Triphasic Nutrient Supplement W Caffeine Aminos Carbs Creatine All the Usual Suspects Allows For Higher Training Volume Lowers Cortisol Dampens Muscle Damage

Do you really need the whole pre-, intra-, post workout supp-arsenal to benefit from your workouts?

Finally, another workout supplementation study! Yeah, I know you are already suffering the side-effects of withdrawl, but its just a couple of lines and you will feel relieve - thanks to Stephen P. Bird and his colleagues from the Charles Sturt University in Bathurst, Australia, whose latest paper is about to be published in one of the upcoming issues of Nutrition Research (Bird. 2013). And as if that was not already enough, the participants were strength trained athletes, the  physical activity and diet were standardized according to pre-recorded habits and the supplementation protocol was extensive! With pre-, intra- and post-workout supplements it was exactly what many people today seem to believe was necessary to see any gains

... but is that true? Do you really need all that stuff?

The Australian researchers probably had a similar question in their minds, when they recruited their 15 strength-trained male field and court sport athletes (mean age 21.7years; 1-RM squat 133.0kg, bench press, 94.7 and 3.1 ± 0.3 years of strength training experience) and randomized them to ingest either a placebo supplement or a supplement "stack" consisting of 15g of Musashi Reactivate Hardcore before, 30g of Musashi Elevator during and 50g of Musashi SPORTS after the workout.

Table 1: Ingredient profile of the "tri-phasic" peri-workout supplement;  the placebo contained an aspartame based flavor that matched the taste of the active supplement (based on data from Bird. 2013)

In view of the fact that this probably sounds similarly "Chinese" to you as to me, Ive provided you with a tabular overview of the ingredient profile of what the scientists call a "triphasic multinutrient supplement". Basically nothing you would not find in the line-up of every major supplement company: Some carbs, EAAs, creatine, beta alanine and AAKG, caffeine and b-vitamins (not listed in table 1) before workout, carbs, EAAs and creatine intra-workout and the obligatory protein- (whey/casein mix), carb-combination garnished with some creatine and glutamine after the workout. Add in some salt, magnesium and potassium and you can even at the as of late obligatory "contains electrolytes" blend and you are good to go.

Acute effects = stat. significant, long-term physiological significance = ?

Caffeine (pre, only), creatine, EAAs, whey (post, only) and even beta alanine and AAKG, the additional carbhydrates, ... all that should do something right? Yep, you are of course right it should. After all people are paying with their hard-earned money for it!

Figure 1: Serum markers glucose, AST, CRP, CK, cortisol and testosterone before, during, right after, 30min after and 24h after the workouts with the active (SUPP) or placebo beverage (PLA); data expressed relative to group-specific pre-values (Bird. 2013)

That being said, the data in figure 1 provides at least initial relieve. There are statistically significant effects for almost all measured hormonal parameters,  if we compare the supplemented with the non-supplemented trials in this double-blind, placebo (PLA)-controlled, crossover study.

Figure 2: Supplement & blood draws (top); overview of the exercises, set x rep scheme and equipment used in the lower body workout (Bird. 2013)

The study design allowed for a 7-day washout before the "crossing" took place and those participants who had been randomized to the supplement group after an obligatory 28-day washout to clear all previously used supplements (and what not ;-) from the system had to perform the test workout (4 sets of 8 to 15 repetitions for 5 lower-body exercises; see figure 2) with/without the "triphasic nutrient supplement" on top of their 33.6 ± 1.8 kcal/kg body mass diet (macros: 3.8g/kg, 1.5g/kg carbs and protein, respectively.

The supplement, or rather the supplements, had to be ingested 15 minutes preexercise, in small, regular doses during the exercise, and the whole 300ml of their post-workout drink right after the workout. and thus according to the manufacturers suggestions.

Aside from the hormonal and inflammatory response (see figure 1) to the workout the scientists also measured the muscular performance and perceptual response during the workouts:

Figure 3: Perceptual measures of exertion & muscle soreness (Bird. 2013)

• the total training volume was higher for SUPP (15 836 ± 518 kg⋅repetitions) compared with PLA (14 390 ± 491 kg⋅repetitions) (P <.05;d = 0.70); 
• countermovement jump peak power (CMJ) did not differ between groups at any timepoint (P> .05;d= 0.05-0.18); in the SUPP group there was however a trend (P= .08;d= 0.32) for increased countermovement jump peak power was yet observed on the third of the four tests 30min after the workout (exact timing see figure 2, top)

• the global rate of perceived exertion (RPE) did increase after the workout in both groups, and was higher 30min after the supplement trial (P < .01; d= 0.89)
• the perceptual responses for muscle soreness was elevated and did not differ between treatments
  after the workouts

However, even for the statistical significant inter-group difference in msucle perceived exertion, the overall effect size is pretty small. It is therefore by no means "obvious", whether the 10% lower perceived exertion during the placebo trial which is probably a direct result of the +10% increase in total training volume, anyways, is of physiological relevance.

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So what do we make of these results? On the one hand it is unquestionably true, that the peri-workout supplementation (I refuse to keep using the hilarious sciency expression "triphasic") did increase the total workout volume, It is also true that it did lower the cortisol increase and produced lower areas under the curve for creatine kinase, but it also lowered the testosterone response to the workout (that the post-workout increase in testosterone is not a legitimate predictor of muscle growth is something you should now, after countless articles on the matter, be aware of; read more about testosterone).

Whey is more insulinogenic than white bread and creatine could make you fatt True for the 1st, remotely possible for the 2nd! And still both simply work....

Much ado about nothing? No, not really. While the hormonal changes are more or less irrelevant an increase in total volue that does not entail greater muscle damage could in fact make a difference thats not just statistically, but also physiologically significant.

What I do yet doubt is that the same results could not have been achieved with a cup of oatmeal, water and protein powder 1h before the workout, a coffee right before the workout and 3-5g of creatine, two bananas and a regular whey protein afterward. All you would have to buy then is a pouch of whey and a 500g jar of creatine monohydrate, which will last you for months. Both SuppVersity supplement staples, as you know and actually among the few supps with physiologically significant effects almost every trainee can benefit from... and did I mention that they are dirt cheap and can be combined with real foods?

References:

• Bird SP, Mabon T, Pryde M, Feebrey S, Cannon J. Triphasic multinutrient supplementation during acute resistance exercise improves session volume load and reduces muscle damage in strength-trained athletes. Nutrition Research. April 2013 [EPub ahead of print].

Carnitine Shoot Out L Carnitine Acetylcarnitine Propionyl Carnitine Which One Has the Highest Bioavailability Plus 2g LCAR Contain More Carnitine Than 2g ALCAR or PLCAR

What if we dont know whats most bioavailable? Does it really matter?

After years of being labeled as the supplemental non-starter #1, carnitine is got back on the radar of the average and extraordinary gymrat. The reasons are obvious - at least if you read the following SuppVersity articles: "Carnitine Wards Off Fat Gain by Increasing Fatty Acid Oxidation and Total Energy Expenditure" | more, "Carnitine as Repartitioning Agent?" | more, "L-Carnitine Increase Expression of Genes Implicated in Fatty Acid Oxidation, Glucose & Lipid Metabolism" | more. There have been quite a few impressive studies on the benefits of carnitine, lately, and their publication attracted a significant amount of attention in the bodybuilding, health and fitness community.

