Vitamin A, B6, B12, C, E, Folate & Iron: Deficiency Nutrients in the US - 31% are Deficient | Plus: What About Athletes?

Few US citizens get all the nutrients they need from their diets.

You may argue that I've addressed this in a previous article. The fact that there's now updated data from the National Health and Nutrition Examination Survey (NHANES)  does yet (IMHO) warrant to take another look at the prevalence of nutrient deficiencies in the US.

The bad news first: The study found sign. deficiency rates for all the investigated nutrients: vitamins A, B6, B12, C, D, E, folate and iron. The good news: It's easy and - with the exception of iron and folate 100% unproblematic to supplement your diet.

Looking for more ways to improve your diet? Increase your potassium (K) intake!

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In their analysis, Bird et al. aggregated data from the from the 2003–2004 and 2005–2006 NHANES data cycles to determine the overall risk of multiple concurrent deficiencies in U.S. children and adults (n = 15,030) aged >9 years.

Table 1: Proportion of the population with usual intakes below the EAR (estimated average requirement), the RDA (recommended dietary allowance) and excessive intake according to TUL (total upper limit | Bird 2017)

As you can see in Table 1 the number of people who don't get enough of at least one of the nutrients is significant. In fact, the scientist's calculations show that 31% percent of the U.S. population was at risk of at least one vitamin deficiency or anemia. 23%, 6.3%, and 1.7% of the U.S. population is at risk of deficiency in 1, 2, or 3–5 vitamins or anemia, respectively. Further analyses of the data-set revealed...

• significantly higher deficiency risks in women (37%), non-Hispanic blacks (55%), individuals from low-income households (40%), or without a high school diploma (42%); 
• significantly higher deficiency risks in underweight (42%) or obese individuals (39%);
• that women aged 19–50 years (41%), and pregnant or breastfeeding women (47%) are at particular risk of nutrient deficiencies;
• that dietary supplement non-users had the highest risk of any deficiency (40%), compared to users of full-spectrum multivitamin-multimineral supplements (14%) and other dietary supplement users (28%)

The symptoms that can arise from not getting enough of these nutrients (you don't have to get 100% every day, though) range from 

• impaired immunity, growth and night blindness from vitamin A deficiency, over 
• impaired wound healing and bleeding from vitamin C deficiency, 
• anemia from iron deficiency, and 
• rickets and osteomalacia from vitamin D deficiency, to
• megaloblastic anemia with low folate intakes, 
• microcytic anemia with B6 deficiencies, and 
• pernicious anemia and neurological damage due to impaired myelination with low B12. 

As the scientists point out, an adequate status of micronutrients in combination is required for many important processes in the body. 

"For example, erythropoiesis requires not only iron, but also folate, vitamin B12, and vitamin A, and dietary vitamin C can improve the absorption of non-heme iron. Sub-clinical deficiency symptoms for many vitamins and minerals are non-specific, and may include fatigue, irritability, aches and pains, decreased immune function, and heart palpitations" (Bird 2017).

Previous reports estimated the deficiency prevalence for each of the vitamins B6, C, and D, and the mineral iron, between 5–10% (similarly, previous studies underestimated the risk of missing out on not just one but two nutrients, i.e. 5.7% vs. 23%). 

What kind of data are we talking about? Food questionnaires? Yes, we are talking about questionnaires (two 24h recalls, to be specific), but the scientists also used data from blood draws that were conducted as part of the NHANES cycles. 

If you take another look at Table 1 the study at hand found significantly higher prevalences of nutrient deficiency. Racial and social disparities have been observed before, but the prevalence rates in risk groups such as pregnant and breastfeeding women, low-income households, or according to educational status, body mass index (BMI), or measures of dietary intake have not been investigated previously. 

Figure 1: Risk of biochemical vitamin deficiency or anemia, by DS use and dietary vitamin/mineral inadequacy/insufficiency (Bird 2017).

The study also investigated in detail the effect of dietary supplement use, with full spectrum multi-nutrient supplements being defined as FSMR, i.e. “full spectrum” multivitamin-multimineral DS (≥12 vitamins and 7 to 16 minerals), being the most effective tools in the arsenal of pills and powders the study participants used. FSRMs reduced the risk of deficiency from 70% in nonusers to still impressive 31% in full-spectrum users. People who supplemented with individual vitamins (see DS in Figure 1) ended up being deficient for at least one nutrient in 51% of the cases. 

All that is bad news, but the fact that only a small number of subjects ended up above the Tolerable Upper Limit (TUL) was low - 1.1%, 0.68%, and 0.31% of the population had excessive intakes of iron, folate, and retinol, respectively - is unquestionably good news. After all, all three of them have potentially health-threatening side effects, most prominently, probably the birth defects (> 8,000 IU / day), risk of osteoporosis, hair loss, bone pain, elevated blood sugar, liver damage, and liver damage (> 25,000 IU / day) for retinol (vitamin A).

What about athletes and gymrats

The data from studies in athletes tend to show generally reduced risks of nutrient deficiency because (a) athletes tend to eat more, (b) athletes tend to eat more healthy, and (c) athletes tend to take more supplements. For their immune-competence, an adequate intake of iron, vitamins A, E, B6 and B12 is particularly important for athletes (Gleeson 2001).

Are "natural vitamins" better than "artificial" ones? For many vitamins, the "natural" version isn't better than "artificial" one. For others there's good evidence (discussed here) in favor of "natural vitamins"; and, even more importantly, if you get the vitamins from whole foods you usually get all necessary co-factors you will be missing w/ most of the dietary supplements (natural or artificial).

It should be emphasized, though, that "acute or short-term marginal deficiencies, identified by blood biochemical measures of vitamin B status, [have] no impacts on performance measures" (Lukaski 2004). Particularly folate and B12 are still deficiency nutrients - especially in endurance athletes who will often suffer from anemia as a consequence of not getting enough of these important B-vitamins. "Evidence of vitamin A and E deficiencies in athletic individuals is lacking apparently because body storage is appreciable" (Lukaski 2004).

Table 2: Energy expenditure in various sports - measured by doubly-labeled water compared to data from dietary recall, (M) male subjects, (f) female subjects (from Meyer 2016)

Interestingly enough, the IOC only recently warned about general energy deficiencies in athletes. In fact, next to sports of which you'd already expect that athletes purposefully consume less than optimal amounts of energy, you can see in Table 2, that other sports, like Tour de France cycling, simply burn so much energy that the athletes cannot keep up (Meyer 2016). For many athletes, this lack of energy intake translates into a lack of micronutrients - with calcium and vitamin D deficits being both prevalent and risky; risky because they significantly increase the risk of stress fractures.

Cumulative meta-analysis of the effect of vitamin B supplementation on the risk of cancer incidence (A), death due to cancer (B), and total mortality (C | Zhang 2016).

Isn't is obvious that everyone should take a multi? Not really.... While this is what the industry wants to make you believe, the actual scientific evidence that taking a multi-nutrient supplement is good for you is... well let's say "inconclusive". There's, for example, the claim that B-vitamins will combat the cognitive decline with age - which makes absolute sense, theoretically, has been observed in some trials (e.g. Douaud 2013), but is not supported by the majority of RCTs and epidemiological studies (Raman 2007; Kang 2008; Wald 2010). In contrast to popular claims, B-vitamin supplementation doesn't lower cardiovascular disease, cancer, and cause-specific mortality, either (Clarke 2010).

Similarly disappointing results have been reported for multivitamin supplements by Grodstein et al. (2013) - with respect to dementia. Likewise a null-result was reported by Macpherson et al. (2013) who didn't find sign. effects on all-cause mortality in their meta-analysis. Multis don't seem to reduce the infection risk in the elderly (El-Kadiki 2005). They don't reduce the risk of progression atherosclerosis (Bleys 2006) or protect you from CVD (Myung 2013). They don't protect you from prostate or breast cancer (Stratton 2011; Chan 2011) and/or general cancer mortality (Park 2011). And the list can be extended (e.g. Song 2011; Sesso 2012...).

