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| Gram negative bacteria, as these E. coli bacteria which have been photographed with a low-temperature electron micrograph (magn. x10,000) tend to produce endotoxins in your gut, while gram positive bacteria tend to produce exotoxins on your food - nasty, ha? |
It has been estimated that a single cell of
Escherichia coli contains approximately 106
Lipid A or endotoxin molecules with a mass of about 1
00,000 Da (the exact mass varies according to the LPS type). The typical
human intestinal tract can harbor approximately one gram of endotoxin, which is ~2-4x more than what scientists used in previous rodent studies as a "lethal dose" (Kawai. 1991). Aside from the information about the lethal dose of endotoxins in rodents, these figures, which are at the same time the
SuppVersity figures of the week are part of the study by Mani et al. with which we are going to kick off this week's installment of
On Short Notice. I guess these figures give you an idea of the toxic potential within your gut and why all the hoopla about leaky guts, the human microbiome, pro- and prebiotics, endotoxemia and co. is probably not all hype, but a hitherto largely neglected aspect of human health (and disease)
Saturated fat < > gut interaction sheds a dark shadow on the "benign fat of our ancestors"
(Mani. 2013) -- According to a study from the
University of Iowa, the endotoxemia response to a meal, i.e. the amount of inflammatory innately produced toxins from your gut that enter circulation in the postprandial phase, is increased in response to a meal that's high in saturated fat.
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| Figure 1: Endotoxin permeablity and changes in serum endotoxin levels in the hours subsequent to the ingestion of a test meal containing either 50ml coconut (CO), vegetable (VO) and fish oil (FO) in otherwise healthy pigs (Mani. 2013). |
The scientists also found that omega-3 fatty acids from fish and cod
liver oil reduced the amount of endotoxins hitting the blood stream and
that olive, as well as vegetable oils exhibited a neutral effect. As the data in
figure 1 (left) goes to show you, the underlying mechanism behind the saturated fat induced influx of toxins was a whopping +60% increase in the endotoxin permeability (Papp) of the guts of the 24 pigs on which the experiments have been conducted.
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| Click here to read more about a previous study that shed some light on the effects of certain nutrients on the gut microbiome. |
Now you can certainly argue that the ground corn-soybean meal dough that was at the base of the test-meal was "the devil" here, but let's be honest, for the average Jane and Joe, there are similar "devils" in any standard meal, they consume, so that the finding that the addition of 50 ml fish oil (FO), vegetable oil (VO) or coconut oil (CO) made such a difference in terms of the influx of pro-inflammatory endotoxins is nothing you can simply ignore. The same goes for the fact these effects occurred in response to the ingestion of
organic coconut oil (according to the researchers purchased from Spectrum Naturals Inc.), is actually somewhat unsettling and certainly not in line with some of the previously established benefits of coconut oil consumption, such as it's waist reducing effects in overweight subjects (
click here to learn more).
What's also interesting is that previous rodent studies yielded different results. Laugerette et al., for example, found a similar increase as Mani et al. in mice, but in response to canola and sunflower oil (Laugerette. 2012). This raises the question in how far the effects may be mediated by the baseline diet and the corresponding bacterial composition of the small and large intestine (or species specific effects?). After all, the gram negative bacteria of which scientists believe that they increase in response to high fat diets have the highest endotoxin content. They populate the distal ileum and the colon and are supposedly the main sources for circulating endotoxin (Berg. 1999) - if you had less of them to begin with, you are not as likely to suffer from an acute influx of endotoxins in response to the ingestion of SFAs. Moreover, what it the endotoxins were released in response to the antimicrobial effects of coconut oil?
Update: Wyatt Brown left an
interesting comment on this issue on the
SuppVersity facebook wall, I do not want to deny anyone, so I thought I'd just update the post with it:
I'm glad people are talking about the endotoxemia thing, that's what we do at SuppVersity, have the discussions nobody else does! I think it's important to recognize that, especially for the paleo/ancestral types who accuse grains of inducing intestinal permeability and then go and eat diets that cause intestinal permeability...and because endotoxemia is bad...
But I don't think that all is lost, the evolutionary argument may just need to be modified a little. The current paradigm involves looking at individual foods, or worse yet (though that was supposed to be an improvement) broad classes of macronutrients, and our adaptation to them. Well, it looks like those might have been wrong in some ways, maybe we aren't fully adapted to some foods, but then again maybe we are adapted to a particular kind of diet that makes those foods all right.