The question that remains, though, is: Which of the various forms of carnitine works best? Basically thats also what a group of scientists from the University (Hospital) Bern had in mind, when they put gavaged they put their mice on "supplement regimen" containing 2 mmol/kg/day carnitine from plain l-carnitine (LCAR), acetyl-l-carnitine (ALCAR), or propionyl-l-carnitine (PLCAR) for 4 weeks.

Rel. Carnitine content of l-carnitine, acetyl-l-carnitine (ALCAR), propionyl-l-carnitine (PLCAR) and l-carnitine-l-tartrate (LCLT)

Millimol vs. grams - for the carnitines thats a tremendous difference! I know that most of you will be annoyed when they get dosing regimen in millimoles instead of grams, milligrams of micrograms. Thats understandable, cause its inconvenient to have to check the molar mass of the given compound, grab the next best calculator and type 2 × 10-3mol * 161.199g/mol to eventually find out that the daily dose we are talking about here is 322.398mg/kg for the mice and thus ca. 26mg/kg or 2g for a human being with a body weight of 80kg (learn how to calculate HEDs).

The inconvenient moles do yet have one major advantage: We dont get into trouble, when we compare "compound molecules" such as the acetyl-carnitine. ALCAR is after all produced by combining L-carnitine and acetyl-CoA and does therefore have a ca. 21% higher molecule mass than the "original" molecule. Practically speaking 500mg ALCAR caps do thus contain 21% less actual carnitine that the basic l-carnitine caps of your neighbor. Aside from increasing the molecular weight, the acetyl-CoA attachment does yet also change its biological function - in other words: You may get the most carnitine for your money if you buy l-carnitine caps, but whether that equals the most "bang for your buck", is a whole different (non-mathematical) question.

Between week 1 and 2 of supplementation, the mice spent 24 h individually in metabolic cages with supplemented water and food ad libitum. During this period, 24-h urine was collected to assess the excretion of carnitine and acylcarnitines.

After 4 weeks of supplement

tion, the mice were submitted to an exhaustive exercise on a treadmill, after which they were anesthetized to take the muscle samples that were used to measure the carnitine content you see in Figure 1. 

What you cannot see in Figure 1 is that the mice gained an identical amount of weight, and that there were minimal, due to intra-group difference yet statistical non-significant differences in water and thus effective carnitine intake between the LCAR, the ALCAR and the PLCAR groups (its worth noting that all rodents on carnitine consumed 13-45% more water, so if you feel freaking thirsty, when youre "on" carnitine that may be a natural reaction to the increased). Likewise not shown is are the effect of carnitine on the skeletal muscle architecture, i.e. the ratio of fast-twitch glycolytic and slow-twitch oxidative fibers. The latter remained unchanged - the "specific trophic effect on type 1 fibers which are characterized by an oxidative metabolism" (Spagnoli. 1990) about which Spagnoli et al. speculated in 1990 was absent.

No changes in Skeletal muscle oxidative capacity! In spite of the fact that this is one of the classic promises of carnitine supplementation, the scientists did not observe significant difference in oxygen uptake between animals treated with carnitine or acylcarnitines and control animals and conclude: "These findings indicate that mitochondrial content and capacity (the activity of complexes I, II, and IV of the respiratory chain) remained unchanged in the supplemented compared to the control group" (Morand. 2013)

What you do see in Figure 1, on the other hand, may be misleading, because the existing differences in total carnitine after 4 weeks on the different forms of carnitine were non-significantly increased compared to the control group, so that the bioavailability, the researchers calculated based on the tissue accumulation and urinary excretion of various forms of carnitine were identical, i.e. l-carnitine - 19.8%, acetyl-l-carnitine - 18.6%, propionyl-l-carnitine - 19.1 % (see Figure 3).

It is not unlikely that the absence of significant differences in bioavailability is a direct result of the fact that the acylcarnitines and propionyl-l-carnitine were fully and partially hydrolyzed before reaching the systemic circulation, respectively. Whether there really is a difference to humans, as the scientists claim appears questionable, because the difference between Morand et al.s rats and Eders pigs, on the one hand, and the 11 Alzheimers patients in Parnetti et al. (1992) could well be brought about by age-/health-, and not species-specific differences.

Preformance, not tissue carnitine concentrations count, right?

In the end this may not even be that important given the fact that supplementing with all three forms of carnitine associated with a lower plasma lactate concentration and a better maintenance of the glycogen stores in white skeletal muscle after exhaustive exercise (Figure 2).

As the researchers point out, similarly lowered post-exercise blood lactate concentrations have recently also been reported in humans treated with 4.5 g glycine propionylcarnitine before exercise (Jacobs. 2009).

"These findings indicate that the animals supplemented with carnitine or acylcarnitines tolerated exhaustive exercise metabolically all in all better than the control animals. This may at least partially explain the beneficial effects of carnitine supplementation on physical recovery after intense exercise." (Morant. 2013)

The fact that this occured in the absence of extreme increases in the intramuscular carnitine stores supports a hypothesis that has been put forward by Rebouche et al. in a review about the pharmacokinetics and metabolism of carnitine and acetyl carnitine (Rebouche. 2004), where the researchers asked the question whether an increased carnitine content in target tissues is even necessary for a pharmacological effect of carnitine or whether an increased exchange between the plasma and tissue carnitine pools could be sufficient. Based on the results of the study at hand, the latter appears pissible, if not likely, "the molecular mechanisms responsible for this effect remain speculative, however" (Morant. 2013). Possible explanations Morant et al. propose are:

• The export of potentially toxic acyl groups from skeletal muscle, as shown in patients on hemodialysis supplemented with carnitine (Vernes. 2006).
• An effect of carnitine and/or acylcarnitines on capillary endothelial cells, possibly resulting in vasodilation and improved skeletal muscle perfusion and nutrient supply during high-intensity exercise (Jacobs. 2009).

In the end it is thus likely that you can benefit from the provision of 2-5g of carnitine, irrespective of the form you chose (this goes only for LCAR, ALCAR and PLCAR, to make a similar statement about LCLT, which has - among other things - been shown to increase testosterone receptor expression, is a whole different animal).

Bottom line: Despite the pathetic increases in muscle carnitine, the non-existent effects on body weight, carcass and muscle composition and the significant loss of the orally administered carnitine, the study at hand does provide evidence of the ergogenic effects of carnitine. The maintenance of white skeletal muscle glycogen stores, which would actually suggest an increase in fatty acid oxidation, although the corresponing mitochondrial enzymes werent elevated, the improved lactate concentrations and the minimal, statistically non-signficant, but measurable increases in time to exhaustion are after all ergogenic effects that could provide a metabolic advantage to any trainee.

Figure 3: Comparison of l-carnitine kinetics of  in rodents and humans in response to chronic and acute oral suppl., respectively (Coa. 2009; Morant. 2013)

Whether this metabolic advantage is relevant for the average trainee is yet about as questionable, as the question: "Plain carnitine, ALCAR or PLCAR, whats the best form of carnitine to take?" Based on the results of the study at hand, it would appear that it does not really matter.