For specific vitamins, like vitamin E, the evidence is even downright disconcerting. Next to evidence suggesting that it's only useless (Vivekananthan 2003), there are also studies showing increased mortality with high(er) doses (>400IU per day | Miller 2005) and an increased risk of stroke (Schürks 2010), which is the exact opposite of what you see with veggies and fruit (He 2006). Just as usual, there's yet also evidence to the contrary. Ye & Song report a reduced risk of coronary heart disease in their meta-analysis of cohort studies (Ye 2008) - and guess what: they analyzed data from studies that used the often bashed vitamins C+E + beta carotene.

So what? Well, if you asked me: I still think it's not necessary. A low (RDA) dosed multi is yet probably not going to kill you (or what frightens some readers even more "impair your gains" - that takes much higher doses of vitamin C + E than the RDA).

The #1 deficiency in athletes is yet one that you will find in the general population, as well. Iron deficiencies (Zourdos 2015)... and that often in the presence of normal hemoglobin values:

Figure 2: Treatment algorithm based on plasma ferritin and haemoglobin levels (C reactive protein is considered normal). Hb = haemoglobin (Chatard 1999).

"De Wijn et al. reported that 7% of male and 17.5% of female athletes studied had a transferrin saturation index be low 20% [you need to have both, a high transferrin saturation andenough serum iron], but very few were anaemic. 

Clement et al. (1977) studied elite Canadian endurance runners, and found that 29% of the men and 82% of the women had extremely low ferritin values (<25 µg/L), even though their blood haemoglobin and serum iron levels were normal" (Chatard 1999).

Supplementation has been found to improve athletic performance significantly, even in marginal deficiency states (Schoene 1983) - even in the absence of anemia (Burden 2015).

Update from August 15, 2017: Do multis even protect you from nutrient deficiencies? Yes, they do. Only recently Blumberg et al. found that except for calcium, magnesium, and vitamin D, the subjects with the most frequent use of multivitamin- and multimineral-supplements (MVMS use ≥21 days/30 days) virtually eliminated inadequacies of micronutrients, and were thus at significantly lower risk of deficiency for the examined nutrient biomarkers except for iron (guess what: that's  because most multis don't contain iron).

And while female athletes are for obvious reasons (menses) at highest risk of low iron, Peeling et al. argue quite convincingly that exercise induced inflammation, the release of cytokines, which increase the hormone hepcidin that in turn reduced impairs iron transport and absorption put athletes at particular risk of iron deficiencies (Peeling 2008).

Table 3: Adequacy of micronutrient intake (%) in men and women presented for users and non-users of nutritional supplements (Wardenaar 2017). Non-users of nutritional supplements (‘non-users’), users of dietary supplements (DS), users of sport nutrition products (SNP) and users of a combination of both (DS + SNP).

The likewise prevalent deficiencies in magnesium and zinc can have similar, albeit less far-reaching ill effects on athletes' performance; just as other less prevalent nutrient deficiencies of Dutch athletes, you can delineate from the data in Table 3.

The ill effects of cold-water immersion on muscle gains are just one out of dozens of examples, where things that should work - theoretically.

Bottom line: Better safe than sorry? When we're talking about classic "multis" or FSMRs as they were called in the study at hand, the strategy the scientists describe as "nutritional insurance to cover unintended gaps in dietary intakes" probably isn't the worst one (cf. Bailey 2013).

This is especially true, because many classic deficiency nutrients were not even included in the analysis: vitamin D, of which 14-18% of all US citizens have way too little (full deficiency w/ 25(OH)D <40 nmol/L) in their blood (Schleicher 2016), zinc deficiency (a global problem esp. for women | Hess 2017), or magnesium deficiency which plagues every third American and of which 62% get only insufficient amounts (Deng 2013).

Needless to say: Logging your food intake over 1-2 weeks and calculating potential deficiencies to then buy exactly the supplements you really need would be the better choice. Even better probably than many of the expensive tests, the accuracy or relevance (e.g. serum magnesium = not representative of your real magnesium status) of which is vastly overstated by their providers.

Also, if you want to know more, catch up w/ previously discussed nutrient deficiency articles on choline, various nutrients, potassium | Or tell me what you think in a comment on Facebook!

References:

• Bailey, Regan L., et al. "Why US adults use dietary supplements." JAMA internal medicine 173.5 (2013): 355-361.
• Bird, Julia K., et al. "Risk of Deficiency in Multiple Concurrent Micronutrients in Children and Adults in the United States." Nutrients 9.7 (2017): 655.
• Bleys, Joachim, et al. "Vitamin-mineral supplementation and the progression of atherosclerosis: a meta-analysis of randomized controlled trials." The American journal of clinical nutrition 84.4 (2006): 880-887.
• Blumberg, Jeffrey B., et al. "Impact of Frequency of Multi-Vitamin/Multi-Mineral Supplement Intake on Nutritional Adequacy and Nutrient Deficiencies in US Adults." Nutrients 9.8 (2017): 849.
• Burden, Richard J., et al. "Is iron treatment beneficial in, iron-deficient but non-anaemic (IDNA) endurance athletes? A systematic review and meta-analysis." Br J Sports Med 49.21 (2015): 1389-1397.
• Chan, Agnes LF, Henry WC Leung, and Shiao-Fung Wang. "Multivitamin supplement use and risk of breast cancer: a meta-analysis." Annals of Pharmacotherapy 45.4 (2011): 476-484.
• Chatard, Jean-Claude, et al. "Anaemia and iron deficiency in athletes." Sports Med 27.4 (1999): 229-240.
• Clement, D. B., R. C. Asmundson, and C. W. Medhurst. "Hemoglobin values: comparative survey of the 1976 Canadian Olympic team." Canadian Medical Association Journal 117.6 (1977): 614.
• Deng, Xinqing, et al. "Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III." BMC medicine 11.1 (2013): 187.
• De Wijn, J. F., et al. "Hemoglobin, packed cell volume, serum iron and iron binding capacity of selected athletes during training." Annals of Nutrition and Metabolism 13.3-4 (1971): 129-139.
• El-Kadiki, Alia, and Alexander J. Sutton. "Role of multivitamins and mineral supplements in preventing infections in elderly people: systematic review and meta-analysis of randomised controlled trials." Bmj 330.7496 (2005): 871.
• Fortmann, Stephen P., et al. "Vitamin and mineral supplements in the primary prevention of cardiovascular disease and cancer: an updated systematic evidence review for the US Preventive Services Task Force." Annals of internal medicine 159.12 (2013): 824-834.
• Gleeson, Michael, Graeme I. Lancaster, and Nicolette C. Bishop. "Nutritional strategies to minimise exercise-induced immunosuppression in athletes." Canadian journal of applied physiology 26.S1 (2001): S23-S35.
• Grodstein, Francine, et al. "Long-term multivitamin supplementation and cognitive function in mena randomized trial." Annals of internal medicine 159.12 (2013): 806-814.
• Guallar, Eliseo, et al. "Enough is enough: stop wasting money on vitamin and mineral supplements." Annals of internal medicine 159.12 (2013): 850-851.
• He, Feng J., Caryl A. Nowson, and Graham A. MacGregor. "Fruit and vegetable consumption and stroke: meta-analysis of cohort studies." The Lancet 367.9507 (2006): 320-326.
• Hess, Sonja Y. "National risk of zinc deficiency as estimated by national surveys." Food and nutrition bulletin 38.1 (2017): 3-17.
• Kang, Jae Hee, et al. "A trial of B vitamins and cognitive function among women at high risk of cardiovascular disease." The American journal of clinical nutrition 88.6 (2008): 1602-1610.
• Meyer, Nanna L., and Melinda M. Manore. "2 Evaluation of Nutrient Adequacy of Athletes’ Diets." Nutritional Assessment of Athletes (2016): 51.
• Myung, Seung-Kwon, et al. "Efficacy of vitamin and antioxidant supplements in prevention of cardiovascular disease: systematic review and meta-analysis of randomised controlled trials." Bmj 346 (2013): f10.
• Lukaski, Henry C. "Vitamin and mineral status: effects on physical performance." Nutrition 20.7 (2004): 632-644.
• Park, Song-Yi, et al. "Multivitamin use and the risk of mortality and cancer incidence: the multiethnic cohort study." American journal of epidemiology 173.8 (2011): 906-914.
• Peeling, Peter, et al. "Athletic induced iron deficiency: new insights into the role of inflammation, cytokines and hormones." European journal of applied physiology 103.4 (2008): 381.
• Raman, Gowri, et al. "Heterogeneity and lack of good quality studies limit association between folate, vitamins B-6 and B-12, and cognitive function." The Journal of nutrition 137.7 (2007): 1789-1794.
• Schleicher, Rosemary L., et al. "The vitamin D status of the US population from 1988 to 2010 using standardized serum concentrations of 25-hydroxyvitamin D shows recent modest increases." The American journal of clinical nutrition 104.2 (2016): 454-461.
• Sesso, Howard D., et al. "Multivitamins in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial." Jama 308.17 (2012): 1751-1760.
• Schoene, Robert B., et al. "Iron repletion decreases maximal exercise lactate concentrations in female athletes with minimal iron-deficiency anemia." The Journal of laboratory and clinical medicine 102.2 (1983): 298-305.
• Song, Yiqing, et al. "Multivitamins, individual vitamin and mineral supplements, and risk of diabetes among older US adults." Diabetes care 34.1 (2011): 108-114.
• Stratton, Julie, and Marshall Godwin. "The effect of supplemental vitamins and minerals on the development of prostate cancer: a systematic review and meta-analysis." Family practice 28.3 (2011): 243-252.
• Wald, David S., Anuradhani Kasturiratne, and Mark Simmonds. "Effect of folic acid, with or without other B vitamins, on cognitive decline: meta-analysis of randomized trials." The American journal of medicine 123.6 (2010): 522-527.
• Wardenaar, Floris, et al. "Micronutrient Intakes in 553 Dutch Elite and Sub-Elite Athletes: Prevalence of Low and High Intakes in Users and Non-Users of Nutritional Supplements." Nutrients 9.2 (2017): 142.
• Vivekananthan, Deepak P., et al. "Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials." The Lancet 361.9374 (2003): 2017-2023.
• Ye, Zheng, and Honglin Song. "Antioxidant vitamins intake and the risk of coronary heart disease: meta-analysis of cohort studies." European Journal of Cardiovascular Prevention & Rehabilitation 15.1 (2008): 26-34.
• Zhang, Sui-Liang, et al. "Effect of vitamin B supplementation on cancer incidence, death due to cancer, and total mortality: A PRISMA-compliant cumulative meta-analysis of randomized controlled trials." Medicine 95.31 (2016).
• Zourdos, Michael C., Marcos A. Sanchez-Gonzalez, and Sara E. Mahoney. "A brief review: the implications of iron supplementation for marathon runners on health and performance." The Journal of Strength & Conditioning Research 29.2 (2015): 559-565.

