Who Wants To Live Forever? 5+ Survival Techniques That Will Help You Make it Past the 100 Year Margin Healthily!

This article will teach you how to make sure you'll see your great, great grand children.

This is one of the many things I have learned from my good friend Carl Lanore, whose radio show, Super Human Radio, I have been following for years before I became what Carl once called "semi-famous": We, that is humans in general and researchers in particular, tend to focus way too much on the sophisticated, the innovative and the revolutionary stuff, when oftentimes the answer to ostensibly open question is lying openly before our eyes. Athletics and bodybuilding, is one of these areas, where practitioners have been doing everything right for decades... and what was their reward? World-records and mind-boggling physiques, for example.

This is yet by no means the only example. The "paleo movement", as bizarre and disfigured as it may have become does still exemplify that the same can be said of "healthy eating", as well.

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There have always been people who (instinctively?) knew how to do it - hell, even the hailed Mediterranean Diet is no invention of brainy scientists (certainly not of dumb dietitians). And when we are honest, we don't need websites like Longecity and tons of useless supplements to make the most of our genetic longevity potential: We all know what we should do, but unfortunately, many of us tend to forget that we don't do what it takes to join the ranks of those people about whom Marilynn Larkin wrote in their 1999 paper "Centenarians point the way to healthy ageing" (Larkin. 1999).

Today's SuppVersity article is an homage to these people and the well-known but often overlooked research on what helps and hinders us from joining the ranks of people like Betsy Baker (supposedly 113, when she died in 1955), Marie-Louise Meilleur (supposedly 117, when she died in 1988) or Jiroemon Kimura (supposedly 116, when he died last year). I mean, they must have done many things right and only a few things wrong, right? Based on the contemporary evidence, I've compiled a list of rules. I guess, neither Betsy or Marie-Louise, nor Jiroemon will have followed all of them to the "T", but hey, this leaves room for you to decide whether you'd rather indulge in one or another passion or stick to all of them to the "T" top Marie-Louise's 117 or Jiroemon's 116 years of age :-)

• Use the available medical care to your advantage: Within the health and fitness community, the things our regular doctors can do for us have gotten a surprisingly bad rep. It does, however, stand out of question that the availability and use of modern medicine is one of the cornerstones of the ever-increasing longevity in centennials and other healthy elderly. From basic treatments to complicated operations, all these things the availability of which we usually take for granted has helped us (and the living centenarians) to do what Thomas Perls calls "to ‘compress morbidity’ and live most of our lives in good health, with only a short period of ill health at the end." (Perls. 1999)

  

  Figure 1: Luckily, your place of birth is not the only determinant of life expectancy; map depicts life expectancy (in years) at birth (created by Panagiotis V. Lazaridis based on WHO & CIA data in 2008)

  At first this may contradict findings Engberg et al. present in a paper with data from a 29-year follow-up of hospitalizations among 40 000 Danes born in 1905, but in the end, it should be obvious that the low hospitalization rates, the Danish researchers observed in centenarians and almost centenarians were rather a consequence than a cause of their longevity and probably also due to timely non-stationary medical interventions, when one of them actually got sick (Engberg. 2009)
• Don't smoke, or quit smoking: I know this should be obvious, but I guess too many people still believe that they must belong to the lucky few Lewin and Crimmins, the authors of a recent paper with the intriguing title "Not All Smokers Die Young: A Model for Hidden Heterogeneity within the Human Population." (Lewin. 2014) are interested in. Contrary to these (allegedly) genetic outliers, the majority of us will suffer a significant reduction in life expectancy. Estimations of the number of years you'll lose range from a handful of years to up to 25% (Rogers. 1991). For a US citizen, the latter would equal almost 16 years! Years, of which Susan T. Stewart et al. (2009) say that the average 18-year-old may reclaim 3.76 life-years and, more importantly, 5.16 quality-adjusted years, in which he or she is not hospitalized and wasting away if they managed to avoid the getting overweight/obese instead.

Eat fish, if you can't stop smoking: The -50% reduction in mortality risk for fish eating heavy smokers vs. people who smoke and have a low fish consumption as it was reported by Rodriguez et al. in 1996, actually raises the question whether it wouldn't make more sense to put images of deliciously prepared salmon on cigarette packets - instead of the tar-black lungs and foul body parts, obviously.

• In fact, the increase in BMI after smoking cessation "overwhelmed the positive effects of declines in smoking in multiple scenarios" Stewart et al. calculated and reduced the benefits for an 18-year old to 0.71 years or 0.91 (Stewart. 2009).
  