If we do yet look back at Table 2 in the Amino Acids for Super Humans" article on carnitine, or the bottom of Figure 3 in this article, it would yet appear as if the results Morant et al. present in their latest paper in the European Journal of Nutrition only support the notion that ALCAR and PLCAR, both of which are sold as a form of "improved" carnitine by the supplement industry, are not the go-to forms of carnitine for the average physical culturist. For him or her, if anything, buying plain l-carnitine over at a bulk supplier of his / her trust would probably be the best option.

Reference:

• Eder, Klaus, et al. "Free and total carnitine concentrations in pig plasma after oral ingestion of various L-carnitine compounds." International journal for vitamin and nutrition research 75.1 (2005): 3-9.
• Parnetti, L., et al. "Pharmacokinetics of IV and oral acetyl-L-carnitine in a multiple dose regimen in patients with senile dementia of Alzheimer type." European journal of clinical pharmacology 42.1 (1992): 89-93.
• Rebouche, Charles J. "Kinetics, Pharmacokinetics, and Regulation of l‐Carnitine and Acetyl‐l‐carnitine Metabolism." Annals of the New York Academy of Sciences 1033.1 (2004): 30-41.
• Spagnoli, Luigi G., et al. "Morphometric evidence of the trophic effect of L-carnitine on human skeletal muscle." Nephron 55.1 (1990): 16-23. 
• Vernez, Laurence, et al. "Effect of L-carnitine on the kinetics of carnitine, acylcarnitines and butyrobetaine in long-term haemodialysis." Nephrology Dialysis Transplantation 21.2 (2006): 450-458.
• Wang, Yong-Xu, et al. "Regulation of muscle fiber type and running endurance by PPARδ." PLoS biology 2.10 (2004): e294.

How would you Acquire microorganism Vaginosis

Bacterial vaginosis infection is concerning the foremost frequent conditions related to womens feminine organ. though it should not be as recognized compared to chlamydia and Cupids disease, microorganism vaginosis infection continues to be a menace to womens health and well being that can not be unnoticed.

There isnt one successful issue that makes microorganism vaginosis. Fact is,, consultants area unit having a tough time work out what the explanation for microorganism vaginosis infection could be. What we have a tendency to area unit awake to is often that there ought to be the existence of many completely different mixtures of microorganisms for microorganism vaginosis to manifest.

Bacterial vaginosis can even be the top results of chemical distinction within the feminine organ. girls with this health probem sometimes have reduced amounts of oxide within the private parts. oxide ıs a chemical substance that generates lactobacilli within the feminine organ. Lactobacilli area unit often called the great bacteria in our body that battles off the dangerous small organism.

In addition, youll get microorganism vaginosis infection through a selected sort of bacterium acknowledged as anaerobic strain of bacterium. this can be a form of bacterium that grows up in cavities wherever theres fully no element. the gathering of bacterium that might generate the ill health causes it to be sophisticated for medical doctors to spot and combat effectively. lots of screening is also required to identify these microorganisms in your private parts to assist eradicate them.

Acquiring microorganism vaginosis can also be hooked in to variety of risk factors. many of the danger issue for microorganism vaginosis infection consists of enjoying many alternative sex partners, attracting new sex partners, symptoms of canal douching, and cigaret smoking. however bear in mind, these area unit merely risk factors and therefore the chance of microorganism vaginosis will still vary lots. True enough, the association of sexual activity and microorganism vaginosis infection area unit usually not clear, and there area unit circumstances of microorganism vaginosis occurring in females WHO didnt have sexual intercourse however.

Avoiding microorganism vaginosis starts with working out however we have a tendency to tumble. its vital to listen to our canal hygiene to shield yourself from it. Wash your feminine organ at the terribly least once daily, ideally with a formula that will balance the acidity or hydrogen ion concentration level of your feminine organ. do not have interaction in many alternative sex behaviors to scale back the possibilities of microorganism vaginosis.

Bacterial vaginosis isnt a dangerous sickness in the slightest degree. However, its essential to invariably maintain our procreative organs entirely freed from infection.

Are You ABCDE Deficient Common Nutrient Deficiencies in the US Plus How Food Fortification New Daily Values Affect the Intakes of Vitamin A E Calcium Iron Co

Nutrition labels on fresh blueberries - do we really need them?

I sill remember that I was shocked, when I bought a pack of blueberries and found a nutrition label underneath the plastic cover of my expensive 150g health-investement...

Thats probably 2 months ago and the reason I do remember this event now is the publication of a paper that examines the effect a change in the "daily values" (i.e. the references), the figures in the obiquitous black and white table are based on, would have on the average US citizens nutritional intake of the vitamins A, D, E, C, B-12 and folate, and the minerals calcium and iron.

"Daily Values" (DV), fortified foods and nutrient adequacy: Before I dig deeper into the actual study results, its probably wise to point out that fortified foods are the link between the DVs and micro-nutrient intake of the average American. If manufacturers continue to fortify foods to the same %DV for each nutrient, the extent to which potential changes in DVs would affect nutrient intake adequacy depends on the proportion of nutrient intakes derived from fortified foods and the magnitude and direction of change in the DV.

According to the data Mary M. Murphy and her colleagues from the National Institutes of Health/Office of Dietary Supplements present in their latest paper, there is still a large gap between the current DV values, which represent the RDAs (recommended daily allowances) from 1968 and have been matched to

"the highest level of intake judged to be adequate to meet the known nutrient needs of practically all healthy persons in a specific age-gender group" (Murphy. 2013)

on the one hand, and supposedly "improved" candidates that could replace them: The population weighed and the population coverage varieties of the RDA & EAR.

• RDA = the average daily dietary nutrient intake level that is sufficient to meet the nutrient requirements of nearly all (97–98%) healthy individuals in a particular life-stage and gender group
• EAR = the average daily nutrient intake level that is estimated to meet the requirements of half of the healthy individuals in a particular life-stage and gender group

As you can see in Table 1 these new recommendations are not - as you may have expected -  significantly higher than the current daily values. If you look closely, you will in fact notice that some of them are significantly lower!

Table 1: Current DVs for select vitamins and minerals and potential DVs based on population-weighted and population-coverage RDAs and EARs. AT,a-tocopherol; DV, Daily Value; EAR, Estimated Average Requirement; RAE, retinol activity equivalent; RE, retinol equivalent (Murphy. 2013).

In the case of vitamin B12 and copper, for example, the difference between the "reformed" recommendations would amount to -50%. The population-coverage RDA for vitamin C, on the other hand, is 50% higher than the old "daily values" (DV) and still more than 10x lower than the 1,000mg of ascorbic acid, of which you may have read on the Internet that it was the bare minimum intake of vitamin C (more about vitamin C). 

Figure 1: Percentage of U.S. population aged >4y with dietary intakes below the EAR based on current intakes and assuming
constant %DVs in fortified foods under the current, as well as two potential DV scenarios, i.e. the population-weighed EARs or the population-coverage RDAs become the revised DV values (Murphy. 2013)

Irrespective of the "low" RDA and the high number of fortified foods, ascorbic acid is yet still one of the those micro-nutrients the diets of more than 40% of the US are deficient in. And as the overview in Figure 1 goes to tell you, this would not change, if any of the new RDAs or EARs became the new DVs, so that the amounts of vitamin C in fortified food was adjusted.