Potassium-Magnesium Aspartate, an Overlooked Endurance Enhancer? Acute 100% Increase in Time to Full Exhaustion

1952, Italian Fausto Coppi is drenched with water by a fan during the golden years of the Tour. Question: Can the topical application of K & Mg do the same magic? Answer: That's very unlikely, ...

What sounds like a supplement producer was trying to sell his product with a sponsored study is, in fact, the gist of a 1968 study from the Departments of Clinical Physiology and Internal Medicine at the venerable Karolinska Institute in Stockholm, Sweden (Ahlborg. 1968).

The authors' conclusion that "[a]fter administration of potassium-magnesium-aspartate [KMgA] the capacity for prolonged exercise increased about 50 per cent" (Ahlborg. 1968) can thus not be discarded as marketing babble. And, before we decide whether it's too good to be true, I'd suggest we take a closer look at the way the data was generated before we either (a) discard it as outdated or (b) get totally excited for nothing.

Mineral water will contain some K and Mg, too - and it will have other benefits:

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Mineral Water Supercharges 'ur Performance?!

Another ten years before Ahlborg et al. published their study, an effect of potassium and magnesium salts of aspartic acid on muscular fatigability has been demonstrated experimentally in animals by several independent research groups. Back in the 1960s, humans studies had yet only subjectively assessed the effects of KMgA on endurance performance in man. Ahlborg et al. were thus right to consider it... "to be of interest to investigate, whether a positive effect on the capacity for prolonged standardized physical exercise after oral administration of potassium-magnesium-aspartate can be objectively demonstrated" (Ahlberg. 1968).

Table 1: Some anthropometric and other data in the test subjects (Ahlborg. 1968).

The scientists recruited 6 out of a group of 300 military recruits who had been examined at the Military Medical Examination Centre at the Karolinska Institute back in the 1960s. All subjects were subjected to the following routine: On 4 consecutive days, which will be called day 1, 2, 3 and 4, prolonged exercise to exhaustion was performed every day beginning at 1 p.m. The subjects were not fasted.

To get the results they wanted and to make sure the subjects' performance was not thwarted, the scientists required all subjects to record all foods they'd been consuming for the 4 days of the test. This practice was meant to avoid interference with of high carbohydrate intakes of which people back in the day still knew and appreciated that they can "increase the capacity for prolonged exercise markedly" (Ahlborg. 1968).

Does this work for strength training as well? While it may help you up your workouts, a study by Consolazio et al. (1964) found  no measurable beneficial effects on muscle strength. This disappointing result was later confirmed by De Haan, et al. (1985). So, I'd venture the guess that - if KMgA is a thing at all - it's an endurance athletes' thing.

To test each subject against itself while still having averages to compare, the authors had all subjects perform the "W170", a bicycle ergometer ride at a pulse rate of 170 beats/min (duration ~90 minutes until physical exhaustion) on days 1, 2, 3 and four. And here's how the supplementation worked:

"Beginning at 6 p.m. on the day before day 1, 5 tablets were administered every sixth hrs. last 5 tablets were given 1 hr before the prolonged exercise test on day 4, see Fig. 1. All subjects were given placebo tablets before the tests on days 1, 2 and 4. Before day 3 active substance was given. The subjects were told that the tests were aimed at elucidating the influence of a vitamin tablet on maximal performance time. No information was given to the test supervisor (the same nurse on all days) or to the subjects as to when placebo or active substance was administered. The placebo and active tablets were identically looking" (Ahlborg. 1968)

This is admittedly not exactly standard procedure, and one could argue that what we are seeing here is a vitamin placebo effect, but the effect (a) appears to be a bit too large (see data in Figure 1) and you could (b) also argue that the previous two 170Ws may have had a negative effect on the subjects' performance during cycling to exhaustion.

Figure 1: Duration of prolonged exercise (y-axis) in the 6 test subjects after administration (x-axis) of placebo (striped area) and after administration of aspartate (black area) and individual data in the table (Ahlborg. 1968).

As you can see in Figure 1 the effect differed from subject to subject but was (a) highly significant in all of the 6 men and (b) doesn't have a residual effect. The latter suggests that the ~100% increase in time to exhaustion is not the result of K or Mg repletion, but an acute response to the KMgA supplement.

Research overview and supplement suggestion: In order to put the results into perspective I've curso-rily searched subsequent studies on aspartate bound minerals with the following results (in random order): [1] Sign. increased ergogenic effects in with 10 g of potassium-magnesium as-partate over a 24 hr in Wesson et al. (1988) in subjects cycling at 70% VO2Max; [2] no benefits in trained indiv. cycling at lower intensities in Hagan, et al. (1982); [3] no benefits were likewise seen, when the supplement was taken in lower amounts chronically, i.e. 5 weeks, only 2g/day (Consolazio. 1964) and / or when the supplement was controlled against equimolar amounts of "regular" (HCL) Mg + K (Maughan. 1983).

