Aluminum More of a Threat Than Thought? German "Feds" Say: Stay Away From Antitranspirants and Beware of the Dozen of Other Aluminum Containing Junk in Your Life

Cancer, Alzheimer's - The X* effect?
*Most deodorants don't contain aluminum.

I have to admit that I missed the original publication of the inconspicious statement of the Bundesintitut für Risikobewertung (BfR. 2014). I am not sure if there is a US or UK equivalent to the BfR, but if there was an US counterpart, those would be the guys that would tell the FDA what they should do, if the industry, the FDA is actually supposed to control had not already taken their job ;-)

All (sadly true) jokes aside, basically the short paper is a re-evaluation of the safety of aluminum - not aluminum in general, but the amount of aluminum in our immediate surrounding. Sources like the particularly nasty Aluminum from antitranspirants

Table 1: Overview of the "worst offenders" among foods and bakery products scientists from the University of Kentucky (Saiyed. 2005)

Processed foods provide the toxic baseline: Antitranspirants are part of the problem, but as usual it's processed food that supplies the baseline of yet another hazardous substance. If you take a look at the list of "worst offenders" Saiyed et al. identified in a 2005 study in a random selection of food from US supermarkets, it's obvious that all of them belong to the processed, convenient or as some of the enlightened people would say "junk" food category.

The BfR assessed the aluminum absorption from antitranspirants based on experimental data on the its dermal obsorption in healthy individuals and found that the systemic absorption for people with intact skin health is 10.5µg. That's ~2µg more than the EFSA says, the contemporary available evidence would suggest to be safe for a healthy 60kg human being.

This means that the uptake of aluminium from antitranspirants is above the maximal tolerable daily exposure levels. For people with skin problems or someone who uses the antitranspirants after damaging the protective layer of the skin while shaving the systemic aluminum uptake is several magnitudes larger. Consequently someone who shaves and applies his antitranspirant afterwards may exceed his total weekly limit (1mg per week) within the first hour of the day!

Figure 1: Tabular overview of the risk profile the BfR released for aluminum containing transpirants; I have translated the relevant parts of the overview, if you want to, you can download the original here.

As the scientists point out, antitranspirants are yet by far not the only potential aluminum sources in our life. Foods like tomatoes, kitchenware and - above all - other cosmetic products like shampoo, lipsticks, cremes (esp. anti-wrinkle and -aging - funny, eh?), toothpaste, and sunscreen all contain significant amounts of aluminum that can make it through our skin or digestive tract right into our blood.

It is thus no wonder that the following tabular overview (I deliberately use the German original) with translated captions) informs us that it is well possible that the aluminum in antitransparent is a health-hazard for the general population. Luckily, "keine unmittelbare Beeinträchtigung" means that you do not have to expect immediate serious adverse health effects - great, ha?

Much ado about nothing and all is good, right?

In view of the fact that the significance of the currently available data is also still insufficient, one could thus assume that you would be overreacting if you threw your aluminum containing antitranspirants away. If you take a closer look at the last row in tabular overview in Figure 1, though, you see the words "kontrollierbar durch Vorsichtsmaßnahmen" = "manageable by safety measures", though. Now what kind of safety measures could you possibly take?

Figure 2: Auluminum has been linked to all sorts of pathologies. The only decently convincing does yet exist for breast cancer (mechanism | left; cf. Darbre. 2013) and Alzheimer's where the negative effect on cognitive abilities has even been confirmed in controlled animal studies (right | exposure to increasing amounts of aluminum leads to corresponding increases in the rates of cognitive decline; cf. Walton. 2013)

Personally I know only two, though: Never apply aluminum-containing antitranspirants to damaged skin parts - A rule that applies for freshly shaved skin, as well! Or, even better stop using aluminum containing antitranspirants altogether.  I know that this is not feasible for some people, but many of us are just so used to it that we do not realize that the stench from puberty is no longer around.

In the end, the message of the statement that provides additional information about the potential involvement of chronic aluminum exposure in the etiology of breast cancer and Alzheimer's, as well as the more recent publication of a similar warning about aluminum containing cometics in general (BfR. 2014) would yet still suggest that you better replace the shampoo, creme, tooth paste, lipstick, sunscreen and antitranspirant of your choice, if they contain aluminum.

What the wise FDA says: It's funny, that the FDA documents say about thee "GRAS" additives, i.e. substances that are generally recognized as safe, such as the aluminum based food additives that "ingested in excessive amounts, their [sic!] appears to be associated with interference in phosphorus metabolism resulting in rachitic or osteomalacic effects, kidney damage, and interference with glucose metabolism, apparently due to interference with phospho- rylating enzymes." Now, this is obviously no reason to be concerned, because "[t]he high intake of phosphorus in the American diet may provide a protective effects"... hmm, great! So the high amount of phosphor of which scientists long say that it's making people sick "protects" you, my American friend from something the FDA is supposed to protect you from - glorious!

Bottom line: Start with the cosmetics! Unlike the aluminum that leaches into the food from its packaging, the aluminum that makes it from the soil into conventional and organic produce, the aluminum that makes it from the feed into the animals and animal products you eat and the good damn aluminum the f*** up "food" industry adds to their products in form of colorings E 173, stabilizers E 520 (aluminum-sulfate), E 521 (aluminum-sodiumsulfate), E 522 (aluminum-potassiumsulfate), E 523 (aluminum-ammoniumsulfate) and as the leavening agent 541 (acid sodium-aluminumphosphate) in all sorts of baked goods, the "alu lipsticks" are comparatively easy to avoid - to find alternatives that last for a similarly long time and survive kissing and making out, on the other hand, is not going to be easy, I suppose.