Not an improvement by any means

In a more thorough sub-analysis, the scientists observed that the differences in the proportion of the total population with usual intakes less than the EAR would be <2% of 5 out of 8 nutrients (vitamins D, E, and B-12; folate; iron), regardless of whether the policy makers sued the population weighted EARs or the population-coverage RDAs as a basis for the revision of the DVs.

To put it plainy: This means that the micronutrient intake of more then 3 million individuals would still fall below the EAR in the total population (U.S. Census Bureau. 2005).

Even worse, if someone in the upper echolons was bribed.... ah, I mean convinced by the conclusive evidence we have that using the population-weighted EARs instead of the population coverage RDA would be the best thing to do, this would increase the risks of inadequate iron and folate intake in women of childbearing age. 

Both, iron and folate deficiency, can result in irreversible damage to the unborn child (Scholl. 2000; McArdle. 2013). The same is true for vitamin A (Wallingford. 1986) of which Murphy et al. write that it "was identified as a shortfall nutrient (although intakes are not currently in the category ‘‘of concern’’) for the U.S. population" (Murphy. 2013)

.

"The Standard American Diet Has Optimal Fatty Acid Ratio to Induce Diabesity." | read more

What has to be done? I hope you dont actually want me to answer this question - do you? I mean lets be honest - if people get 17–28% of total intakes of folate, iron, and vitamins A, B-12, and C and 8–12% of calcium and vitamins D and E from fortified foods (this is what Murphey et al. found) and are still deficient, you could obviously argue that we simply have to put even more vitamins and minerals into the nutrient deficient, energy dense junk the average Westerner is shoveling his piehole everyday.

But lets be honest: Wouldnt it be better to kill two birds with one stone by educating people that the stuff they eat is making them fat and sick - no matter how much artificial vitamins the "food" industry is pumping into their highly addictive, revenue-centered high-tech designer products?

References:

• McArdle, Harry J., Lorraine Gambling, and Christine Kennedy. "Iron deficiency during pregnancy: the consequences for placental function and fetal outcome." The Proceedings of the Nutrition Society (2013): 1-7.
• Murphy, Mary M., et al. "Revising the Daily Values May Affect Food Fortification and in Turn Nutrient Intake Adequacy." The Journal of nutrition 143.12 (2013): 1999-2006.
• U.S. Census Bureau. 2005 Middle series data from annual projections of the resident population by age, sex, race, and Hispanic origin: lowest, middle, highest, and zero international migration series, 1999 to 2100 (NP-D1-A). Washington: Department of Commerce; 2000 [cited 2012 Jun 16]. Available from: http://www.census.gov/population/www/projections/natdet-D1A.htm 
• Scholl, Theresa O., and William G. Johnson. "Folic acid: influence on the outcome of pregnancy." The American journal of clinical nutrition 71.5 (2000): 1295s-1303s.
• Wallingford, J. C., and B. A. Underwood. "Vitamin A deficiency in pregnancy, lactation, and the nursing child." In: Bauernfeind JC, ed. "Vitamin A deficiency and its control." New York: Academic Press, 1986:101–52.

True or False Washing Your Fruit and Veggies is Useless You Cant Wash Away the Pesticides Anyway!

Its a good idea to wash your veggies, but this is not the most effective method. Bath them in warm water, dont wash them under the faucet.

Despite the fact that I had my reasons to end the SuppVersity "True or False" Series back in the day. The popularity of the corresponding articles that appear from time to time as SuppVersity Classics on Facebook does yet tell me that you wont be mad at me, if I revive it and try to tackle a statement Ive overheard in one of those infamous gym conversations between two ladies on the cross-trainer: "I always wash those pepper extra thoroughly, you know... tomatoes are among the veggies with the highest amounts of pesticides on them." Answer lady two: "Ha, you dont really believe the pesticides are on the outside of the tomatoes only, do you? They are in the tomato. Washing them will at best remove some of the dirt on their skin!"

True or False: "Its useless to wash your peppers."

False - I was surprised, when I realized that the answer to this True or False item was much easier to find than I had thought. It took me a while, though, before I found a study that analyzed data from more than just one vegetable variety, but the basic answer,  i.e. "No, its not useless to wash your peppers - quite the contrary!" popped up right in my first cursory database search.

Figure 1: Amount of ethylenebisdithiocarbamates and chlorpyrifos on selected vegetable (µg/kg) before and after washing; the figure above the bars indicate %-change from pre to post washing (Chavarri. 2004; Randhawa. 2007)

If you look at the data of two studies I selected more or less randomly (see Figure 1) you will yet see that the effectiveness of the "wash away the pesticide approach" depends on both, the type of vegetable and the type of pesticide. With a mean total endusulfan reduction of >20% it should however be absolutely obvious that not washing your veggies would be wreckless. 

Table 1: Current European Union Maximum Residue Levels in mg/kg (Council Directives 76/895/EEC and 90/642/EEC, last revised in June 2004)

Artificially contamination ➫ standardization: The baseline pesticide level of the vegetables in the Chavarri study was achieved by spraying fresh produce from controlled plots with no previous pesticide applications with those pesticides farmers usually use in the EU. The reason should be obvious: standardization. Thus, the pesticide levels were within the contemporary EU limits (s. Table 1) - something you cannot necessarily expect from every product you buy in the supermarket.

I mean, I shouldnt have to tell you to that its unquestionably healthy not to be exposed to the full load of 24µ/kg chlorpyrifos and 1,626µg/kg ethylenebisdithiocarbamates (both have carcinogenic effects in humans; cf. Houeto. 1995, Josephson. 2005), from the tomatoes - specifically in view of the fact that 5.% of the tomatoes that are sold in the EU exceed the contemporary pesticide limits (Nasreddine. 2002) and would thus contain way more of these hazardous substances to begin with.

Aprospos washing! How do you do that?

You dont know how to wash veggies? Well, I obviously cant tell you what the absolute optimal way is, but what I can tell you is how scientists washed the specimen that were used in the studies the data in Figure 1 is based on: They placed the veggies in a dish or a clean lavatory with warm tap water and cleaned them with "gentle rotations of the hand" (Randhawa. 2007), before they grapped a conventional paper towel and blotted them dry.

Figure 2:  Illustration of the processing steps in Chavarri et al. (2007).

Thats similar to what you do? Great, and you know what, I would bet thats not the only similarity between yourself and the average scientist. Just like you, scientists dont eat all their veggies raw. Consequently, both Chavarri et al. as well as Randhawa et al. conducted additional analyses of the pesticide content of their veggies after the produce had been blanched (the peppers were roasted, not blanched), peeled, pureed (Chavarri. 2004; see Figure 1) and cooked or peeled and cooked (Randhawa. 2007), respectively.

Figure 3: Relative ethylenebisdithiocarbamates and total endosulfan levels (in % of baseline) after washing, peeling, blanching / cooking & co. (Chavarri. 2004; Randhawa. 2007)

As you can see in Figure 3, each of these processing steps lead to a further reduction of pesticides. For the initially highly intoxicated asparagus, for example, even the last traces of pesticides ended up in the cooking water. If you would now decide to recycle the water for a soup or whatever, all your efforts to rid yourself of the pesticide would have been in vein.