Overall, the research, there-fore, appears to suggest that athletes who perform high-intensity endurance exerci-ses could benefit most from the serial administration of a total of 10g/24h of Mg and K - not necessarily bound to aspartate, for which scien-tists have not conclusively proven benefits when it's taken on its own, either (Trudeau. 2008).

So what's triggering these benefits? As you will know I am not happy if I don't understand the cause-and-effect relationships in any field of research that does not belong to quantum sciences. Unfortunately, I have to admit that, in this particular case, where Heisenberg's uncertainty principle obviously doesn't apply, I still cannot explain exactly what the reason for the surprisingly pronounced ergogenic effects is.

What appears to be certain (also based on previous studies) is that the 100% increase is not a normal day-to-day performance variation. As Ahlborg et al. point out, the antifatigue effect in previous research in rodents was often interpreted as the result of an ATP and phosphocreatine sparing effect, i.e. a decreased consumption of ATP and phosphocreatine. The authors of the paper at hand, however, believe that it is "more likely that the resynthesis of the energy-rich phosphates ATP and phosphocreatine might be accelerated by potassium-magnesium-aspartate" - quite obviously, the net result will be the same, an increased available amount of energy-rich phosphates in the muscles. This, in turn, was suspected to be due to a glycogen sparing effect of the Mg and K esp. with a focus on aspartate co-administration ('cause Asp is a major source of gluconeogenesis during exercise). Since the latter has been refuted by Trudeau, et al. in 1993, we are thus stuck with hypothesis #2, i.e. a direct effect on the (accelerated) rate of resynthesis of phosphocreatine.

Well, back in the day Ahlborg et al. wrote that "investigations are in progress to evaluate these theories". Unfortunately, the final answer to the question "how does that work" has yet not been found (see box on the right). Increased heart rate, increased lipolysis and glucose oxidation as they have been observed in Wesson et al. who confirmed the benefits on endurance performance in 1988 are probably rather a consequence than the cause of the performance enhancement you may be able to see in the conditions I outlined in the box to the right | Comment!

References:

• Ahlborg, Björn. Capacity for exercise in man. Forsvarets sjukvardsstyrelse, 1967.
• Ahlborg, Bjorn, et al. "Human muscle glycogen content and capacity for prolonged exercise after different diets." Forsvarsmedicin 3.Suppl 1 (1967): 85ą89.
• Ahlborg, Björn, et al. "Muscle glycogen and muscle electrolytes during prolonged physical exercise1." Acta Physiologica Scandinavica 70.2 (1967): 129-142.
• Ahlborg, Björn, Lars‐Göran Ekelund, and Carl‐Gustaf Nilsson. "Effect of Potassium‐Magnesium‐Aspartate on the Capacity for Prolonged Exercise in Man." Acta Physiologica Scandinavica 74.1‐2 (1968): 238-245.
• Consolazio, C. Frank, et al. "Effects of aspartic acid salts (Mg and K) on physical performance of men." Journal of applied physiology 19.2 (1964): 257-261.
• Ekelund, Lars-Göran. "Circulatory and respiratory adaptation during prolonged exercise." Acta physiologica Scandinavica. Supplementum 292 (1967): 1.
• De Haan, A., J. E. Van Doorn, and H. G. Westra. "Effects of potassium+ magnesium aspartate on muscle metabolism and force development during short intensive static exercise." International journal of sports medicine 6.01 (1985): 44-49.
• Hagan, R. D., et al. "Absence of effect of potassium-magnesium aspartate on physiologic responses to prolonged work in aerobically trained men." International journal of sports medicine 3.03 (1982): 177-181.
• Maughan, R. J., and D. J. M. Sadler. "The effects of oral administration of salts of aspartic acid on the metabolic response to prolonged exhausting exercise in man." International journal of sports medicine 4.02 (1983): 119-123.
• Trudeau, François, and René Murphy. "Effects of potassium-aspartate salt administration on glycogen use in the rat during a swimming stress." Physiology & behavior 54.1 (1993): 7-12.
• Wesson, Matthew, et al. "Effects of oral administration of aspartic acid salts on the endurance capacity of trained athletes." Research Quarterly for Exercise and Sport 59.3 (1988): 234-239.

Hair Mineral Analysis: Significant Correlations Between Calcium, Magnesium, Potassium & Sodium and Met. Syn., Insulin Resistance, Waist, BP etc. - Implications?

Does her hair hold the secret to her fitness body? Actually that's unlikely, but it appears possible that a hair analysis could reveals what's keeping you back from a similarly amazing physique.

Hair mineral analyses have been discredited by certain snake oil vendors who use them to sell their "oils" in form of an endless list of "essential" supplements you'd have to take if you don't want to end up as dead as the hair they used to produce the analysis. Still, they share one big strength with the more expensive RBC or other cell tests: They give you an idea of your actual calcium, magnesium, sodium and potassium balance.

Much in contrast to serum levels, by the way. If those are off, it's either due to an acute event (like diarrhea, for example ;-) or you have a real reason to be concerned. There is after all a really good reason these minerals are also called "electrolytes": They are heavily involved in the ion and thus charge-exchange that keeps your heart beating!

Serum analyses tell you if your heart will keep beating, but what do hair analysis tell you? That's a very valid question and the answer is NOTHING! You can use them to estimate your mineral balance, but a high calcium level in the hair, does not necessarily imply a high level in other body parts. Moreover, correlations as I am about to report them in today's SuppVersity article allow for hypotheses about causative effects, what they don't do, though is to prove cause and effect! Please keep that in mind while reading this article and before your next visit at your favorite quack.

Before we get to the actual hair mineral analysis data, let's briefly have a look at another set of striking and not so striking differences between the "normal" subjects and those with established metabolic syndrome:

Figure 1: Serum mineral concentrations, visceral (VAT) and subcutaneous body fat and smoking status in subjects w/ and w/out metabolic syndrome (Choi. 2014)

If you take a closer look at the data in Figure 1 you will see that - aside from marginal, but statistically non-significant differences in serum phosphor - the often-checked total Ca, Mg, K, Na & Ph concentrations did not differ between the two groups.

Potassium, insulin resistance & obesity: Later in this article you will learn that there was a negative association between the amount of potassium in the hair of the subjects and their HDL and insulin sensitivity. It's important not to confuse this with the message "potassium is bad for your insulin sensitivity" - in fact, in 1980, Rowe et al. observed significant decreases in plasma insulin response  to sustained hyperglycemia and a ~30% reduction in glucose metabolism (Rowe. 1980).

Moverover, visceral fat was a much more reliable parameter to distinguish the healthy and unhealthy subjects than subcutaneous fat and... a bit to my surprise: Smoking appears to be associated with a lower metabolic risk than non-smoking.

Let's take a look at the hair analysis, now

Much in contrast to the serum levels, the hair mineral analysis did reveal significant inter-group differences and corresponding correlations:

Of all potentially toxic molecules the researchers measured only the levels of arsenic and lead differed significantly between the two groups. The concentrations of cadmium, mercury, and aluminum were not different between the two groups, on the other hand, did not.

And what does that mean? If we take a parting look at the data in Table 1, you will see that, the one parameter that makes all the difference is none of the minerals. It's rather an old acquaintance: The total amount of visceral fat. With a p-value of p = 0.000 it's the best parameter we have to identify someone with metabolic syndrome. The hair minerals, on the other hand, may present with associations with individual features of the metabolic syndrome, namely...

Table 1: Multiple logistic regression analysis for hair mineral concentrations with metabolic syndrome (Choi. 2014)

• low calcium, low magnesium ➮ high blood pressure, high blood sugar, triglycerides, weight and waist,
• high sodium, high potassium ➮ low HDL,
• high copper ➮ low blood pressure, low weight, low waist, high insulin sensitivity,
• high chromium ➮ high weight, high waist, and
• high cobalt ➮ low blood pressure

Now, since, we don't know how exactly the hair mineral content ant the nutritional intake are connected, it is very difficult to make any recommendations based on these observations.