  But don't worry, other studies report much more beneficial effects. Taylor et al. (2002), for example, estimate that the life expectancy among smokers who quit at age 35 will exceed that of continuing smokers by 6.9 to 8.5 years for men and 6.1 to 7.7 years for women. And in spite of the fact that early smokers will obviously realize greater gains in life expectancy, even those even those who quit much later in life gained some benefits: among smokers who quit at age 65 years, men gained 1.4 to 2.0 years of life, and women gained 2.7 to 3.7 years.
• Avoid drinking alcohol in amounts >0.5 glasses of wine per day: Notwithstanding the overcited epidemiological evidence which suggests that a moderate alcohol consumption will have beneficial effects on your life-expectancy, the margin between "just enough" and "already too much" is simply too narrow for me to suggest you drink more than the literal half glass of wine that's supposed to lower the all-cause mortality risk of women by ~20-25% (Streppel. 2009).
  
  

  

  Table 1: Relative Risk for Major Chronic Disease Categories, by Gender and Average Drinking Category (Rehm. 2002)

  A high(er) level of alcohol consumption, on the other hand, has been found to be associated with a higher risk of hypertension, alcoholic cardiomyopathy, cancer, cerebrovascular events and dementia (Kloner. 2007) - a fact that should remind you that (a) the evidence regarding the possible health benefits of alcohol is uncertain and that (b) alcohol may not benefit everyone who drinks. Theoretically, genetic polymorphisms that make alcohol the panacea for one, could turn an in innocent glass of wine into a deadly poison for someone else (Hashimoto. 2002).
  
  And just in case the ambiguity of data ain't reason enough for you to let go of all alcoholic beverages on at least360 of 365 days of the year, the data in Table 1 may convince you.
  
  If you take a closer look at "Drinking Category I", where you'll find all the women who consume 0–19.99 g pure alcohol and all the men who consume 0–39.99 g pure alcohol every day (a glass of wine has ~13g), you will see that alcohol increases the risk of liver cirrhosis by 26%, hypertensive diseases and other CVD by 40% and 50%, is associated with 34% and 23% higher risk of epilepsy for women and men, respectively and increases the risk of all cancers esp. those of the esophagus (+80%) significantly.
  
  I am not sure about you, but for me, this alone would be enough to get my sleep, diet and exercise regimen in check instead of trying to use alcohol as a means to reduce my CVD risk.
• Attend to relationships and friends: Individuality has become on of the / the (choose for yourself) highest good(s) of Western civilization and few people are aware that we are paying a very high price for that. The influence of social relations on mortality is, after all, well documented. A meta-analysis of 148 studies (308,849 participants followed for an average of 7.5 years) confirms that the quality of our social networks significantly predicts mortality (Holt-Lunstad. 2010).

  

  Figure 2: Weighted avg. effect sizes across different measures of social relationships (Holt-Lunstad. 2010).

  People with social relationships defined as adequate are 50% more likely to survive than older adults with social relationships defined as poor or insufficient. The overall effect remains consistent across age (see Figure 2).
  
  It is yet still unclear whether specific types of relationships are more advantageous than others. Giles et al. (2005) showed that the beneficial association between social networks and survival among elderly people may be restricted to relationships with friends and confidants rather than with children and relatives. In a meta-analysis of 53 prospective observational studies on older adults, marriage or support from a partner was found be a significant independent predictor of survival; the overall reduction in mortality risk was 9–15%. However, this association was statistically significant in only half of the studies (Manzoli. 2007).

Social support is the also key to get lean and stay lean... at least for men In view of the fact that staying lean is one of the most important longevity promoters, these days, it's actually only logical that a lack of emotional support is associated with a 98% increased obesity risk. What's astonishing is that this is not the case in women, where divorce and thus "being back on the market" will actually reduce a woman's risk of becoming obese by a whopping 61% (Oliveira. 2013)!

• As Rizzuto & Fratiglioni (2014) point out, one hypothesis suggests that strong social connections can buffer significant stress and protect against stress-related outcomes:
  

  "People might be protected from adopting stress-related lifestyle choices that are detrimental to health, such as smoking, excessive alcohol consumption and sleep loss." (Rizzuto. 2014)

  The main-effect hypothesis postulates that social support is beneficial regardless of the stress level a person is experiencing; in other words, social support can act protectively even before a stressor is experienced. For instance, persons with social support could be influenced to engage in protective behaviors such as exercise.
  