Some of the antioxidants in orange juice prevent intestinal permeability from dietary fats it seems the bile acids secreted during digestion are to blame, and it's an oxidative mechanism, so the orange juice prevents this (Ghanim. 2010). It also works with grape polyphenols (Ghanim. 2011).
Moreover, it seems that feeding mice a diet rich in fermentable fibers prevents endotoxemia - maybe due to butyrate production and its protective effects on intestinal cells (Cani. 2007). And acutely, fiber with a high fat meal also prevents the effect (Ghanim. 2012). It's probably due its ability to sequester excess bile acids (Vahouny. 1980)
So it would appear that we are adapted to a diet containing those fats but also containing fruit and fiber.
As you see, Wyatt makes a pretty valid point, when he hints at other contributing factors of which I know that they got forgotten way too often in the paradigmatic and downright stupid and unproductive high fat vs. low fat and the SFA vs. PUFA skirmishes on the Internet.
I guess, there is still much to learn here and I hope you are aware that the
SuppVersity is the place you can do just that:
Learn something new everyday!
Caffeine's effect on muscular fatigability during maximal vs. supramaximal stimulation
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| There is no question that caffeine can have beneficial effects on exercise performance - whether every athlete benefits to a similar degree is yet as questionable as the "ideal" dosage to elicit optimal fat loss effects without the negative side effects that are associated with the chronic overconsumption of any type of stimulant (click here to learn more about the narrow margin between "just enough" and "already too much") |
(Tallis. 2013) -- In a very straight forward in vitro experiment, researchers from the
Coventry University in the UK found that the ergogenic effects of caffeine depend on the intensity of the muscular contractions. When the scientists exposed isolated soleus muscles to up to 70µM of caffeine (that's still within what you would consider a "physiological dosis"), Tallis et al. observed that the muscular endurance increased only, when the muscles were challenged at submaximal intensities (+19.2%), while it decreased by 17.6% upon maximal challenge.
Whether or not this is important for the average strength trainee remains questionable. After all the "endurance" part of your regimen is usually conducted at submaximal intensities and weheter you can do one interval more or less probably doesn't matter as well. For a professional cyclist participating in a time trial, those 17.6% may well make the difference between victory and defeat. On the other hand, there is more to "endurance" than local muscular fatique, so that caffeines effects on the central nervous system will at least ameliorate, if not totally counter these potential downsides.
Lactoferrin, an overlooked visceral fat annihilator?
I don't even know if all of you are familiar with the globular glycoprotein lactoferrin that is widely represented in various secretory fluids, saliva, tears, nasal secretions and - above all - colostrum. It has a very important role in the immune defenses of your body and according to a recent review by Japanese scientists, it does also exert direct lipolytic (breakdown and release of fat from) and anti-adipogenic effects in vitro and in vivo.
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| All of you who read the "Ask Dr. Andro" installment on Milk & Colostrum should at least have heard of lactoferrin before. It's one of the anti-microbial, anti-fungal and immune modulating molecules in the white elixir of mammalian life that's also suppose to exert antagonist effects on the opioid receptors (read more). |
A hitherto still unsolved problem is the delivery of the lactoferrin to the target tissue, but with the advent of specifically enteric coated lactoferrin which circumvents the breakdown of the 80kDa protein in the acidic milieu of the stomach and allows its passage via the lymphatic system into the mesenteric (visceral) fat pad, where it accumulates, interacts with the lactoferrin receptor LRP1 which is directly located on the adipocytes of the visceral adipocytes and suppresses the expression of PPARγ reduces the expression of perilipin and thus shuts down lipogenesis and increases lipolysis in existing adipocytes. Accordingly, respective supplements
could in fact become "a highly safe and a promising dietary supplement" that has in addition to its already well-known beneficial effects on the immune system the ability the potential to "be used to promote human health globally" (Ono. 2012). But let's be honest, haven't we heard claims like that before?
Perceived recovery 48h after a workout correlates with free testosterone levels
(Sikorski. 2013) -- Yeah, I know the whole free testosterone after a workout discussion is pathetic,
but what about free testosterone levels 48h hours after the workout, i.e. amidst the hot recovery phase? According to a soon to be published study in the
Journal of Strength and Conditioning Research a standardized test to elicit the perceived recovery (PRS) appears to be surprisingly accurate to predict the drop in free testosterone after a session of high volume resistance training designed to elicit a large amount of fatigue and muscle damage.