If you are no "processed junk junky", ditching antitranspirant & co you cut your intake back to a tolerable 14–35 mg aluminum per week - at least this is what the EFSA estimates a 70kg human being will be exposed to withing 7 days. With a limit of max. 70 mg, you would thus reside in a "green zone" of which no one probably knows how "green" it actually is... in view of an estimated half-life of seven years (Yokel. 1989), I could understand, though, if you say that this is not 100% comforting.

Reference:

• BFR. "Aluminiumhaltige Antitranspirantien tragen zur Aufnahme von Aluminium bei" Position Statement 007/2014 issued by the BFR on February 26, 2014.
• BFR. "Fragen und Antworten zu Aluminium in Lebensmitteln und verbrauchernahen Produkten" FAQ issued by the BFR on February 26, 2014.
• BFR. "Fragen und Antworten zur Risikobewertung von kosmetischen Mitteln" Updated FAQ  issued by the BFR on March 3, 2014.
• Cashman, Allison L., and Erin M. Warshaw. "Parabens: a review of epidemiology, structure, allergenicity, and hormonal properties." Dermatitis 16.2 (2005): 57-66.
• Darbre, Philippa D., Ferdinando Mannello, and Christopher Exley. "Aluminium and breast cancer: Sources of exposure, tissue measurements and mechanisms of toxicological actions on breast biology." Journal of inorganic biochemistry 128 (2013): 257-261.
• FDA. "Aluminum hydroxide." SCOGS-Report 43 (1975). ID Code: 21645-51-2. CFR Section: 184.1139
• Walton, J. R. "Aluminum’s Involvement in the Progression of Alzheimer’s Disease." Journal of Alzheimer’s Disease 35 (2013): 875.
• Yokel, Robert A., and Patrick J. McNamara. "Elevated aluminum persists in serum and tissues of rabbits after a six-hour infusion." Toxicology and applied pharmacology 99.1 (1989): 133-138.

Detrimental Effects of Aerobic & High Oxygen Packaging on Meat Quality: 2x Higher Lipid & Cholesterol Oxidation, Less Tender, More Drip Loss, Less Juicy... but More Convenient!

Rosy, but rusty: "Fresh" meat packaged with 70% oxygen.

I don't know about the US, but most of the "fresh" meat, you buy at the Supermarket here in Germany is packaged in what the label calls a "Schutzatmosphäre". Literally translated this means nothing but a "protective atmosphere" and it refers to the supposedly bacteria-free high oxygen air that's pumped into the airtight packaging in which the chicken breasts and beef steaks, the pork and lamb and all the other appetizingly looking meats are stored for up to a week in the fridges of the meat counter.

Good to now it's protected! Right?

If you ever bought a product like that you will have realized that you can easily store it for the whole 7day+ period in you fridge and - as long as the airtight plastic container is not broken - it will look and smell almost as it did on day one, when you rip the container open and take a closer look, whether the meat you are about to prepare is still good to eat; Looking good!

What you cannot see though, is that the "protective atmosphere" protects, may have protected the looks of the meat, but not its nutritional quality. 

I mean think about it: What happens when you put metal into a wet high oxygen environment? Right! It starts to oxidize. Now guess what has happened to your appetizing piece of chicken, beef, pork or lamb while it was (highly conveniently, obviously) waiting for you in your fridge. Right it began to rust.

Figure 1: Content of cholesterol oxidation products (COPs) in non-irradiated raw chicken/turkey leg and raw beef with packaging, and storage time; data expressed relative to baseline (Nam. 2001)

As the data in figure 1 goes to show aerobic packaging (this is not yet a high oxygen environment) accelerates the rate of lipid and protein oxidation, so that the content of potentially hazardous cholesterol oxidation products (COPs) in your turkey legs, raw beef on day 7 is anywhere between 20-100% higher than on day one.

"Although the packaging conditions of meat during storage were critical for the oxidation of cholesterol in raw meat, irradiation synergistically increased it." (Nam. 2001)

And as Nam et al. point out this effect is even more pronounced if the meat has been irridated before packaging. The vacuum packaging, most producers and vendors are reluctant to use, because the meat does not look anywhere as fresh as the one that's packaged with highly oxygenated air (in fact it's the oxidized oxyhaemoglobin MbO2 that's responsible for the rosy color, cf. Rennere. 1999), on the other hand, "was enough to protect cholesterol and fatty acids from oxidation regardless of irradiation dose." (Nam. 2001)

Red deception in the "fresh" food corner

Figure 2: T-bar levels (a marker of lipid oxidation) in air, high oxygen and vacuum packaged pork during refrigeration for 0-20 days (Cayuela. 2004)

Now, with normal air, the nice red color will at some time give way to a brownish one, with extra high oxygen air that's used in high oxygen packaging, it will prevail, but at the same time,

"[t]he use of modified atmospheres with a high oxygen concentration (70%) act[s] as a pro-oxidation factor both for fatty acids and for cholesterol (an increase of 86.4% on the initial COPS content)." (Cayuela. 2004)

And that's a plus of almost 90% on top of what you would see with "regular" air packaging, as it was used in the Nam study.

Ah, and did I mention that this "meat" will also be less tender, less juicy and will have a 4-6x higher drip loss than "regular" packaged meat, when it's stored at 4°C for several days (Lund. 2004).

---

Vacuum + Irridation = Plastimeat 2.0 According to a 2012 paper the phtalate DEHP content of vacuumed meats increases "dramatically" by 2.55, 2.75, 2.18 and 2.16 times in comparison to that in control samples having a fat content of 10%, 20%, 30% and 40%, respectively, when it is exposed to 20 h of UV irradiation at an intensity 900µW/cm² (Zhang. 2012).