  Moreover, having a wide range of social ties also provides multiple sources of information that could result in more effective use of available health care and services (Cohen. 2004). No wonder, you have, after all, read only a couple of days ago that education is what protects "poor women from fattening effects of rising wealth" in the SuppVersity Facebook News (read more).
• Stay lean and be active, God damn it! There is this unfortunate and die-hard myth of something scientists refer to as the obesity paradox. A term that is misrepresented by overweight journalists and doctors and misunderstood by the ever-increasing number of obese average Joes, for whom the misleading connotations of terms such as "healthy obese" are downright life-threatening. 
  
  And this is not an exaggeration, by the way. If you look at the 30% increase in mortality risk Whitlock et al. (2009) calculated based on a meta-analysis of data from 57 prospective studies that included almost 900,000 adults for every 5-point increase in BMI the attribute "life-threatening" is by no means an exaggeration.

Ladies, listen up! Being underweight is unhealthier than being obese. Trying to equal the anorexic Hollywood "stars" could cost your life! It sounds drastic, but with a 47% increase in mortality risks being underweight women (BMI <18.4) have a higher mortality risk than obese ones (+44% for BMI 30.0 to 34.9; see Berrington de Gonzalez. 2010)

• Although the proportional increase was greater at younger ages (35–59 years), the corresponding increase in mortality for those in their 70s was nearly 30%, and for those in their 80s, it was still 15% - the notion that older people would benefit from being fat is thus simply hilarious.
  
  What's not hilarious, though, is that a certain amount of healthy, well-distributed body fat that's complemented by a decent amount of life-extending muscle mass (20% reduction in all cause-mortality for men >55years w/ a decent amount of lean mass; see  SuppVersity Facebook News | learn more) and a corresponding BMI between 20-27 offers enough energy reserves to draw on, when you're sick and old. It is thus also not surprising that being slightly overweight (obesity starts with BMI >30) is not a risk factor for people aged ≥ 65 years (Heiat. 2001) and certainly better than being what scientists call "underweight", when it's actually only "under-muscled" for the vast majority of elderly individuals who are affected.

Sleep! Enough, but not too long. What you should never forget, is to stick to a regular sleep rhythm - and this means not tho short, but not too long either. While short sleepers, defined as people who get "commonly < 7 h per night, often < 5 h per night," have a 12% higher all-cause mortality than people who sleep 7-8h on a regular basis, lying around in bed too long could eventually cost you more than just your job. According to a recent meta-analysis of data from 27 independent cohort samples, sleeping "commonly > 8 or 9 h per night" is even more dangerous and will increase your risk of dying 'prematurely' by 30% compared to a 7-8h sleeper (Cappuccio. 2010).

• As a SuppVersity reader, you know: The risk for both, being underweight and overweight can be reduced if not nullified by a high amount of daily physical activity (the 10,000 steps mantra) and working out regularly. Being moderately active, alone, for example, was found to be associated with a 3.6x higher chance of "successful [=healthy] aging" in a recent study from the University of Ibadan - for regular vigorous activity, the chance of aging healthily increased by 711% (Gureje. 2014)!

• Miscellaneous, but worth mentioning: This is where I will list everything that popped up on my radar while doing the research, but did not really appear to make a good standalone item in the list. Things like having sex, for example. At least twice a week, to make sure that you don't increase your risk of fatal coronary heart disease by 180%, guys (Ebrahim. 2002). And the results Smith et al. presented 5 years before are even more promising: According to their study, each increase of 100 orgasms per year is associated with a 46% reduction in all-cause mortality risk (Smith. 1997)!

It is obviously true that some of the things that determine healthy aging are (still) out of your reach. Most prominently, your sex! Scientists are yet struggling to explain the underlying reasons of the sex-specific "longevity bias", but contemporary research would suggest that...

"[...]female centenarians likely exploited a healthier life-style and more favorable environmental conditions, owing to gender-specific cultural and anthropological characteristics" (Franceschi. 2000) 

... and do thus depend to a lesser extend on having the right mtDNA haplogroups, Tyrosine Hydroxylase, and IL-6 genes than men.

Figure 5: Yes, genes matter, but there is more (Franceschi. 2003)

Apropos genes, the "typically male" aka sex–dependent genetic predisposition to produce high levels of IL‐6 is about as detrimental to your goal of making it past the "100+ years finish line" healthily, as being born with the nasty "ε4" variety of the apolipoprotein E gene and the corresponding lifelong problems with high blood lipids and an increased risk of cardiovascular disease, Alzheimer's & co (Panza. 1999; Bonafè. 2001).