"Conventional vs. Organic is not about getting more, but about getting  less for your money" | more

Bottom line: Wash your damn veggies you lazy *****! If you still dont believe that its well worth spending this inconvenient extra-minute it takes to prepare warm water (28-32 °C), put your foods in, scrub a little with your hand and then continue processing them, Id suggest you take a look at a recent meta-analysis from Ghent University in which the authors dealt with the exact same question and conclude:

"Reduction of residue levels was indicated by blanching, boiling, canning, frying, juicing, peeling and washing of fruits and vegetables with an average response ratio ranging from 0.10 to 0.82." (Keikotlhaile. 2010)

References:

• Chavarri, M. J., Herrera, A., & Arino, A. (2005). The decrease in pesticides in fruit and vegetables during commercial processing. International journal of food science & technology, 40(2), 205-211. 
• Houeto, P., Bindoula, G., & Hoffman, J. R. (1995). Ethylenebisdithiocarbamates and ethylenethiourea: possible human health hazards. Environmental health perspectives, 103(6), 568.
• Keikotlhaile, B. M., Spanoghe, P., & Steurbaut, W. (2010). Effects of food processing on pesticide residues in fruits and vegetables: a meta-analysis approach. Food and Chemical Toxicology, 48(1), 1-6.
• Nasreddine, L., & Parent-Massin, D. (2002). Food contamination by metals and pesticides in the European Union. Should we worry?. Toxicology letters, 127(1), 29-41.
• Randhawa, M. A., Anjum, F. M., Asi, M. R., Butt, M. S., Ahmed, A., & Randhawa, M. S. (2007). Removal of endosulfan residues from vegetables by household processing. Journal of Scientific and Industrial Research, 66(10), 849.

Nutrition News Quicky ⤹ Energy Reduction Metabolic Parameters ⤹ Macrobiotic Ma Pi 2 Diabetes Diet 2 0 Plus Remember Youre Eating Foods Not Figures

Review suggests: On the SAD American diet only energy restriction saves the average Joes & Janes form diabesity.

Have you ever wondered what actually happens to your body, when you start dieting? I mean on a molecular / signalling protein level? If so, todays "Nutrition News Quicky" is for you, because one of the two studies this quicky is dealing with talks about just that: The type and onset of changes and the realization that Mr. & Mrs. Average Joe on their standard Western diets will gain weight, if they dont subscribe to life-long energy restriction. If you dont like that, it appears as if the "Macrobiotic Ma-Pi 2 Diet" could be a solution - or is this just too good to be true?

Energy Restriction & Metabolic Parameters

With all the hoopla about macronutrient composition, timing, etc. and the realization that the calories in vs. calories out equation is not as simplistic as most dieticians still want to have it, the word "calorie restriction" has gotten quite a bad rep in the Internet health community. 

Table 1 Comparison of the metabolic effects of caloric restriction after a variable period of time on (Soare. ahead of print).

If you take a look at overview of its effects in on body composition, blood glucose, lipids, etc. in Table 1, it does yet become obvious that you must not underestimate what will happen if you simply cut back on calories (based on overview in Soare. ahead of print). As long as the nutrition remains adequate (= you get the necessary micronutrients), eating less will lead to improvements in insulin sensitivity. This in turn triggers a whole cascade of beneficial effects that start with the reduction of fasting blood glucose levels and insulin concentration and end with significant reductions in body fat, type II diabetes rates, blood pressure and chronic inflammation.

Hey Mr. Average Joe, you are going to be fat and sick!

What is quite shocking, is the comparison of overweight dieters to Mr. & Mrs. average in a recent study by Soare et al. (2013).

If you take a look at the data in Table 1 you will see that the "healthy control" group Soare et al. defined in their review of the literature will almost inevitably develop a diffuse combination of obesity-related pathologies we call the "metabolic syndrom". In other words, if Soares assessment of the situation was correct only the dieters will be able to ward off an insidious increase in body weight, blood glucose, insulin, etc. in the long run.

"What? I am going to be a fat sedentary slob?" Dont worry, you are not going to be either fat or a slob, unless you are sedentary. There is (imho) no debating that you either have to diet for the rest of your life or incorporate a minimal amount of physical activity into your everyday lives. If the focus is on health, recent studies have confirmed: The effects of exercise are more pronounced than that of "healthy dieting" (read more in the SuppVersity Facebook News).

On a more general note, I would like to point out that these "results" (in a way the assumption that everyone who is not dieting is going to become obese is rather a hypothesis) confirms my personal conviction that the ostensibly paradoxical difference between our bodies inability to compensate for increased vs. decreased energy intakes is also a result of chronic overnutrition - or, to put it differently: If there is a 20% margin in our daily energy requirements within which our weight would be stable, 90% of the weight stable population of the Western obesity belt is consuming those extra 20%, anyway.

This would not just explain why each and every additional cookie people eat ends up on their hips "instantaneously"; it would also provide us with a simple, yet logical explanation that significant weight loss can only be achieved, if you reduce your dietary intake by >20%... but hey, I am getting side-tracked, here ;-)

⤹ "Macrobiotic Ma-Pi 2" = Diabetes Diet 2.0?

In their very recent, hitherto unpublished review of the effects of diet on type II diabetes a group of scientists from the University Campus Bio Medico conclude:

Battle diabesity w/ supplements

"Many dietary regimens are available for patients with type 2 diabetes to choose from, according to personal taste and cultural tradition. [...] Additional randomized studies, both short-term (to analyze psychological responses) and long-term, could help reduce the multitude of diets currently recommended, and focus on a shorter list of useful regimens." (Kahzrai. ahead of print)

A diet that was not (yet?) on the list Kahzrai et al. are referring to, here is the "Macrobiotic Ma-Pi 2" diet. A pretty funky name for a nutritional intervention the efficacy of which has been tested by Francesco Fallucca, Carmen Porrata, Sara Fallucca and Mario Pianesi in recent experiment. The results of this experiment are about to be published in a future edition of the peer-reviewed scientific journal Diabetes/Metabolism Research and Reviews in 2014 with a telling subtitle:

" Gut microbiota, inflammation, diet, and type 2 diabetes"

In conjunction with the word "macrobiotic" in the name of the diet, it should be obvious that the main idea behind this "new" anti-diabesity diet is to tackle the imbalance of the intestinal microbiota of which more and more scientists (e.g.. Musso. 2011; Qin. 2012) believe that it was the cause not the consequence of development of several human diseases, including obesity and type II diabetes (T2DM). As Kahzrai et al. mention in their abstract,

"[t]he main regulators of the intestinal microbiota are age, ethnicity, the immune system, and diet. A high-fat dietmay induce dysbiosis, which can result in a low-grade inflammatory state, obesity and other metabolic disorders. Adding prebiotics to the diet may reduce inflammation, endotoxaemia, and cytokine levels as well asimproving insulin resistance and glucose tolerance." (Kahzrai. ahead of print)

In their overview of the currently available literature, on the effects the administration of prebiotics such as fermentable dietary fibers has on the production of incretins (~satiety hormones), i.e.

• glucagon-like peptide 1 (GLP-1; fatty acid oxidation, glucose control ↑)  and 
• peptide YY (PYY; anorexigenic = hunger ↓), 

as well as its anti-ghrelin (orexigenic = hunger ↑), they highlight a very recent 21-day, intervention study in patients with T2DM. It is one of only few contemporarily available human studies of which the researchers say that they

"have not given robust results because of their limitations; most randomized controlled trials have been  short-term studies (no more than six months), with small sample sizes ( less than 50 subjects), and have focused on surrogate markers rather than clinical end points". (Kahzrai. ahead of print)

Many of these studies, which confirmed the previously referenced beneficial effects on GLP-1 and PYY have been conducted with pregnant women. These studies were able to show that the frequency of gestational diabetes is significantly reduced by probiotic intervention - immediate downstream effects on the children’s growth rate, on the other hand, were not observed (Luoto. 2010a).