Bottom line: As inconvenient as it may sound, the lipid and cholesterol oxidation meat undergoes, when it is packaged surrounded by a "protective atmosphere" of highly oxygenated air is just another example of how our urge for "convenience" and immediate 365 x 24/7 availability of whatever we want to eat can contribute to the overall burden of dietary-related diseases.

Don't get me wrong, you certainly won't die when you eat meat from the supermarket and still - the oxidized fats and cholesterol from the gas packaged meats from the supermarket are another on its own probably negligible piece to the puzzle that holds the answer to the complex question why we are fat and sick. One thing appears to be relatively certain, though, the terms "convenience" and "revenue" relate to almost every item on the never ending list of causative and confounding factors of the obesity epidemic in one or the other way.

References:

• Cayuela JM, Gil MD, Bañón S, Garrido MD. Effect of vacuum and modified atmosphere packaging on the quality of pork loin. European Food Research and Technology. 2004; 219(4), 316-320.
• Lund MN, Lametsch R, Hviid MS, Jensen ON, Skibsted LH. High-oxygen packaging atmosphere influences protein oxidation and tenderness of porcine longissimus dorsi during chill storage. Meat Sci. 2007 Nov;77(3):295-303. 
• Nam KC, Du M, Jo C, Ahn DU. Cholesterol oxidation products in irradiated raw meat with different packaging and storage time. Meat Sci. 2001 Aug;58(4):431-5.
• Rennere, M. Factors involved in the discoloration of beef meat. International Journal of Food Science & Technology. 1990; 25: 613–630.
• Zhang SL. Effect of UV Irradiation on the Migration of DEHP from Food-Grade PVC Film into Packaged Ground Meat . Advanced Materials Research. 2012; 601(94).

Mono-Sodium Glutamate (MSG), NAFLD, Leptin Resistance, Trans-Fats, HFCS, Gluttony, Leaky Gut & Brain, the Vagus Nerve and the Chinese Restaurant Syndrome - Bon Appetit!

Image 1 (msg-exposed.com): Is obesity the inevitable, unnatural metabolic long-term equivalent of the dreaded "Chinese Restaurant Syndrome"?

Earlier today, I posted a blurb from a recently published epidemiological study on the effects of mono-sodium glutamate, aka MSG, an umami = all taste receptor activator that is commonly found in all sorts of ready made foods that would otherwise taste as lame as their individual fake ingredients, on the SuppVersity facebook wall (Insawang . 2012). The scientists had evaluated the data from 324 families (349 adult subjects, age 35–55 years) from a rural area of Thailand and found that the prevalence of metabolic syndrome was not just significantly higher in the tertile with the highest MSG intake, but that the "odds ratio", i.e. the chance that a certain parameter, in this case "obese, yes/no" would be found to be true, increased with every 1 g increase in total MSG intake irrespective of  the total energy intake and the level of physical activity.It took roughly 2 minutes for the first sharp-witted "SuppVersity student", in this case that was Wyatt Brown, to spot that post and ask what I believed could explain this observation.

Honestly, I had not really thought about that before, but simply assumed that the effects were probably mediated via not yet fully elucidated effects of dietary glutamate on the balance of excitatory and inhibitory neurotransmitters... after thinking about that for a moment I realized that in the absence of hyperphagia (i.e. extreme hunger and subsequently higher caloric intake), which was obviously not the case for the obese Thais with high MSG intakes, this explanation was not really satisfactory.

Does it all come back to food quality once again?

My next thought was that this could yet again be an issue of food quality vs. food quantity. After all, junk food and all sorts of foodstuff that's made with tons of food-additives to disguise their inferior, nutrient-poor and thus "tasteless" ingredients are the most likely candidates with respect to the MSG exposure in the Western and Eastern "developed" *rofl* world are concerned. In view of the fact that "diet quality" was (as so often) not among the variables Insawang et al. had assessed, their study did not allow for any conclusions in this respect, so that I had to dig deeper and came up with a couple of interesting findings,  I did not want to hold back from me (sorry, Stephen, for postponing the "HIIT Manual"-post, once again, but think about it like that, what's the use of working out if your MSG intake would quash your results anyway ;-)

• * See figure 2 for exact data on the average daily human intake of MSG - with 91mg MSG /kg body weight, an amount that would translate to a daily intake of ~500+mg MSG in humans, the mice in the Collison were representative of the average American, yet not the Thai, Japanese and Korean MSG intake; against that background it is  important to note that MSG ingestion alone did not result in microscopic fat deposits in the liver. These effects were exclusively observed upon co-ingestion of the MSG with a diet with ~9% TFA content!
  "MSG intake at doses similar to human average daily intake[*] caused hepatic microsteatosis and the expression of beta-oxidative genes." - in a 2009 study, Collison confirmed the negative effects of even moderate MSG intake on liver health in a rodent model; only the common combination of trans-fatty acids (TFA) + MSG that is one of the main characteristics of modern "convenience" foods, did yet induce statistically significant increases in liver weight and hepatic triglyceride content; the increases in total, but also HDL cholesterol due to MSG + TFA were accompanied by profound increases in circulating leptin levels, probably in response to developing leptin resistance and increased storage of lipids in the white adipose tissue stores of the nine-week old C57BL/6J mice (Collison. 2009); in a follow up study Collison et al. confirmed that the double-whammy of trans-fatty acids + MSG becomes even more toxic if a third villain is added to the mixture, high fructose corn syrup (Collison. 2011) - and I don't have to tell you where in the human food chain you will find this unholy trinity, do I?
• "MSG ingestion reduces weight gain, body fat mass, and plasma leptin levels" - in a 2008 trial Kondoh and Torii observed a very different and in fact surprisingly pronounced beneficial effect of the ingestion of a 1% solution (in biology this means 1g per 100ml) MSG resulted in decreases in weight gain, body fat mass and plasma leptin levels in male Sprague-Dawley rats irrespective of the energy content of their diets (!) and without effecting total energy intake or food intake, but in the presence of a profound decrease in 24h-water intake (2g vs. 9g); these effects were observed in both adult and young animals, in the latter without any negative side effects on the normal development of body length