What appears to be relatively certain, though, is that these new findings don't change anything about my previous recommendation to make sure that you get enough calcium and magnesium - the thing about potassium, on the other hand, strikes me as odd. As an antagonist to calcium, the negative effects of K may yet simply be a result of a Ca deficiency in the average mid-40s subjects in the study at hand.

References:

• Choi, Whan-Seok, Se-Hong Kim, and Ju-Hye Chung. "Relationships of Hair Mineral Concentrations with Insulin Resistance in Metabolic Syndrome." Biological Trace Element Research (2014): 1-7.
• Rowe, John W., et al. "Effect of experimental potassium deficiency on glucose and insulin metabolism." Metabolism 29.6 (1980): 498-502.

There is More To Glucose Control Than Carbohydrates (4/?): Non-Carbohydrate Nutrients Blood for Glucose Management ➲ Calcium - Bone Builder + Fat Burner + Glucose Stabilizer?

Healthy due to calcium?

In the last three weeks we've already covered the effects of protein, fat and vitamin D in this series about the "non-carbohydrate" (micro-)nutrients which have an impact on your blood glucose levels (browse the previous installments).

With vitamin D as the topic of the last installment, it appears only logical to jump from vitamins to minerals and take a look at the "bone mineral" calcium, of which scientists have long believed that its management was the main, if not the only function of vitamin D.

In view of the fact that the word "calcium" did not even appear in last week's installment about the "sunshine vitamin", it may appear questionable, whether it would even be worth taking a closer look at the soft gray alkaline earth metal. As a SuppVersity reader who has read my previous articles about calcium, you will yet be aware that this would be as inappropriate as the shortsighted idea that the only function of 25OHD was to control the amount of calcium in your blood and bones.

There is more to calcium than bone health, but is glucose management part of the "more"?

There is in fact a plethora of studies to suggest that dietary calcium (specifically from dairy products; see Fumeron. 2011) and, in some cases, also supplements could have beneficial effects on the blood glucose levels of healthy and diabetic subjects (in some cases w/, sometimes w/out vitamin D supplementation; e.g. Pittas. 2007).

You can learn more about this topic at the SuppVersity

Proteins, Peptides & Blood Glucose

SFA, MUFA, PUFA & Blood Glucose

Vitamin D & Diabetes

Glucose Manager Calcium?

Read these ➲ while waiting

Fat to Blunt Insulin?

Vitamin D unquestionably is a top candidate for t One of those vitamin D + calcium studies was conducted by Joanna Mitri et al. in 2011. In their study, the researchers tested the effects of  2000IU vitamin D (cholecalciferol) in conjunction with 2x400 mg calcium per dayt on the pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes. The marginal improvements in β cell function minimal attenuation of the rise in HbA1c Mitri et al. observed in the course of the 16 week study are yet by no means what study titles such as "Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications." (Zemel. 2002) would suggest.

The reasons for this discrepancy will yet become obvious, if we take a look at the results from well-controlled animal trials: While there is albeit inconclusive evidence that high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain, and conclusive evidence that they can promote a modest energy loss through increased fecal fat excretion (Soares. 2010), papers that would confirm direct beneficial effects of calcium on glucose metabolism are rare: Even the often-cited effects Beaulieu et al. observed in a 1993 study are "vitamin D depenent", i.e. they occur only when the subjects are vitamin D depleted (interestingly, these observations were made in the absence of vitamin D supplementation; cf. Beaulieu. 1993).

Protein or calcium: Specifically in the case of the "dairy calcium" studies it's difficult, in many cases even impossible, to know whether the beneficial effects on blood glucose homeostasis are brought about by their high calcium and not by their high protein content and/or quality. Intervention studies with high calcium intake as a single variable, on the other hand, are scarce. It's thus most likely that it's the synergy of the two - a synergy you can get in concentrated form from dairy protein supplements (see box in the bottom line).

At least in the case of calcium supplements, the following examples from the contemporary scientific literature do thus not support the often-heard claim that calcium supplements would have beneficial effects on insulin sensitivity:

• As an adjunct to an energy reduced diet, 1,000mg/day of supplemental calcium will have no effect on either insulin sensitivity or the changes in body composition (Shalileh. 2010).

I guess one of the most important reasons that the myth of the anti-diabetic effects of calcium supplements are so die-hard is the difference between the short and long-term effects of high calcium meals vs. diets:

• Acutely, calcium supplements will have "beneficial" effects on the postprandial expression of hormones that are involved in the control of blood glucose, because it will augment the postprandial production of glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1).

  

  Figure 1: Difference in plasma GIP, GLP, insulin, glucose, lactate and NEFA levels after the ingestion of a standardized breakfast w/ 248mg vs. 1,239mg calcium (Gonzalez. 2013).

  As you can see in Figure 1, the downstream effects of isocaloric breakfasts providing 0.5 g carbohydrate/kg body mass (energy: 1,258 ± 33 kJ, 299 ± 8 kcal; protein: 11 ± 0 g; carbohydrate: 41 ± 1 g and fat: 10 ± 0 g) with either 248mg or 1,239mg of calcium on the blood glucose levels of the young, healthy, physically active study participants of the Gonzales study are negligible.

The increase in GLP-1 & Co is still not useless: On the contrary, it's not unlikely that ~150% increases in postprandial fatty acid oxidation and the protein sparing effects of dairy calcium Nicola Cummings et al. observed in a three-way cross-over study in which subjects were randomly provided breakfast meals either low in dairy Ca, high in non-dairy Ca (calcium citrate; see figure to the left, values expr. rel. to low CA), or high in dairy Ca are eventually triggered by said changes in GLP-1 & Co (Cummings. 2006).

• In the long run, on the other hand, any beneficial effects on blood glucose management (if they occur at all) are probably "side effects" of the accumulating beneficial effects on lipid metabolism, body weight and energy balance of high calcium diets. It is furthermore not clear to which extend these benefits are eventually driven by additional / synergistic nutrients in dairy - the "calcium source of choice" in ~90% of the pertinent long(er) term studies.

If you take a look at the list of "high calcium" foods, which ranges from dairy (obviously), over broccoli, kale, water cress, peas, beans, almonds, brazil nuts, to sardines, salmon, apricots, and figs, it's actually no wonder that eating a diet that's naturally high in calcium is going to be beneficial for your glucose metabolism.

If, on the other hand, the addition of a bunch of calcium carbonate pills on top of the standard (obesogenic) Werstern diet, would protect you against diabesity, those 5% of the US population who are taking calcium or calcium containing supplements on a regular basis (Radimer. 2004) would have to be lean and insulin sensitive... needless to say that this is not the case, right?

Mind your total Ca intake if you use dairy protein: Unless you have been bamboozled into buying overpriced overprocessed specialty whey & casein products, the latter can easily provide you with a whopping 200mg (whey) and 500mg (casein) of calcium per serving... maybe another reason they help you to get and stay lean and insulin sensitive?

So what's the verdict then? When all is said and done, there are two fundamental conclusion you can take home from today's fourth installment of this series (browse the previous installments). The first one is that there is ample evidence that (a) a sufficient intake of calcium (800-1200mg total) is an important prerequisite for optimal glucose management and that (b) high calcium meals, due to their GLP-1-powered (learn more about GLP-1) thermogenic and "fat burning" effects are another valuable tools in your weight loss toolbox.

The second one, on the other hand, will probably sound less exciting to the supplement maniacs among the SuppVersity readers. Conclusion #2 is after all: If you are eating a whole foods diet with significant amounts of dairy and leafy greens in it, and consume a calcium containing mineral water (in Germany 90% of the tapwater qualifies as "mineral water), the use of supplements is at best useless, at worst detrimental to your health (think of the rumors about Ca supps and Prostate cancer, for example).