"A unique follow-up study (Luoto. 2010b) has suggested that gut dysbiosis during the first stages of life may be associated with the development of obesity; this study investigated the bifidobacterial numbers in infant fecal samples and showed they were higher in children of normal weight than in overweight infants." (Kahzrai. ahead of print)

Luoto et al.s follow up study is unfortunately does yet share one of the central limitations 90% of the currently conducted experiments have in common: They did not include all the factors that may be involved in the development of obesity, in particular dietary habits.

Table 2: Macrobiotic Ma-Pi 2 Diet typical composition (Porrata. 2009)

This takes us back to the previously mentioned "recent" series of studies, the results of which have not yet been fully evaluated, yet.

As you can see if you take a look at the typical diet composition of the subjects in the first, prospective trial (Porrata. 2009; see Table 2), the "macrobiotic" intervention was exclusively food based. It was composed of 40–50% whole grains (rice, millet and barley), 30–40% vegetables (carrots, kale, cabbage, broccoli, chicory, onions, red and white radish, parsley),  and 8% legumes (adzuki beans, chickpeas, lentils, black beans), plus gomashio (roasted ground sesame seeds with unrefined sea salt), fermented products (miso, tamari, umeboshi) and seaweeds (kombu, wakame, nori).

Bancha tea (tannin-free green tea) was the main source of liquid. The food intake was measured using the weight method for 7 consecutive days in the 2nd and 4th months of the intervention. The same goes for the compliance with the recommended (100% idiotic) macronutrient composition, according to which the subjects had to consume 15%, 20% and 65% of total energy in form protein, fat and carbohydrates, respectively.

Figure 1: Changes in body composition and glucose & fat metabolism after 6 weeks on Ma-Pi 2 (Porrata. 2009)

If you take a look at the data in Figure 1 there is yet still no debating: The tons of macrobiotic whole foods worked magically - irrespective of the suboptimal protein intake (66g per day, only), the study participants lost tons of fat weight and increased their lean body mass - certainly not bad, if you asked me.

There is yet still one question that needs to be answered: Is this a results of the macrobiotics or a result of the obligatory switch from the Western "convenience" to a whole foods diet that induced these changes? If you asked me, its the latter. This does not exclude the beneficial influence of an increased macrobiotic content of the diet and corresponding changes in the bacterial make-up of the gut. In the end, this is yet a necessarily result of the enforced revisions the sixteen 60-year old adult type II diabetics who were all treated with insulin made to their food selection.

Bottom line: It may be hidden in plain sight, but the two studies I discussed in todays news quicky do have something in common. Something thats not just the term "type II diabetes": Its the way they can remind you of the things that actually matter: Food selection and quantity (well and exercise, or I should say "physical activity" - although its not directly mentioned in the studies).

If I read the questions about diet I receive on an almost daily basis, the majority of them is concerned with irrelevant details that revolve around insignificant changes in macro- and micro-nutrient composition. At times it sounds as if you were eating figures, not foods. No wonder that this does not produce the weight loss or hypertrophy effects you could achieve if you started to count the number of eggs, potatoes and tablespoons of oil you consume instead of obsessing about the different effects of eating 300 and 324 rice corns... Ok, I am exaggerating, but if this exaggeration made you feel insulted, you are probably one of those people who would benefit most from letting go of the fractional digits in his or her food logs.

References:

• Luoto, R., Laitinen, K., Nermes, M., & Isolauri, E. (2010a). Impact of maternal probiotic-supplemented dietary counselling on pregnancy outcome and prenatal and postnatal growth: a double-blind, placebo-controlled study. British journal of nutrition, 103(12), 1792-1799.
• Luoto, R., Kalliomäki, M., Laitinen, K., & Isolauri, E. (2010b). The impact of perinatal probiotic intervention on the development of overweight and obesity: follow-up study from birth to 10 years. International journal of obesity, 34(10), 1531-1537.
• Musso, G., Gambino, R., & Cassader, M. (2011). Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes. Annual review of medicine, 62, 361-380.
• Porrata, C., Sánchez, J., Correa, V., Abuín, A., Hernández-Triana, M., Dacosta-Calheiros, R. V., ... & Pianesi, M. (2009). Ma-Pi 2 Macrobiotic diet intervention in adults with type 2 diabetes mellitus. MEDICC review, 11(4), 29-35.
• Soare A., Weiss E.P., Pozzilli P. (2013) "Benefits of caloric restriction for cardiometabolic health, including type 2 diabetes mellitus risk". Diabetes/Metabolism Research and Reviews [ahead of print]
• Qin, J., Li, Y., Cai, Z., Li, S., Zhu, J., Zhang, F., ... & Yang, H. (2012). A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 490(7418), 55-60.

Effectively watching blood sugar Levels

Effectively watching blood sugar Levels

Living with diabetes isnt easy. you would like to form sure changes on however you reside your life. Managing polygenic disease is straightforward if you recognize the way to effectively monitor your blood sugar level. this can be ready to assist you live a additional traditional life despite the actual fact that you simply square measure full of polygenic disease.

You have to recollect that after you get polygenic disease, you have got it for as long as you reside. theres no cure for this sickness however it is managed. And, so as for you to effectively manage polygenic disease, you would like to be ready to monitor your blood sugar levels. By doing thus, youll be ready to live a additional traditional life.

To monitor your blood sugar levels, you would like to possess a glucometer or a aldohexose meter. This device will inform you the way abundant aldohexose is in your blood. mistreatment this device needs you to supply a comparatively bit of blood for the machine to browse. In most cases, lancets square measure enclosed in aldohexose meter kits furthermore as a lancing device.

The first step is to place a replacement lancet within the lancing device. Then, you would like to require a take a look at strip from the bottle and replace the cap when doing thus. Then, you have got to insert the take a look at strip in to the aldohexose meter to induce it prepared to be used. ensure that you simply make clean your hands initial by laundry it and applying disinfecting alcohol. Also, ensure that your hand is dry as water or liquid will manufacture varied result on the aldohexose reading.

Then, prick the tip of your finger with the lancing device and let blood effuse of it. Take the specified quantity of blood sample and place it on the take a look at strip. Most devices can mechanically browse the blood sugar level from the sample you provided and can manufacture leads to simply a number of seconds. Then, you would like to require disinfected cotton and press it on the realm wherever you Drew blood from.

You then ought to discard the take a look at strip properly furthermore because the used lancet. you have got to record the end in a log book so as for you to effectively monitor your blood sugar levels throughout the day effectively. this can assist you in getting ready meals furthermore as understand what reasonably activities that you simply ought to do or not do.

Diabetes may be a terribly serious sickness that contains a ton of complications once managed improperly. If youre living with polygenic disease, create certain that you understand however to manage it in order for you to live a traditional life. though theres no cure however for polygenic disease, there square measure ways in which to treat it and manage it. its conjointly necessary to frequently visit your medical practitioner so as for you to understand however youll effectively treat and manage the sickness.