  

  Figure 1: Leptin levels (ng/ml) on diets with different energy density and macronturient composition with or without MSG added to the water (data based on Kondoh. 2008)

  this leaves more than enough room to speculate about centrally mediated increases in energy expenditure in response to the ~20mg total MSG (equivalent to 33mg/kg for a rodent and a human equivalent dose of ~5.5mg/kg) intake of which Kondoh and Torii speculate that they may be "mediated via gut [glutamate] receptors functionally linked to the afferent branches of the vagus." (Kondoh. 2008); subsequent studies into the effects of MSG on the "gut brain axis" appear to support this hypothesis (cf. Kondoh. 2009a,b; Otsubo. 2011)
• " MSG, in spite of mild hypophagia [reduced food intake], caused severe increase in fat body weight ratio, via leptin resistance" - in 2011 Afifi and Abbas, two researchers from the Department of Biochemistry at the Zagazig University in Egypt, report that feeding high amounts of MSG to pregnant rat dams had similar negative effects on body composition and leptin sensitivity as a hypercaloric diet and that despite an overall reduction in total food intake; moreover, despite similar gains in body fat, the negative effects on the offspring of those pregnant rats was more pronounced than in the rats on the "normal" hypercaloric diet (Afifi. 2011)
• If you suffer from "Chinese Restaurant Syndrome", you should check whether increased gastrointestinal permeability could be the root cause of your problems and avoid all foods with any of the following "ingredients": E620 Glutamic acid, E621 Mono-sodium glutamate, E622 Mono-potassium glutamate, E623 Calcium diglutamate, E624 Mono-ammonium glutamate, E625 Magnesium diglutamate!
  "Findings from the literature indicate that there is no consistent evidence to suggest that individuals may be uniquely sensitive to MSG" - in one of the few reviews evaluating exclusively human studies, Freeman did not find any placebo controlled research that would confirm the universal existence of side-effects (e.g. headaches, chest pain, flushing, numbness or burning in or around the mouth, sense of facial pressure or swelling and sweating) as a direct consequence of the consumption of food-borne mono-sodium glutamate; e.g.
  

  "The present study led to the conclusion that 'Chinese Restaurant Syndrome' is an anecdote applied to a variety of postprandial illnesses; rigorous and realistic scientific evidence linking the syndrome to MSG could not be found." (Tarasov. 1993)

  instead, the author suggests that "unique sensitivities" could explain the documented case reports (Freeman. 2008 // see also Walker. 2000; Geha. 2000); given the emerging evidence of the existence of something you could call a "leaky brain" (in analogy to "leaky gut"), it appears likely that an unnaturally increased permeability of the blood-brain-barrier and subsequent penetration of large amounts of glutamate into the brain even at lower serum concentrations could well explain those differences (although not directly related to MSG, I would still like to point you to the results of a recently released study, which found a profound decrease in the permeability of the BBB in response to an oral 1mg/kg (HED ~0.16mg/kg) Lycium barbarum extract in an experimental stroke model; Yang. 2012)
• "dietary antioxidants have protective potential against oxidative stress induced by MSG" - in 2006 Faromby and Onyema observed that previously described oxidative damage to the liver and subsequent steatosis (lipid accumulation) in response to the intra-peritoneal administration of ridiculously high amounts of MSG (4g/kg body weight) could be ameliorated by vitamin C + vitamin E + quercitin; these results suggest that exorbitantly high doses of MSG (human equivalent ~51g/day) are probably a result of an increase in reactive oxygen species
• "after intragastric administration of MSG, the MSG is preferentially metabolized through gluconeogenesis in B6 mice, whereas thermogenesis is the predominant process for 129 mice" - in previous studies scientists had observed profound differences in terms of the effects of MSG on food intake and preference; in 2009 Bachmanov et al. traced those differences back to genetic polymorphisms and respective differences in the metabolic response to / utilization of MSG - if we assume that similar differences exist in human beings, those would provide another explanation for the different incarnations of the "Chinese Restaurant Syndrome" with the classic headaches, high blood pressure and sweating in people who would be long to the human equivalent of the 129 mice and the highly rewarding and appetite stimulating gluconeogenic (hepatic production of glucose from the glutamate) effects in those humans with a similar genetic programming as the B6 mice

I could certainly go on for hours, citing study after study with "evidence" and "counter-evidence", or rather what the respective authors consider as such, but I believe that you have read enough to see a couple of basic patterns emerge, here.

So what about those differences? Genes, dosages, or what?

One of these patterns is also brought up by Kondoha and Torii in the discussion of the results of their study (remember: decrease in body fat and increase in energy expenditure; purported mechanism = activation of glutamate receptors that are linked to the vagus nerve), in which the researchers state that they believe that the diametrically opposed results of their, compared to other studies (most of which report an increase not a decrease in body fat that is accompanied by increases in circulating leptin and decreases in leptin sensitivity and not vice versa as in the Kondoh study), may well be explained by

[previous] studies [being] designed specifically to produce toxic effects in the brain (where GLU is an excitatory neurotransmitter), through the administration of extremely high doses (2000 mg/kg or more, administered repeatedly) to infant animals, either by single, direct injection or intubation (Kondoh. 2008).

Those high dosages could in fact have lead to blood glutamate concentrations that would allow the flux of the excitatory amino acid even across intact blood-brain-barriers. The more realistic, orally administered dosages  Kondoh and Torii used in their experiment, on the other hand, did not induce any (not even statistically non-significant) elevations of serum glutamate levels.