Other genes that have been highlighted as factors that contribute to exceptional longevity are certain variants of the FOXO3A gene (Flachsbart. 2009), ...

You are stronger than your genes: That's a good thing because it means that you can attenuate if not nullify the increased disease/obesity risk you may be born to (Kilpeläinen. 2011). For far more of us, it's yet rather a bad thing, because they are deliberately throw- ing away their chance to lead a long and above all healthy life by the way they eat, don't exercise and wake all night.

Bottom line: I guess I could list at least a dozen of additional gene of which researchers believe that they were linked to extraordinary longevity (see Sebastiani. 2010), but that would hardly be useful. It could even contradict the message of this article which is "NOT to go to 23andme.com and get tested!".

It's a matter of fact that the most important reason people die fat and sick before their time is because they don't take responsibility for their health ...[deliberate pause] ...and trying to find the cause of your health problems in your genome is the #1 strategy to dig up an excuse that will allow you to put the blame on your parents and grand parents. And this just one day before mother's day! Shame on You! You really think someone blaming his mother deserves to live forever?

References: 

• Berrington de Gonzalez, Amy, et al. "Body-mass index and mortality among 1.46 million white adults." New England Journal of Medicine 363.23 (2010): 2211-2219.
• Bonafè, Massimiliano, et al. "A gender–dependent genetic predisposition to produce high levels of IL‐6 is detrimental for longevity." European journal of immunology 31.8 (2001): 2357-2361. 
• Cohen, Sheldon. "Social relationships and health." American psychologist 59.8 (2004): 676.
• Ebrahim, S., et al. "Sexual intercourse and risk of ischaemic stroke and coronary heart disease: the Caerphilly study." Journal of epidemiology and community health 56.2 (2002): 99-102.
• Flachsbart, Friederike, et al. "Association of FOXO3A variation with human longevity confirmed in German centenarians." Proceedings of the National Academy of Sciences 106.8 (2009): 2700-2705.
• Franceschi, C., et al. "Do men and women follow different trajectories to reach extreme longevity?." Aging Clinical and Experimental Research 12.2 (2000): 77-84. 
• Franceschi, C., and M. Bonafe. "Centenarians as a model for healthy aging." Biochemical Society Transactions 31.2 (2003): 457-461. 
• Giles, Lynne C., et al. "Effect of social networks on 10 year survival in very old Australians: the Australian longitudinal study of aging." Journal of Epidemiology and Community Health 59.7 (2005): 574-579. 
• Gureje, Oye, et al. "Profile and Determinants of Successful Aging in the Ibadan Study of Ageing." Journal of the American Geriatrics Society (2014).
• Heiat, Asefeh, Viola Vaccarino, and Harlan M. Krumholz. "An evidence-based assessment of federal guidelines for overweight and obesity as they apply to elderly persons." Archives of internal medicine 161.9 (2001): 1194-1203.
• Holt-Lunstad, Julianne, Timothy B. Smith, and J. Bradley Layton. "Social relationships and mortality risk: a meta-analytic review." PLoS medicine 7.7 (2010): e1000316. 
• Kilpeläinen, Tuomas O., et al. "Physical activity attenuates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children." PLoS medicine 8.11 (2011): e1001116.
• Kloner, Robert A., and Shereif H. Rezkalla. "To drink or not to drink? That is the question." Circulation 116.11 (2007): 1306-1317.
• Larkin, Marilynn. "Centenarians point the way to healthy ageing." The Lancet 353.9158 (1999): 1074.
• Manzoli, Lamberto, et al. "Marital status and mortality in the elderly: a systematic review and meta-analysis." Social science & medicine 64.1 (2007): 77-94. 
• Oliveira, Aldair J., et al. "The influence of social relationships on obesity: sex differences in a longitudinal study." Obesity 21.8 (2013): 1540-1547.
• Panza, Francesco, et al. "Decreased frequency of apolipoprotein E ε4 allele from Northern to Southern Europe in Alzheimer's disease patients and centenarians." Neuroscience letters 277.1 (1999): 53-56.
• Perls, Thomas T., Margery Hutter Silver, and John F. Lauerman. Living to 100: Lessons in living to your maximum potential at any age. 1st ed. New York: Basic Books, 1999.
• Rehm, Jürgen, et al. "Alcohol-related morbidity and mortality." Mouth 140.208 (2002): C00-C97. 
• Rizzuto, D., and L. Fratiglioni. "Lifestyle Factors Related to Mortality and Survival: A Mini-Review." Gerontology (2014).
• Rodriguez, Beatriz L., et al. "Fish Intake May Limit the Increase in Risk of Coronary Heart Disease Morbidity and Mortality Among Heavy Smokers The Honolulu Heart Program." Circulation 94.5 (1996): 952-956. 
• Rogers, Richard G., and Eve Powell-Griner. "Life expectancies of cigarette smokers and nonsmokers in the United States." Social science & medicine 32.10 (1991): 1151-1159.
• Sebastiani, Paola, et al. "Genetic signatures of exceptional longevity in humans." Science 10 (2010): 1126. 
• Smith, George Davey, Stephen Frankel, and John Yarnell. "Sex and death: are they related? Findings from the Caerphilly cohort study." Bmj 315.7123 (1997): 1641-1644.
• Stewart, Susan T., David M. Cutler, and Allison B. Rosen. "Forecasting the effects of obesity and smoking on US life expectancy." New England Journal of Medicine 361.23 (2009): 2252-2260.
• Streppel, Martinette T., et al. "Long-term wine consumption is related to cardiovascular mortality and life expectancy independently of moderate alcohol intake: the Zutphen Study." Journal of epidemiology and community health 63.7 (2009): 534-540.