If youre full of polygenic disease, a technique to manage its to require a blood sugar reading many times every day. fashion amendment is additionally necessary. By effectively watching your blood sugar levels, youll take care that managing polygenic disease are easier in your half and can permit you to measure a additional traditional life.

Keep these items in mind and youll be ready to conquer polygenic disease.

Conjugated Linoleic Acids Whats the Difference Between cis 9 11 and trans 10 12 CLA and Should We Label Them as Transfats Plus What Makes CLA Potentially Harmful

If Hayden Panettiere drinks it dairy cant be bad - despite (or because?) CLA, right? Well, what if I told you that Mrs. Panettiere was advertising milk in the "Got Milk" campaign despite being lactose intolerant?

As a SuppVersity veteran you will be familiar with the idea that trans-10, trans-12 conjugated linoleic acid is the "fat burning" CLA isomer, while 9 cis,11 trans linoleic acid appears to blunt some of the pro-inflammatory actions of its cousin and has been shown to have specific physiological effects on its own (e.g. increased bone health, cf. Platt. 2009; anti-cancer, cf. Corl. 2003).

As I already mentioned, this is probably nothing new for you, if you make sure to get your daily dose of SuppVersity wisdom everyday. What you may however not be aware of is the fact that researchers like Ye Wang and Spencer D. Proctor are - despite the never-ending hoopla around potential weight loss effects of CLA - still contemplating, whether CLA could not pose a major health threat to all or at least certain subgroups of the population and whether this should or shouldnt be reason enough to change the current food labeling practices.

Do we have to label CLA as "transfat"?

From a technical perspective the above question is obsolete. CLAs are transfats and would thus (technically, again) have to be labeled as such on the product label. From a health perspective, however, things do in fact look different. Due to the fact that the aforementioned ruminant (=naturally produced in the stomach(s) of ruminents) trans-fats have been associated with health benefits (Gebauer. 2011), we could effectively risk to scare consumers away from healthy foods if they were listed as part of the "transfat" category on the product labels.

Whats actually the reason that one the same CLA isomer that will have you lose body fat will also "inflame" you? Due to the fact that most of the research on "fat loss supplements" is conducted in sick, obese individuals, people tend to get the false impression that "fat burners" were anti-inflammatory and that anti-inflammatory agents would burn fat.

Effects of 10-trans,12 CLA on fatty acids & glucose metabolism and IL-6 gene expression in isolated fat cells in the petri dish (Hartwig. 2013)

Now, while it is correct that soothing inflammation will help the future Mr. Average Joe, who is going to be an obese (pre-)diabetic, lose weight, this has little to do with any active contribution to the oxidation of body fat. 10-trans,12 CLA, on the other hand, has been shown to block lipid storage, increase mitochondrial uncoupling (UCP-2), lower PPAR-alpha and ramp up the oxidation and release of fatty acids from the fat stores (Hartig. 2013). Unfortunately it will also block the uptake of glucose and increase the expression of the pro-inflammatory cytokine IL-6 in fat cells. So, if you took 10-trans,12 CLA at very high doses it will probably in fact keep you lean.

If you cannot handle the sudden increase in free fatty acids, pack the glucose into your liver and muscle glycogen stores and deal with the exuberant amount of inflammatory cytokines, however, it will only make you sick.

Currently, the trans-fat content on many food labels (and in legislative documents) does not include ruminant CLA isomers and Wang and Procter acknowledge that:

"As highlighted in a recent quantitative review of prospective cohort studies by Bendsen et al. dietary consumption of ruminanttrans-fat may be protective against total as well as fatal CHD events." (Wang. 2013)

The researchers do however point out that concerns about potential adverse effect on atherogenic cholesterol profiles from supplemental CLA are not unwarranted - at least if they are used by a group of persons - abdominally obese and/or insulin resistant men, for example (Riserus. 2002 a,b).

Australia and New Zealand suggest a re-evaluation

Accordingly, Australia and New Zealand (FSANZ) proposed to re-evaluate their perception regarding the exclusion of CLA from the TFA definition on nutrition labels.

If you re-evaluate something, you do not necessarily have to change them and if you go through the concise summary of results Wang and Procter present in their paper (see table 1 for an overview of the currently published meta-analyses, it does not appear necessary to question the current practice to label only industrually produced trans fats.

Table 1: Meta analysis with beneficial (green), neutral (grey) and potentially negative outcome (red); based on Wang & Proctor (2013)

As the authors point out, the inclusion of CLA in the total amount of transfats on the label would only drive people away from the consumption of whole food products. This is particularly true in view of the fact that the ill-health effects of "trans-fats" are something everyone will have heard about. The fact that these ill health effects are not to be expected from trans fats in dairy and other CLA containing whole foods, on the other hand, is still news to many costumers.

Moreover, how would you, me and everyone else who may well be aware that CLAs are not the bad guys and the "trans-fat" in grass fat butter is not going to hurt us know if the 3g of transfats in another product we buy are actually from the undisclosed amount of butter (and thus CLA) in it? It could likewise be that the producer added a little extra partially hydrogenated vegetable oil to cut the product costs and neither you nor me would know that.

Suggested read: "A Higher Intake of CLA and Vaccenic Acid from Dairy, Beef, Veal and Lamp Could Prevent Subtle Weight Gain" | read more

Only the obese have to be worried: Based on the currently available evidence the healthy and lean person (hopefully you) has absolutely no reason to avoid products with a "high" natural CLA content and thus both the pro- (trans-10,12) and (partly) anti-inflammatory (cis-9,11) form of CLA in them.

For obese and insulin resistant individuals things do however look somewhat different. A 2004 study by Risérus et al., for example, has been able to show that even the allegedly "harmless", 9 cis,11 trans linoleic acid can worsen both lipid peroxidation and insulin resistance in 25 abdominally obese men. (Risérus. 2004).

With 3g/day the dosage that was used in the Risérus study, the amount of CLA was yet much hither than the amount of CLA you can possibly ingest with nourishing foods such as butter, full-fat dairy, grass-fed beef (and beef in general, by the way). Instead of these you are thus better advised to avoid CLA supplements... but dont worry if you take another look at the data in table 1 you will have to concede that they are pretty much useless, anyway.