Hence, the effects seen in the present study, as discussed above, are probably linked via a physiologic mechanism, to a local action of GLU in the gut, rather than via a pharmacologic/toxicologic mechanism to a distant action of exogenous GLU forced on the brain (Kondoh. 2008).

If you review the brief rundown of the literature I've provided in the previous paragraphs you will have to acknowledge the validity of this remark (remember: the steatosis in the Collison study required co-administration of trans-fatty acids /TFA/ and even then the increase solely due to MSG was marginal compared to that of the TFAs, alone).

Without a leaky gut, you would probably have to eat pure MSG all day to do harm

If you also take into account, that in healthy individuals only <5% of the dietary glutamate are actually absorbed into systemic circulation, while the rest is used as an oxidative substrate by the intestinal mucosa (Smriga. 2007), the difference between thhe orally consumed 33mg/kg MSG that helped the rodents in the study by Kondoh and Torii to lean out and the intraperitoneally injected 4,000mg/kg that were necessary to induce the touted hepatic side effects in the study by Faromby and Onyema are way above the average intake even the worst offenders among the MSG abusers are exposed to (cf. figure 2):

Figure 1: Average per capita daily MSG intake in different countries (adapted from Löliger. 2000)

Even if we discard the oxidative loss within the intestine, those 4,000mg/kg for a rodent (in previous studies Onyema et al. had even used 6,000mg/kg to elicit the hepatic damage; Onyema. 2006) would translate to ~650mg/kg in humans and would mean that you would have to shovel down anywhere between 32g and 64g of pure MSG (depending on whether you weigh 50 or 100kg), i.e. 20-40x more than the average daily intake of a Korean (note: The "rodent model of MSG induced obesity" is induced by injection of 10,000mg/kg body weight; cf. Bunyan. 1976) and the whopping MSG equivalent of 400-800ml of soy sauce (avg. MSG content 80mg/ml), which is probably the worst offender in the E-number-laden ingredient arsenal of the Asian cuisine.

Figure 3: Protein-bound and free glutamate content of "high" glutamate foods (left) and total glutamate content of selected plant proteins (right; data adapted from Loliger. 2000)

Your best bet to ingest similar amounts of free glutamate from real foods is, as the data from a review by Loliger suggests (cf. figure 3), would be parmesan cheeese, but in all honesty, in view of the fact that you would have to consume 2.6kg of the Italian delicacy, it is pretty unlikely that the glutamate and not the sheer amount of pure energy in the cheese would be the underlying reason for subsequent weight gain. Against that background it should not be surprising that negative side-effects as they occur as a result of high to unrealistically high MSG intakes and or in especially susceptible individuals, are not exactly common in people who don't eat out and/or consume pre-packaged convenient foods on a regular, if not daily basis.

Too much of a vitally important thing at the wrong time and as part of the wrong foods...

The mere presence of non-negligible amounts of glutamate in all sorts of "real" foods, should yet remind you that glutamate is not a toxin, or a "foreign substance" we are not evolutionary adapted to, but an amino acid that is of utmost importance for the health of your central nervous system (Platt. 2005). So that at the end of this analysis we may not be back at square one, but still have to concede that it brought us back to a set of very common motifs here at the SuppVersity:

• When consumed in excess, substances that are good, healthy, beneficial and even "vitally" (=vitamin ;-) important can easily turn against you
• When substances do not have to pass the gut, the dose-response relationship can differ so substantially that results that are acquired using route A (e.g. intraperitoneal injection) cannot simply be transfered to scenarios employing different administration routes (e.g. oral ingestion)
• Inter-individual/-species differences and differences between healthy and unhealthy individuals / animals, warrant utmost caution, when it comes to interpreting data - the "Chinese Restaurant Syndrome", for example, could be a result of increased gut and blood-brain-barrier permeability that would lead to an increased absorption of glutamate from the intestine into the blood and from there across the blood-brain-barrier right into the brain.
• Oftentimes, differences due to the aforementioned factors are not of simple quantitative, but of qualitative nature, in the case of MSG this would be the difference between the metabolic activation in response to the local activation of glutamate receptors in the gut that are connected to the vagus nerve, on the one hand, and the systemic / central obesogenic (fattening) effects of glutamate that leaks from the gut into the blood and from there into the brain.

And lastly, to eventually come full circle and remind you of the results of Collison et al., we cannot ignore that MSG is one of those substances that is usually found in foods with a whole host of other nutrient-poor ingredients, anti-nutrients and proven obesogenic, pro-inflammatory and otherwise unhealthy substances and food additives. They are wrapped in plastics have an extended shelf life due to tons of preservatives and highly adorned with stickers and labels saying "low this", "extra that", "only X amounts of calories", etc. - as long as you avoid those foods on 360+ days of the year, prepare your meals from whole foods, don't dine at cheap restaurants, fast-food outlets and snack bars too often or try to find the "optimal amount of supplemental MSG to stimulate your vagus nerve and help you shed fat" *lol*, you can calmly watch the ever-recurring MSG scares on the Internet and other mass media ;-)

References:

1. Afifi MM, Abbas AM. Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring. Acta Physiol Hung. 2011 Jun;98(2):177-88.
2. Bachmanov AA, Inoue M, Ji H, Murata Y, Tordoff MG, Beauchamp GK. Glutamate taste and appetite in laboratory mice: physiologic and genetic analyses. Am J Clin Nutr. 2009 Sep;90(3):756S-763S. Epub 2009 Jul 1.
3. Bachmanov AA, Inoue M, Ji H, Murata Y, Tordoff MG, Beauchamp GK. Glutamate taste and appetite in laboratory mice: physiologic and genetic analyses. Am J Clin Nutr. 2009 Sep;90(3):756S-763S. Epub 2009 Jul 1.  
4. Bunyan J, Murrell EA, Shah PP. The induction of obesity in rodents by means of monosodium glutamate. Br J Nutr. 1976 Jan;35(1):25-39.
5. Collison KS, Maqbool Z, Saleh SM, Inglis A, Makhoul NJ, Bakheet R, Al-Johi M, Al-Rabiah R, Zaidi MZ, Al-Mohanna FA. Effect of dietary monosodium glutamate on trans fat-induced nonalcoholic fatty liver disease. J Lipid Res. 2009 Aug;50(8):1521-37. Epub 2008 Nov 11.  
6. Collison KS, Zaidi MZ, Saleh SM, Makhoul NJ, Inglis A, Burrows J, Araujo JA, Al-Mohanna FA. Nutrigenomics of hepatic steatosis in a feline model: effect of monosodium glutamate, fructose, and Trans-fat feeding. Genes Nutr. 2012 Apr;7(2):265-80. Epub 2011 Dec 6. 
7. Farombi EO, Onyema OO. Monosodium glutamate-induced oxidative damage and genotoxicity in the rat: modulatory role of vitamin C, vitamin E and quercetin. Hum Exp Toxicol. 2006 May;25(5):251-9.
8. Freeman M. Reconsidering the effects of monosodium glutamate: a literature review. J Am Acad Nurse Pract. 2006 Oct;18(10):482-6.nonalcoholic fatty liver disease. J Lipid Res. 2009 Aug;50(8):1521-37. Epub 2008 Nov 11.
9. Geha RS, Beiser A, Ren C, Patterson R, Greenberger PA, Grammer LC, Ditto AM, Harris KE, Shaughnessy MA, Yarnold PR, Corren J, Saxon A. Review of alleged reaction to monosodium glutamate and outcome of a multicenter double-blind placebo-controlled study. J Nutr. 2000 Apr;130(4S Suppl):1058S-62S.
10. Hermanussen M, García AP, Sunder M, Voigt M, Salazar V, Tresguerres JA. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite. Eur J Clin Nutr. 2006 Jan;60(1):25-31. 
11. Insawang T, Selmi C, CHa'on U et al. Monosodium glutamate (MSG) intake is associated with the prevalence of metabolic syndrome in a rural Thai population. Nutrition & Metabolism 2012, 9:50 doi:10.1186/1743-7075-9-50
12. Iwase M, Ichikawa K, Tashiro K, Iino K, Shinohara N, Ibayashi S, Yoshinari M, Fujishima M. Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue. Hypertens Res. 2000 Sep;23(5):503-10.
13. Kondoh T, Torii K. MSG intake suppresses weight gain, fat deposition, and plasma leptin levels in male Sprague-Dawley rats. Physiol Behav. 2008 Sep 3;95(1-2):135-44. 
14. Kondoh T, Tsurugizawa T, Torii K. Brain functional changes in rats administered with monosodium L-glutamate in the stomach. Ann N Y Acad Sci. 2009a Jul;1170:77-81.
15. Kondoh T, Mallick HN, Torii K. Activation of the gut-brain axis by dietary glutamate and physiologic significance in energy homeostasis. Am J Clin Nutr. 2009b Sep;90(3):832S-837S.
16. Loliger J. Function and importance of glutamate for savory foods. J Nutr. 2000 Apr;130(4S Suppl):915S-20S. 
17. Otsubo H, Kondoh T, Shibata M, Torii K, Ueta Y. Induction of Fos expression in the rat forebrain after intragastric administration of monosodium L-glutamate, glucose and NaCl. Neuroscience. 2011 Nov 24;196:97-103.
18. Onyema OO, Farombi EO, Emerole GO, Ukoha AI, Onyeze GO. Effect of vitamin E on monosodium glutamate induced hepatotoxicity and oxidative stress in rats. Indian J Biochem Biophys. 2006 Feb;43(1):20-4.
19. Pavlovic V, Sarac M. The role of ascorbic acid and monosodium glutamate in thymocyte apoptosis. Bratisl Lek Listy. 2010;111(6):357-60. 
20. Platt SR. The role of glutamate in central nervous system health and disease--a review. Vet J. 2007 Mar;173(2):278-86.
21. Ren X, Ferreira JG, Yeckel CW, Kondoh T, de Araujo IE. Effects of ad libitum ingestion of monosodium glutamate on weight gain in C57BL6/J mice. Digestion. 2011;83 Suppl 1:32-6. Epub 2011 Mar 10. 
22. Smriga M. COFAG comments on: "Monosodium glutamate-induced oxidative damage and genotoxicity in the rat: modulatory role of vitamin C, vitamin E and quercetin". Hum Exp Toxicol. 2007 Oct;26(10):833-4; author reply 835-6. 
23. Tarasoff L, Kelly MF. Monosodium L-glutamate: a double-blind study and review.
    Food Chem Toxicol. 1993 Dec;31(12):1019-35.
24. Walker R, Lupien JR. The safety evaluation of monosodium glutamate. J Nutr. 2000 Apr;130(4S Suppl):1049S-52S.
25. Yang D, Li SY, Yeung CM, Chang RC, So KF, Wong D, Lo AC. Lycium barbarum extracts protect the brain from blood-brain barrier disruption and cerebral edema in experimental stroke. PLoS One. 2012;7(3):e33596. Epub 2012 Mar 16.

Is it Your Neighbor(hood)'s Fault That You are an Obese Couch Potato? Plus: Higher Incomes Increase Obesity Risk in Men, Better Education Decreases Risk in Men & Women

Image 1: If this photo looks as if it was taken in your neighborhood, statistics say that you will have a harder time than others warding off obesity.

