more numerous "Short News". In case you are still hungry for more, I suggest you make take a slight detour to the SuppVersity Facebook Wall before you you sally into the weekend. There are a couple of appetizers waiting for you there:

• 

  "Does the Usefulness of Vitamin E Supplementation Depend on Your Activity Level?" While the marathon runners in the facebook study took only 50IU, 400IU is what most supplements have to offer as a minimum. Is that too much, for you? Do athletes need more? What about the hormetic response to exercise - it it even hormetic? (learn more)

  EGCG is an "anti-folate" - You still don't have to worry, nature has made sure that those who value the synergy of whole foods, or in this case drinks, won't be harmed (read more)
• LOW(!) doses of vitamin C & E (125mg & 50IU) don't diminish the benefits of exercise - On the contrary, in marathon runners that's enough to blunt the neutrophil damage (read more)
• Smart Kids = Lean Adults  - General intelligence as assessed in childhood has a significant and direct effect on adult obesity risk (read more)
• Valine, vanadium and oxygenated water - All useless for athletes. That's at least what the latest installment of the "A–Z of nutritional supplements" says (read more)

When you are done with those, it's about to start news fasting, for a couple of hours until tomorrow's morning news (for you probably today's late evening news) will be published on Facebook. Have a great "Post-Valentine's Day", everyone - I just  hope your spouses were happy with their presents ;-)


References:

• Castro B, Sánchez P, Torres JM, Preda O, Del Moral RG, Ortega E. Bisphenol A Exposure during Adulthood Alters Expression of Aromatase and 5α-Reductase Isozymes in Rat Prostate. PLoS One. 2013;8(2):e55905.
• Hall WL, Millward DJ, Long SJ, Morgan LM. Casein and whey exert different effects on plasma amino acid profiles, gastrointestinal hormone secretion and appetite. Br J Nutr. 2003 Feb;89(2):239-48.
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