References: 

• Beaulieu, Christine, et al. "Calcium is essential in normalizing intolerance to glucose that accompanies vitamin D depletion in vivo." Diabetes 42.1 (1993): 35-43. 
• Cummings, Nicola K., Anthony P. James, and Mario J. Soares. "The acute effects of different sources of dietary calcium on postprandial energy metabolism." British journal of nutrition 96.01 (2006): 138-144.
• Fumeron, Frédéric, et al. "Dairy consumption and the incidence of hyperglycemia and the metabolic syndrome results from a French prospective study, Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR)." Diabetes Care 34.4 (2011): 813-817.
• Gonzalez, Javier T., and Emma J. Stevenson. "Calcium co-ingestion augments postprandial glucose-dependent insulinotropic peptide1–42, glucagon-like peptide-1 and insulin concentrations in humans." European journal of nutrition (2013): 1-11.
• Mitri, Joanna, et al. "Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial." The American journal of clinical nutrition 94.2 (2011): 486-494.
• Pittas, Anastassios G., et al. "The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults." Diabetes care 30.4 (2007): 980-986.
• Soares, Mario J., and Wendy L. Chan She-Ping-Delfos. "Postprandial energy metabolism in the regulation of body weight: is there a mechanistic role for dietary calcium?." Nutrients 2.6 (2010): 586-598.
• Shalileh, Maryam, et al. "The influence of calcium supplement on body composition, weight loss and insulin resistance in obese adults receiving low calorie diet." Journal of research in medical sciences: the official journal of Isfahan University of Medical Sciences 15.4 (2010): 191.
• Zemel, Michael B. "Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications." Journal of the American College of Nutrition 21.2 (2002): 146S-151S.

Quackery or Solid Science: The Zinc Tally Test - Does it Work? How Does It Work? And How Reliable is It?

"Any idea if zinc tally test is reliable? Google spits somewhat mixed conclusions." That's what SuppVersity reader David Salda asked two days ago on the SuppVersity Facebook Page and this article is a somewhat lengthy answer to a short, but very valid question.

I know that only few of you are running a website, let alone one with daily updates, but if you do you the following incident may sound vaguely familiar: You are just trying to keep up with the comments on questions on the Facebook page of your website, when an innocent question like "Any idea if zinc tally test is reliable? Google spits somewhat mixed conclusions." someone (in this case David Salda) posted on your Facebook wall, reminds you of the written, yet never finalized and published articles that lie dormant in the depth of your website's draft folder... don't get me wrong, this is unquestionably a good thing - I mean I guess there will be more people than David, who would like to have the following two questions answered, correct?

How does the Zinc Tally Test work?

Actually the procedure is pretty straight forward. You hold a 10ml solution of zinc sulphate hydrate in a distilled water base (can be bought at the pharmacy) in your mouth for 10 seconds (don't swallow it!) and see how it tastes: (1) If you don't taste anything you are zinc deficient, (2) if there is no immediate taste, but a furry/dry mineral taste develops, your are low on zinc, (3) if a definite taste is detectable right away, you are supposedly in the lower normal range, and (4) if a strong unpleasant taste is immediately present, you got plenty of zinc already.

Is the Zinc tally test an adequate means to test whether you should Supplement W/ Zinc?

No. While it cannot be totally excluded that you can identify individuals with low zinc status on the basis of the Zinc Tally Test the scientific evidence for the accuracy of this method is clearly insufficient, highly conflicting and in large parts bugged with the usual methodological flaws you see in studies on topics most allopath would deem nuturapathic *bs*.

Take a short cut to the answer to your question: If we take into consideration the currently available literature (an ebook someone sells on his own website is no "literature"), there is little to add to the conclusion the researchers from the Southern Cross University in Lismore,  Australia fomulate in the abstract of their study: Despite being widely used, the Zinc Tally Test does is not sensitive and specific enough to assess marginal zinc status in humans. It's thus not really surprising that a 1999 study by Jenna Jameson shows that its results don't even correlate with with dietary zinc intake (Jamison. 1999)

In 2012 Gruner & Arthur conducted a systematic review of the available literature in which they included only studies which provide full reports of clinical trials comparing the tally test (ZTT) to at least one other zinc test within the same sample population. The mere number of studies which matched these more or less self-evident minimum requirements, is telling, already: "3", in words "three" studies matched the criteria of inclusion.

If your breakfast looks even close to this extraordinary beans, eggs and bacon breakfast, it's him time that you learn and apply(!) the "Three Simple Rules of Sensible Supplementation" | more

"Study I compared the ZTT with sweat zinc in patients with food intolerance, reporting moderate correlation. Study II recruited pregnant women using the ZTT and serum zinc to assess zinc status, with above 70% congruence between the two tests at the start of the trial and 100% congruence at the end. Study III also recruited pregnant women at three stages during gestation, assessing ZTT and leukocyte zinc initially, later adding dietary zinc intake and at delivery cord blood zinc. No significant correlation was found between the results of these different methods; however, statistically significant differences in the ZTT responders (tasters and nontasters) were found for pregnancy outcomes." (Gruner. 2012)

And guess what: Even these studies suffered from all sorts of methodological problems. The laboratory assays that were used in the studies lacked sensitivity to zinc status. They were poorly standardized and did often deviate from the original design of the zinc tally test as it is described on the Internet.

Zinc deficiency alters general taste acuity - but not in a linear / reliable fashion

Something else that's worth mentioning in this context is the influence of low zinc levels on taste acuity in general. While the number of respective studies is not exactly high, there is good evidence that subjects with a generally impaired ability to taste tend to have lower zinc concentration in the blood and exhibit a lower ratio of apo/holo-activities of angiotensin converting enzyme (ACE), a zinc dependent enzyme in the serum (ACE ratio), than controls (Ueda. 2006). A 2010 follow up study did yet reveal that a definitive correlation between serum zinc levels and the scores on a visual analogue scale for the severity of the symptoms of did not correlate in after supplementation - whether zinc is the the cause or as so often just a corollary factor is therefor still in the open (Takaoka. 2010)

Suggested: " Zinc: 15mg Are Plenty - After 120 Days Rodents on Diets Containing 2xRDA of Zinc Develop Metabolic Syndrome" | more

Bottom line: While it stands out of question that the zinc tally test should not be your method of choice, when it comes to testing your zinc status, the observation Ueda et al. and Takaoka et al. made with respect to the ratio of apo/holo-activities of angiotensin converting enzyme (ACE) could actually be used as a measure of your zinc status. It would provide an alternative and accurate tests to determine the adequacy of your dietary zinc intake.

That's at least what the results of a 2012 experiment by Sarakura et al. in the course of which mice were zinc depleted for 9 days would suggest (Sarakura. 2012). The ACE ratio would thus be #4 on the list of tests that are considered to reflect the zinc status human beings more or less adequately. The other three tests are plasma, urinary, and hair zinc analysis (Lowe. 2009).

References:

• Jamison, JR. Mineral Deficiency: A Dietary Dilemma? Journal of Nutrition and Environmental Medicine.1999; 9(2):149-158.
• Lowe NM, Fekete K, Decsi T. Methods of assessment of zinc status in humans: a systematic review. Am J Clin Nutr. 2009 Jun;89(6):2040S-2051S.
• Sarukura N, Takai S, Ikemoto S, Korin T, Ueda Y, Kitamura Y, Kalubi B, Yamamoto S, Takeda N. Effects of dietary zinc deprivation on zinc concentration and ratio of apo/holo-activities of angiotensin converting enzyme in serum of mice. Auris Nasus Larynx. 2012 Jun;39(3):294-7.
• Takaoka T, Sarukura N, Ueda C, Kitamura Y, Kalubi B, Toda N, Abe K, Yamamoto S, Takeda N. Effects of zinc supplementation on serum zinc concentration and ratio of apo/holo-activities of angiotensin converting enzyme in patients with taste impairment. Auris Nasus Larynx. 2010 Apr;37(2):190-4.
• Ueda C, Takaoka T, Sarukura N, Matsuda K, Kitamura Y, Toda N, Tanaka T, Yamamoto S, Takeda N. Zinc nutrition in healthy subjects and patients with taste impairment from the view point of zinc ingestion, serum zinc concentration and angiotensin converting enzyme activity. Auris Nasus Larynx. 2006 Sep;33(3):283-8.