Reference:

• Corl BA, Barbano DM, Bauman DE, Ip C. cis-9, trans-11 CLA derived endogenously from trans-11 18:1 reduces cancer risk in rats. J Nutr. 2003 Sep;133(9):2893-900.
• Gebauer SK, Chardigny JM, Jakobsen MU, et al. Effects of ruminanttrans fatty acids on cardiovascular disease and cancer: a comprehensive review of epidemiological, clinical, and mechanistic studies.Adv Nutr. 2011; 2, 332 – 354.
• den Hartigh LJ, Han CY, Wang S, Omer M, Chait A. 10E,12Z-conjugated linoleic acid impairs adipocyte triglyceride storage by enhancing fatty acid oxidation, lipolysis, and mitochondrial reactive oxygen species. J Lipid Res. 2013 Nov;54(11):2964-2978. 
• Lenz TL & Hamilton WR. Supplemental products used for weight loss. J Am Pharm Assoc. 2004; 44,  59– 67, quiz 67– 58.
• Onakpoya IJ, Posadzki PP, Watson LK, Davies LA, Ernst E. The efficacy of long-term conjugated linoleic acid (CLA) supplementation on body composition in overweight and obese individuals: a systematic review and meta-analysis of randomized clinical trials. Eur J Nutr. 2012 Mar;51(2):127-34.
• Platt I, El-Sohemy A. Effects of 9cis,11trans and 10trans,12cis CLA on osteoclast formation and activity from human CD14+ monocytes. Lipids Health Dis. 2009 Apr 29;8:15.
• Risérus U, Arner P, Brismar K, Vessby B. Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. Diabetes Care. 2002 Sep;25(9):1516-21.
• Risérus U, Basu S, Jovinge S, Fredrikson GN, Arnlöv J, Vessby B. Supplementation with conjugated linoleic acid causes isomer-dependent oxidative stress and elevated C-reactive protein: a potential link to fatty acid-induced insulin resistance. Circulation. 2002 Oct 8;106(15):1925-9
• Salas-Salvadó J, Márquez-Sandoval F, Bulló M. Conjugated linoleic acid intake in humans: a systematic review focusing on its effect on body composition, glucose, and lipid metabolism. Crit Rev Food Sci Nutr. 2006;46(6):479-88. Review.
• Schoeller DA, Watras AC, Whigham LD. A meta-analysis of the effects of conjugated linoleic acid on fat-free mass in humans. Appl Physiol Nutr Metab. 2009 Oct;34(5):975-8.
• Tricon S, Yaqoob P. Conjugated linoleic acid and human health: a critical evaluation of the evidence. Curr Opin Clin Nutr Metab Care. 2006 Mar;9(2):105-10. Review.
• Whigham LD, Watras AC, Schoeller DA. Efficacy of conjugated linoleic acid for reducing fat mass: a meta-analysis in humans. Am J Clin Nutr. 2007 May;85(5):1203-11.

Fish Oil Oleic Acid Counter Each Others Beneficial Health Effects MUFAs Improve Cholesterol Glucose Metabolism Fish Oil Lowers Triglycerides But Only On Their Own!

Oleic acid and fish oil dont mix.

Everybody is still talking about the omega-3 to omega-6 ratio, but SuppVersity readers are, as always, one step ahead and will (as of now) closely eye-ball their omega-3 to MUFA or precisely their DHA + EPA vs. oleic acid ratio, as well.

In a recent study, Sani Hlais and his colleagues from the Department of Nutrition and Food Sciences at the American University in Beirut, Lebanon, analyzed the effects of 12 weeks of differently dosed fish and/or high-oleic acid sunflower oil (OSO) supplementation in 98 healthy subjects (18–35 not on meds and supplement abstinent; Hlais. 2013)

"Hold on!? Healthy sunflower oil?"

I know, the current dogma is: "There is no oil beside fish and coconut oil... well maybe virgin olive oil." But just as the term "dogma" implies this is just a deeply ingrained pattern - no universal truth. The statistically significant reductions of total and LDL cholesterol in the OSO group (8g/day; 6.5g oleic acid content), which was absent in the fish oil (2g/day) group would be one of those effects that contradict this dogma. And as it turns out - the effects probably will not even even manifest themselves in those of you who apply the "better I take any supplement on earth, to make sure I dont miss something", when you stand in front of the virtual or real shelves of supplement vendors.

Figure 1: Changes in total, LDL, HDL cholesterol and triglycerides (in mg/dL; Hlais. 2013)

Allegedly, the fish oil (49.5 % PA, 19.6 % DHA), which was just as the the high oleic acid sunflower oil (81.6 % oleic acid) provided in capsules, had its own advantages, but if you take a closer look, you will see the same hitherto not fully "paradigmatized" pattern arise: Take both and negate the effects of one.

Figure 2: Changes in BMI, fasting glucose and insulin over the 12-week study period (Hlais. 2013)

And no, this is not just about trigs and cholesterol, it also happens for body weight, glucose and insulin, where the "happy medium" of 2g fish oil + 8g oleic acid is not as "happy", let alone "golden" as one may think. Or, to express that in the words of the scientists:

Trigs or phospholipids whats in your fish oil caps + why does it matter? (learn more)

"In conclusion, glycemic and blood pressure parameters were not affected by the different supplements. Intake of fish oil (2 g/day) was found to reduce TAG by about 13 % and not to affect other lipid parameters. Intake of oleic acid (6.5 g/day) was found to reduce both total and LDL cholesterol by about 10 %. These effects seem to be diminished when using a combination of the two oils (n-3 and n-9), which may be attributed to a competition in the metabolism of the two fatty acids." (Hlais. 2013)

For omega-3 vs. omega-6 we already know that the conversion of the short chain omega-3 fatty acid ALA to its long-chain brethren EPA and DHA is hampered by high intakes of linoleic acid (LA: short chain omega-6), because they require the same enzymes needed for the generation of arachidonic acid (ARA) from LA. The "competition" the scientists suspect to be working here is instead probably on a cellular or receptor level. Well, I guess future studies are going to elucidate that in more detail... right?

---

Supercharged Phenol-Enriched Virgin Olive Oil - would it be worth the extra-money (learn more)?

So what can we learn from these results? "If you want everything, you rarely get anything..." well, I guess that is a bit platitudinous. Rather, the results from the study at hand complicate the already overtly complex interplay between different forms and quantities of fatty acids in our diet. The magic really is in the ratios and while I cannot tell you what the most beneficial ratios are, I can tell you that everybody telling you they know exactly how your and everyone elses optimal omega-3-to-6-to-9-ratio looks like is a quack - you can take my word on that.

References:

• Hlais S, El-Bistami D, El Rahi B, Mattar MA, Obeid OA. Combined Fish Oil and High Oleic Sunflower Oil Supplements Neutralize their Individual Effects on the Lipid Profile of Healthy Men. Lipids. 2013 Jul 26.

Causes of Breast Pain in Women

WOMEN are often worried when their breast pain and pain, fear as a sign of breast cancer. However, pain is not necessarily a sign of breast cancer.

Pain or pain in the breast does make a woman feel uncomfortable. The following are some of the causes of pain or pain in the breast as reported by Boldsky.

Water Retention

There are some women who experience pain in the breast due to water retention, and it has nothing to do with the menstrual cycle. Many observations have been made by researchers to determine whether the pain is caused due to environmental factors or nutrients. However, no clear evidence was found regarding the cause.

Fibrocystic Breast

More than half of women will experience fibrocystic breast changes in some parts of the breast, and one of the main causes of breast pain. Very normal indeed experiencing fibrocystic breasts, but they cause pain on the outside of the breast and chest. Take care of yourself to ease the pain.

Breast Cysts

Cysts in the breast can make you feel like a small lump or containing dangerous liquids. Breast cysts are considered benign are the most common problem among women before menopause, and usually occurs between the ages of 35 and 40 years. Meanwhile, for some people, breast cysts can be uncomfortable and painful.

Costochondritis

This is the type of inflammation of the junction of the ribs to the breastbone. Costochondritis causes less pain at around the sternum and ribs. In addition, the pain can range from mild to extremely painful.

Hormonal changes

Some women worry when experiencing pain in their breasts, yet they may be normal and anxiety caused due to hormonal changes. Several types of hormonal changes is menopause, menstruation, and premenstrual syndrome, pregnancy and puberty.