If you have not already been aware that the major weightloss obstacles are not so much of physio- than of psychological, or I should say behavioral natural, Monday's blogpost on the inability or unwillingness of the majority of the study participants in the Krebs study should have reminded you that there is more to losing weight than having an "optimal" diet plan. In this context, the results of a recently published paper from the University of Ottawa, Canada (Prince. 2012), comes to mind, in which Stepanie A. Prince and her colleagues report the results of a large-scale cross-sectional multi-level analysis of the association between neighborhoods, physical activity and obesity in Ottawa.

Mislead and misfed, but by no means unable to afford leading a healthier life-style

Although obviously of epidemiological nature, the study is remarkable in that it relies on relatively recent data (2006-2008) from 494,000 residents from 86 neighborhoods in Ottawa, who were part of the Ottawa Neighborhood Study (ONS). My usual advice not to confuse correlation (no matter how "significant") and causation, does yet still apply. A statement like "for each additional km² of park area per 1,000 inhabitants, the odds of being physically active increased by 17% in the female inhabitants of the respective neighborhood" (cf. figure 1, left; respective value: 1.17) does thusly signify that readily available parks areas seem to encourage women to be more physically active in their leisure time. It does not mean that moving to an apartment from which you can see the joggers doing their rounds in Central Park will turn a couch potato into a sporting ace. After all, it is at least as likely that people who like to jog try to make sure that they move to an area, where they can easily pursue their hobby.

Figure 1: Model predictions for the influence of environmental, social and contextual parameters on physical activity (left) and overweight/obesity rate (right) in men and women; * p < 0.05 (data based on Prince. 2012)

Against that background, I decided to include only factors which showed a statistically significant association with either obesity or physical activity in at least one of the two sexes in the data in figure 1. Now, you rarely have a rule without exception, and in this case, I also included the associative strength with the so-called census-based socio-economic status (SES) index, because the non-existent influence of social status on obesity rates goes just about as nicely against the notion that you cannot eat healthy if you are on a budget, as the +39% increased obesity risk of men in households with incomes >30,000$ (cf. figure 2)

Figure 2: Model predictions for the influence of the individual parameters household income and education overweight/obesity rate in men and women; * p < 0.05 (data based on Prince. 2012)

Moreover, the strong negative association -44% for men and -45% for women between having at least a college degree and being overweight/obese, would would support the argument that it is less about not being able to afford a "healthy lifestyle" than about not having learned / not being able to teach oneself to do so... or, if you will, being more susceptible to the misleading information from the food industry and less aware of the pitfalls of shopping in convenience stores (+17% increased risk of obesity in women per additional convenience store for 1,000 inhabitants) and eating at fast food outlets.

Note: Neither the age nor parameters, such as the number of indoor or outdoor recreational facilities, grocery stores, specialty stores and (normal) restaurants which, at least taken in isolation, had no statistically significant influence on either physical activity or obesity rates.

With respect to the +22% and +39% increased obesity risk per additional fast-food outlet (per 1,000 inhabitants), it should also be mentioned that this is only one out of several of the environmental factors, which had statistically significant influence only on obesity rates in women from the respective neighborhoods - a phenomenon, which could yet be a consequence of the fact that men are less likely to be in their respective neighborhood during working hours than women, so that the susceptibility to fast food stores is probably not gender-specific ;-)

The bitter or delighting truth about your neighbor(-hood ;-)

It is nevertheless quite remarkable that the associative strength of individual criteria such as age, income, education etc. showed an overall much more pronounced variation (0.98, p<0.05), than one of the area-specific variables, the variance of which did not reach statistical significance for either of the two study outcomes, i.e. physical activity level or overweight/obesity (cf. figure 1). This would suggest that environmental influences in the area we live in is in fact a more reliable indicator of our likelihood of ending up as an overweight couch potato or lean physical culturist than our incomes, education or say our age. A finding, which I would say is actually quite remarkable, don't you think so?

Reduced Exertion High Intensity Training - A Minimalist 2x20s HIIT Protocol For The Male Convenience Generation.

Image 1: Looks like humans are not the only lazy creatures, in these days of unhealthy convenience.

Laziness, it seems, is utterly human. If you look around, these days, it appears as if we were genetically programmed to be bone idle. And, from an evolutionary perspective, we may actually be. After all, moving around, hunting and gathering was an obligatory part of our lives in 99% of the human history. It was thus only consistent that our genes would tell us to sit down at the fireplace and relax, once we had found enough to eat on a given day... (un-)fortunately things have changed since those early days. Not only have we moved out of our caves, we have also found ways to radically reverse the ratio of activity to inactivity in our lives.

"Convenience" is the buzzword of the modern western civilization and the obesity epidemic is its unwanted consequence.

A consequence, which is yet by no means inevitable. After all, we all know that getting our behinds off our couches and into the gym, and setting the dietary recommendations of the (fast-)food industry, ahh... pardon, the government at naught would solve the problem, if ... yeah, if there was not this aforementioned genetically programmed laziness that makes the couch so much more appealing to us than the hard benches in the gym...

Sacrifice 30min per week of your TV-time and live to see your grandchildren graduate

A recent study from scientists from the United Kingdom does yet show that you could still spend more than enough time in front of your beloved television set, if you just performed what what Richard S. Metcalfe and his colleagues from the United Kingdom call the "minimal amount of exercise for improving metabolic health" (Metcalfe. 2011) - a 3x per week 10min exercise regimen with no more than two (yes, only 2x!) all-out sprints.