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...

That's 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 citizen's 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, it's probably wise to point out that fortified foods are the link between the DV's 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 don't actually want me to answer this question - do you? I mean let's 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 let's be honest: Wouldn't 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.

Science Round-Up Seconds: The Macro-Mineral Alphabet & the Potential Health Hazards of Diet-Induced Latent Acidosis

You lose 600x more sodium than magnesium during a workout. The RDA is yet only ~3-4x higher (Montane. 2007).

If you already listened to the podcast of yesterday's installment of the SuppVersity Science Round Up (if you have not already done so, you can dowload the podcast, here), you may have noticed that I confused the minimal potassium (K) to sodium ratio (Na), which is probably ~1:1, and the "original" K:Na ratio in the "paleo diet".

According to Sebastian et al. (2002) the latter is ~8-9:1 in other words: 8-9 mols of potassium per mol of sodium. That's miles apart from the 1:2-3 ratio the average Westerner (the exact ratio varies depending on which study you refer to) uses as a springboard to hypertension ;-)

The (un-)definite mineral synergism/antagonism chart

Another thing you may have noticed with yesterday's show is the fact that the show was pretty "topic centered". My personal feeling is that it has a much better flow this way and that not despite, but because Carl and I did not cover such a broad range of topics. I cherish the hopefully non-futile hope that you feel the same but am obviously open for any constructive criticism from your side

The SuppVersity macro mineral chart provides a general overview of the complex interactions that exist between calcium, phosphorus, magnesium, sodium, chloride, and potassium (compiled based on various sources)

. This, by the way, does also apply to the corresponding installment of the Seconds, of which you will soon realize that it is not a non-related add-on, but will expand, explain and summarize interesting aspects we've covered in the live show (note: from next week on the Science Round-Up will air at 12 PM EST, the same URL as usual).

On that note, let's start with an "expansion" I already promised to deliver towards the end of the show: some information on the synergism and antagonism of the macro minerals. It's a pretty complex matter and the following illustration is based on generalizations. Some of them, like the low-level exception to the antagonism between calcium and magnesium, of which I believe that it is important to know are explicitly mentioned, others are not.

A very good example of the former, i.e. the important second order interactions is the influence sodium has on the antagonism between potassium and magnesium. The latter disappears, when sodium levels are high and magnesium is needed as a sodium antagonist. Similarly, the often-touted antagonism between magnesium and calcium is actually a co-factor relation, where any "antagonism" is only the result of imbalances between the two.

The good, the bad and the ugly: Just a question of the "wrong" perspective

One thing that should actually be obvious, but is often ignored in all the hoopla about the "good" and "bad" guys among the macro-minerals is that "antagonisms" do not contradict the essential nature of all of the electrolytes, which are - antagonistic or not - in the end, all actors in the same metabolic play.

Figure 1: Average ratio of mineral content (new:old) of 20 vegetables and 20 fruit: data based on comparison of  UK Government’s Composition of Foodsdata at two-time points separated by approximately 50 years (Mayer. 1997)

I mean, take calcium and phosphorus as an example, they are both essential for the structural integrity of your bone and the fact that calcium has a reputation of being the "good guy", while phosphorus is the "bad guy" is just a necessary consequence of the overabundance of the latter, i.e. phosphorus from grains, soft drinks, dairy products, meats, fish, seeds, nuts, eggs and due to the change in mineral ratios (cf. figure 1) even most fruits and vegetables in the food chain of Mr. Joe Average, these days.

According to a 2009 paper by Dana Cordell et al. this may well change in the not all too distant future, after all "the quality of remaining phosphate rock is decreasing and production costs are increasing" (Cordell. 2009). With estimates saying that the demand for phosphorus is going to double within the next 40 years, it stands to reason that the decried overabundance of phosphorus, which is, among other things, also responsible for lowering the zinc content of the produce (cf. Peck. 1980) may be partly reversed within the next decades... I mean, we all know that nothing is as "convincing" as with financial interests, right?

The strong ion difference determines your pH levels

What's the difference between macro-minerals and their "little brothers" the trace minerals? Calcium, sodium, potassium, phosphorus, magnesium, chloride and sulfur are macro-minerals because you need them in amounts that are greater than 100mg per day. Of the trace minerals, on the other hand, you need less (in most cases much less) than 100mg per day. That does not mean though that Iron, zinc, copper, chromium, fluoride, manganese, iodine, molybdenum and selenium were less important - it's merely a quantitative distinction.

While it stands to reason that there is a reason, calcium, sodium, magnesium, and potassium are also called "electrolytes", astonishingly few people can actually give an ad hoc explanation why this is the case - and that despite the fact that their lives depend... no, not on the answer, but on the existence and physiological function of electrolytes ;-)

If you have listened closely to your physics teacher, you will yet probably be aware that an "electrolyte" (electro- ~ charge, -lyte ~ carrier) is a positively or negatively charged molecule (ion) and nothing out of the ordinary in nature.

In your body electrolytes are used to establish ionically charged gradients, similar to the gradient that exists between the positive and negative pole of a battery. These gradients are situated on the cell membranes in excitable tissues, such as muscle and verve, where they facilitate or hinder the influx/efflux of other charged particles.

One of these gradients, in fact probably the physiologically most significant one, by the way, is established by positive sodium (Na+) and potassium (K+) ions and their negative counterpart chloride (Cl-) - exactly those electrolytes you've heard about in yesterday's show (remember: whenever you hear "salt" it actually means Na + Cl).

The electrolytes are not the only charged particles ...

From your chemistry lessons, you may remember that there are not just ionic atoms, but also ionic molecules and that the electron configuration of these particles will determine how they bind, interact and react. But I guess, we have had more than enough complicated theory for today, so if you want to know how the anions and how the strong ion difference (SID) is calculated, check out this brief overview over at acid-base.com.

Rather than going into the details of the mechanism, I decided that it would probably of greater value to wrap the Seconds up with a brief overwiev of the downstream effects of a metabolic state, of which Pizzorno, Frassetto and Katzinger point out that it is not necessarily characterized by acedemia, i.e. pH levels below the "magic" (if we were honest, we'd you'd have to write arbitrary, here) cut-off limit of pH 7.35:

High intensity exercise can also lower your blood pH, an effect you can counter with sodium bicarbonate

"Acidosis only becomes acidaemia when compensatory measures to correct it fail. To illustrate the difference between acidosis and acidaemia, take the following example: two processes occurring simultaneously in the same individual, such as a respiratory acidosis combined with a metabolic alkalosis. In this case, if the respiratory trend toward acidosis is greater than the metabolic trend, a pH of less than 7·35 may be reached, and would be considered acidaemia, despite the presence of a metabolic alkalosis. The intensity of each ‘process’ will determine the pH, but the terms themselves (acidosis, alkalosis) do not indicate a certain pH." (Pizzorno. 2009)

In other words, you don't have to suffer from diabetic or otherwise pathogenic "acidosis", to suffer from one of the following ill health-consequences:

• 

  Hip fracture incidence per 100,000 study participants; aggregated data from cohorts from 33 countries (Frassetto. 2001)

  Calcium loss, bone loss, osteoporosis - Unfortunately, this is not only the best-known side effect of "being too acidic", it's also the only one people take seriously. In that, scientists and lay press alike have zoned in on the high intake of animal proteins as the main confounding factor. But despite the fact that the high sulfur content (methionine, cysteine & co) does certainly contribute to the problem, the data in the figure at the right should make it quite clear that the stuff we eat and don't eat with our meats is at least as much to blame for the misery. In view of the fact that
  

  "[...] cereal grains themselves are net acid-producing and alone accounted for 38% of the acid load yielded by the combined net acid-producing food groups in the contemporary diet" (Sebastian. 2002)

  the average (processed) grain addicted US citizen with his/her quasi-non-existent vegetable intake would end up way on the left side of the x-axis of the graph on the right-hand side, even if he ate not a single gram of animal protein - we would just have to relabel the axis to vegetable/acidd forming food intake (including grains!)".
• Increased renal nitrogen excretion and hampered protein synthesis - One of the less known effects of an increased acid/base ratio is an increase in nitrogen excretion that will obviously not simply hamper your gains, but can also set you up to sarcopenia (age-induced muscle loss).
  