"All subjects participated in a high volume resistance training session consisting of 3 sets of 10-12 repetition maximum loads for each of the following exercises: full squats, bench press, deadlifts, pullups, bent over rows, dips, shoulder press, barbell curls and triceps extensions. Rest periods were 1 minute between sets, and 2 minutes between exercises." (Sikorski. 2013)
The scientists from the
University of Tampa recruited 35 highly resistance-trained subjects (aged 21.3 ± 1.9 years) with an average squat, bench press, and deadlift of 1.7± 0.2, 1.38 ± 1.9 and 2.07 ± 2.7 times their bodyweight for their study. The subjects had a minimum experience of 3 years of resistance training and were thus probably way more capable to access their own recovery status than the average Jane or Joe after with a dozen of irregular workouts under her / his belt. Blood analyses, soreness and PRS tests were conducted at before, immediately after and 48h after the workout (total weight lifted in the training session was 16,353 ± 3,691.8 kg) and revealed ...
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| Read more about the hormonal effects of different workout styles in this previous SuppVersity post |
- a significant increases in leg, chest and arm soreness from pre to post exercise,
- a significant increases in creatine kinase (CK; measure of muscle damage) from 189.4 ± 100.2 to 512 ± 222.7 U/L (p < 0.05),
- no changes in cortisol, testosterone, and free testosterone from pre to immediately post workout,
- a significant moderate, and inverse relationship between leg soreness and PRS scores and low, inverse relationships between chest and arm soreness and PRS scores,
- a significant, moderate inverse relationship between CK and PRS
yet only when the CK values peaked 48h after the workout, however, the aforementioned "low, direct relationship with PRS" (Sikorski. 2013) was observed. As the researchers point out this result could be
"[...] important for those individuals that have neither the resources (time, monetary or otherwise) nor the expertise to draw blood and perform chemical assays to determine recovery status and or muscle damage. [...] This, in the bigger picture, may help appropriately design periodization plans designed aimed at functional overreaching and ensure proper overload. Moreover, and perhaps more importantly, the ability to indicate level of recovery following heavy resistance training expeditiously and accurately may be a critically important step in prevention of overtraining." (Sikorski. 2013)
The scientists do yet also emphasize that "future work is needed addressing other variable influencing recovery and long-term studies investigating the usefulness of the PRS in training" before a more general recommendation can be issued.
That's it for today folks. As usual there are a couple of interesting
facebook posts for you to check out and discuss
- Upping your vitamin D levels does nothing to reduce knee pain or cartilage loss in patients with symptomatic
knee ostearthritis (read more)
- "The one-two punch", retinoic acid suppresses obesity by both promoting energy expenditure and by inhibiting adipogenesis (read more)
- More evidence of intrauterine dietary priming: Low protein in the womb + high caloric diet afterwards => insulin resistance (read more)
and obviously, you are invited to post your thoughts or questions on any of today's items in the comment area of this post.Aside from that, I wish all of you an exciting weekend ;-)
References:
- Berg RD. Bacterial translocation from the gastrointestinal tract. Adv Exp Med Biol 1999, 473:11–30.
- Cani PD, Neyrinck AM, Fava F, Knauf C, Burcelin RG, Tuohy KM, Gibson GR,
Delzenne NM. Selective increases of bifidobacteria in gut microflora improve
high-fat-diet-induced diabetes in mice through a mechanism associated with
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- Laugerette F, Furet JP, Debard C, Daira P, Loizon E, Geloen A, Soulage CO, Simonet C, Lefils-Lacourtablaise J, Bernoud-Hubac N. Oil composition of high-fat diet affects metabolic inflammation differently in connection with endotoxin receptors in mice. Am J Physiol Endocrinol Metab. 2012;302:E374–386.
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- Ono T, Morishita S, Murakoshi M. Novel function of bovine lactoferin in lipid metabolism: Visceral fat reduction by enteric-coated lactoferrin. Pharma Nutrition. 2012 [accepted manuscript]
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Naimo MA, Averbuch B, Gilchrist P. Changes in Perceived Recovery Status Scale
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