Figure 1: Outline of the training protocol, the black bars indicate all-out sprints at a breaking force equivalent to 7.5% of the individuals body weight (directly adapted from Metcalfe. 2011. Fig. 1)

As you can see in the outline of the experimental protocol, the 29 healthy and normal-weight, but sedentary young (~23y) men (n=13) and women (n=16) did not even have to start with 2x20s sprints. They rather built up to it, by starting out with a single 10s all-out cycle-ergometer sprint at a braking force equivalent to 7.5% of their body weight in the first week of the 6-week study period and built their exercise capacity from there.

Image 2: "Cardio" does not have to be steady state.

Note: If you have not read my previous blogposts on HIIT, you may have missed the information that interval training (not necessarily at the maximal intensity, though) is suitable for everyone - even heart disease patients (cf. Interval, not Steady State Aerobics is the Way to Go - Even for Patients with Myocardial Infarctions!). This has been confirmed only recently by Neil A. Smart et al. who found that "[i]ntermittent exercise may improve functional capacity [of congestive heart failure patients] to a greater extent than continuous exercise" (Smart. 2011) - and that despite the fact that both continuous (30min), as well as interval training (60min, 1 min cycling, 1 min rest) were performed at the same low intensity.

The rest of the 10-min exercise sessions, the subjects were pedaling along at 60W, which is about as much as it takes so that you do not fall off the bike, because of the lack of resistance that is required to stabilize yourself on the bike. The latter would have been tragic, at least if you are a man, because that would have counteracted the surprisingly (not for who has read about the magic of HIIT here at the SuppVersity before) profound effects this regimen, for which the scientists coined the name "reduced exertion high intensity training" (REHIT), had on the glucose homeostasis of the male subjects.

Figure 2: Changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test in men and women after 6 week of "reduced exertion high intensity training" (data calculated based on Metcalfe. 2011)

As the data in figure 2 shows, the statistically more than significant decreases in the area under the glucose (-12%) and insulin (-39%) curve (AUC) measured during an oral glucose tolerance test was exclusive to the 13 male participants - and that despite the fact that both, male as well as female study participants exhibited similar improvements in their individual VO2Max (+15% in men; +12% in women).

(RE)HIIT only for men?

As far as the underlying reasons for these gender differences are concerned, the scientists are pretty much at a loss, stating that this could be due to "the low statistical power of our study, with only eight female subjects performing the REHIT", " differences in metabolic perturbations during the brief high-intensity cycle sprints",  and the 3-day delay after the last HIIT session before the glucose tolerance test was done (as a SuppVersity reader you will be familiar with the notion that the "anabolic barn door" is wide open for 24-48h), so that "insulin sensitivity was improved in female subjects at an earlier time-point". Now, I do not want to sound like a himbo, but I would say that another observation the scientists made, provides a much better explanation:

[...] we observed that some of the female volunteers struggled with the transition from 60 W to the all-out sprints, and were unable to substantially increase their pedal frequency, and thus their power output during the sprints. This may have increased the aerobic contribution to energy supply and reduced glycogen depletion.

In other words, what was supposed to be a sprint turned out to be a sluggish ordeal. The slightly, but statistically significantly higher rates of perceived exertion (+10%) in the female study participants corroborates the assumption that the women simply did not burn enough glycogen. If we do now also consider the results of a 2008 study by Hagobia et al. who report that

[...] in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained.

It appears obvious that an increase in pedaling frequency by adapting the resistance to the individual fitness levels and dietary controls may be necessary to render this minimalist "REHIT" protocol productive for the fairer sex.

Figure 2: Comparison of changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test subsequent to 6 weeks of REHIT, or 10 months of "classic cardio" exercise, or dietary intervention (data calculated based on Metcalfe. 2011 and Dengel. 1996)

The comparison of this 6 week exercise program with the results of a 10 months intervention program in likewise healthy sedentary, but older men (45y) who exercised 3x a week for 40min (steady state) at 75-85% of their maximal heart rate, goes to show that it would well be worth making the REHIT protocol work for women, as well (Dengel. 1996). After all, the steady state endurance protocol in the Dengel study was not only four times more time-consuming (plus, the intervention period was 6.6x longer) than the modified HIIT protocol in the Metcalfe study, it also failed to improve the glucose response to the oral glucose tolerance test and produced less pronounced improvements in insulin sensitivity (cf. insulin AUC in figure 3). The mild caloric reduction (-300-500kcal/day) that was imposed on another group of the study participants, on the other hand, yielded similar reductions in glucose and insulin AUCs as the REHIT protocol in the Metcalfe study that was accompanied by a body weight reduction of ~10%, a reduction in body-fat of -5.8% and essentially no loss in fat free mass!

Note: Unfortunately, Metcalfe et al. did not measure the body composition of the study participants. In view of the results of the Whyte study (Whyte. 2010), I cited in the Intermittent Thoughts on Healthy Weight Loss, where the participants lost -2.4cm of their allegedly obese bellies within no more than 2 weeks of doing HIIT, as well as the well-established correlation between insulin resistance and the size of your beer-belly, it is very well possible that the male participants in the Metcalfe study will have lost some body fat doing no more than 8.67 minutes of all out cycling spread across 18 training sessions in 6 weeks... and if they didn't their diet probably was still too convenient ;-)

The (in-)convenient truth about your future

Taken together the results of these studies suggest that a) steady state aerobic exercise is pretty pointless, b) even a minimalist HIIT regimen goes a long way, as long as c) you really hit it hard and d) adhere to your regular (hopefully non-convenient) diet, or even better e) introduce a slight calorie deficit. In other words, without at least some "inconveniences" as far as nutrition and exercise are concerned, chances are that YOU will either remain or become one of the 34,004,946 obese human beings that are now populating a planet where the US alone spend 1,550,566$ per day on the detrimental health consequences of the"convenience" of its citizens (data from Obesity Statistics).