  

  

  Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women (Frassetto. 1997)

  In the end, the excretion of nitrogen is nothing, but an adaptive mechanism and a consequence of the catabolism of tissue protein. It is, if you will, a basic necessity for your body to rob your muscle and other tissue of glutamine and all other amino acids, that can be convert to glutamine in the liver, from where it is delivered to the kidney where it's used to synthesize ammonia and excrete the potentially toxic acid load. This will obviously mitigate the severity of the acidosis, it does yet also entail a net loss in muscle and organ protein that cannot be compensated for by an increase in acid forming protein in your diet.
  
  As the data in the figure to the right goes to show you this is a process that's regulated on a day to day basis and the relief in nitrogen loss (data in mg/day/60kg) provided by bicarbonate supplementation (days 0-18) is transient and disappears as soon as you return to your regular low-base, high acid diet (days 19-30).
• Impairments of the growth hormone / IGF-1 axes - Brunnger et al. tested in 1997 whether experimental acidosis would have an effect on the growth hormone / IGF-1 axis and observed a "significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3", which points towards an acid induced "primary defect in the growth hormone/IGF-1 axis" that occurs "via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone" (Brunger. 1997). Interestingly, Mahlbacher et al. were able to show that the administration of IGF-1 can in turn ameliorate acidosis and thus correct the previously discussed nitrogen wasting (Mahlbacher. 1999).
  
  

  

  Learn more about the effects of GH, IGF1 and it's splice variants MGF & co and their influence on skeletal muscle hypertrophy in the respective part of the Intermittent Thoughts on Building Muscle (go to the overview).

  In fact, potential physiological effects of the acid-induced impairment of the GH / IGF-1 axes had been observed much earlier, already. McSherry et al. for example report in a 1978 article in the Journal of Clinical Investigations that children with short stature and classic renal tubular acidosis developed normally, when they were treated with adequate amounts of alkalizing agents.
  
  That similar negative effects can be observed even in the presence of "low-grade 'tonic' background metabolic acidosis" was confirmed by Frassetto et al. who observed statistically significant increases (+11%) in 24-hour mean growth hormone secretion in post-menopausal women with diet-induced low-grade metabolic acidosis, when their dietary acid load was neutralized with adequate amounts of potassium bicarbonate (Frassetto. 1997).
  
  In a subsequently published study the scientists argue that the concomitantly observed increases in osteocalcin and bone metabolism would confirm the physiological significance of these changes (Frassetto. 2001). The effects on bone add to the well-known beneficial metabolic effects of growth hormone ( and line up with the recently reported association between low growth hormone levels and memory impairments (Wass. 2010).
  
  In view of the bad press GH and IGF1 are getting, it is important to point out that we are talking about a normalization of the GH/IGF-1 axis, here. It is therefore unlikely that the restoration of a normal acid-base balance will have any of the anti-longevity and pro-cancerous (see next bulletin point) effects of growth hormone and IGF-1 you may have read about in the pertinent literature.
• Potential protective / anti-cancer effects - While conclusive scientific evidence for the involvement of low-grade acidemia in the etiology of cancer is still missing, it has long been speculated that the genetic and epigenetic perturbations, which will turn normal cells into cancer cells may be triggered (among other factors) by disturbances in the acid-base equilibrium. As Ian Forrest Robey points out in his 2012 review of the literature, a diet induced
  

  "[a]cid-base disequilibrium has has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion." (Robey. 2012)

  If you want to learn more about the "state of the art research" on the potential link between latent dietary acidosis and the development of cancer, I suggest you simply read the free fulltext of the paper on PubMed. 

I guess, now that you've learned about some of the intricacies of adequate mineral intakes and balances, the acid / base balance, nitrogen and bone loss, growth hormone and cancer, and listened to the interactions of sodium blood pressure, blood glucose and insulin on yesterday's show, it's about time to come back to the simple things that work - the bottom line, so to say...

"What was that about the nutrient sufficiency of the vegetarian / vegan diet, you said on the air?" The above figure shows the % of omnivores, vegans and vegetarians who meet the RDAs  for protein and fiber and selected vitamins and minerals (DiMarino. 2013)

Bottom line: A whole foods convenient-"food" free with the right balance of vegetables, protein, and a reasonable amount of complex largely unprocessed carbohydrates, fats and fruits - call it "ancestral" or "paleo", if you will - is going to provide you with all the minerals you need, it will contain them in the right ratios and supply your body with all the co-factors it needs to use them. It will stabilize your pH levels, normalize your growth hormone / IGF-1 axis and is beyond any doubt the most effective way to get and stay in shape, to reduce your cancer risk, ward off diabetes and lead a life that's not simply long, but also worth living.

If you adhere to these simple rules, there is no reason to be worried about "not getting your minerals" and other essential nutrients. After all, this is what distinguishes you from the "average" western omnivore, vegetarian or vegan who fails to meet most of his or her nutrient requirements.

References:

• Brungger M, Hulter HN, Krapf R. Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone in sensitivity in humans. Kidney Int. 1997; 51:216–221
• Cordell D, Drangert J-, White S. The story of phosphorus: Global food security and food for thought. Global Environ Change. 2009;19(2):292-305.  
• DiMarino A. A Comparison Of Vegetarian Diets And The Standard Westernized Diet In Nutrient Adequacy And Weight Status. The Ohio State University. A Thesis Presented in Partial Fulfillment of the Requirements for Graduation with Distinction from the School of Health and Rehabilitation Sciences of The Ohio State University. 2013. 
• Frassetto L, Morris RC, Jr., Sebastian A. Potassium bicarbonate reduces urinary nitrogen excretion in post-menopausal women. J Clin Endocrinol Metab. 1997: 82:254–259.
• Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13.
• Mahlbacher K, Sicuro A, Gerber H, Hulter HN, Krapf R. Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. Metabolism. 1999; 48:763–770
• May RC, Kelly RA, Mitch WE. Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism. J Clin Invest. 1986. 77:614–621.
• Mayer AM. Historical changes in the mineral content of fruits and vegetables. British Food Journal. 1997; 99(6):207 - 211
• McSherry E, Morris RC, Jr. At tainment and maintenance of normal stature with alkali therapy in infants and children with classic renal tubular acidosis. J Clin Invest. 1978; 61:509–527. 
• Montain SJ, Cheuvront SN, Lukaski HC. Sweat mineral-element responses during 7 h of exercise-heat stress. Int J Sport Nutr Exerc Metab. 2007 Dec;17(6):574-82.
• Peck NH, Grunes DL, Welch RM, MacDonald GE. Nutritional Quality of Vegetable Crops as Affected by Phosphorus and Zinc Fertilizers Agron. J. 1980; 72: 528–534.
• Pizzorno J, Frassetto LA, Katzinger J. Diet-induced acidosis: is it real and clinically relevant? Br J Nutr. 2010 Apr;103(8):1185-94.
• Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr. Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Am J Clin Nutr. 2002 Dec;76(6):1308-16.
• Wass JA, Reddy R. Growth hormone and memory. J Endocrinol. 2010 Nov;207(2):125-6.
• Williams B, Layward E, Walls J. Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis. Clin Sci. 1991; 80:457–462