Will Glucosamine Make Us Live Forever? Probably Not, But in Mice the Low-Carb Mimetic Effects Make 10% Possible - In Humans, This Would be ~9 Years! Too Good to Be TRUE?

One of the lead scientists is so convinced that the 10% life-extension the resear- chers observed in rodents will occur in humans, as well, that he is already taking glucosamine supps everyday!

Next to not eating at all, not eating any carbs has recently become all the rage in the "how do extend the lifespan of stupid worms"-research all over the world. Now, I am all for eating less carbohydrates than the people who came up with "Your Plate", my American friends consider optimal.

Yes! I am even in for skipping carbs altogether, but not for a lifetime (!) which is what would be necessary to reproduce the life-extending effects Schulz et al. observed in their 2007 study on the effects of carbohydrate restriction on the lifespan of the notorious (not B.I.G but) B.I.R. as in "big bad roundworm" (Schulz. 2007).

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Now, about seven years later, my favorite anti-ROS-theory-of-aging researcher Michael Ristow and his colleagues some of whom had been involved in the previously cited experiment as well was able to show that bathing the worms in glucosamine will elicit similar life-extending effects (Weimer. 2014).

With only 5% the overall increase in life-expectancy was yet significantly lower than in the "carb restriction" study from 2007, but - and that's actually way more important - unlike cutting carbs, which had failed to produce any effects in a rodent model, the mice who received the glucosamine as an adjunct to their diet, when they were already 100 weeks of age (in human years that's approximately 65 years) lived almost 10% longer than their peers in a non-glycosamine-enhanced control group.

Just to make that clear: We are talking about around 8 additional years of human lifespan! If the results translate from a small mouse who does not stuff itself with junk food all day to the average fast-food addicted Westerner, who follows Winston Churchill's motto "No sports!"

Even if the life-extension did not work, though, couch potato and aging athlete will would probably both benefit from the pronounced improvements / amelioration of the age-induced defects in glucose control, which were significantly reduced in the rodents on the high glucosamine groups.

Figure 1: The decreased ATP stores that come with the "low carb mimicry" effect are not exactly what someone who wants to hit the weights in his old age, would want (Weimer. 2014)

Unfortunately, theses improvements in glucose metabolism come at cost. Ristow et al. found out, glucosamine feeding promotes the breakdown of amino acids in both worms and mice - a breakdown of which the scientists say that it is characteristic of the "metabolic state of a low-carb diet".

In view of the fact the both groups of mice consumed identical amounts of carbohydrates, it's thus only logical to assume that the provision of adequate amounts of glucosamine inhibits the use of glucose from the diet and will thus yield similar metbolic (side) effects as a real low-carb diet - yet without having to skip on pasta, pizza and (of course ;-) tons of sweet potatoes.

Figure 2: At normal glucose levels (<35%) glucosamine reduces skeletal muscle  GLUT-4 expression and glucose disposal (Baron. 1995),

Should we now all start to take glucosamine supplements? According to the accompanying press release Michael Ristow thinks so and actually he even acts on his believe stating: "This [i.e. that everyone should take glucosamine supplements] may be considered a valid option, and yes, I have started taking glucosamine myself."

Whether that's actually a good idea or not, is in my humble opinion still questionable. Previous studies have after all linked high glucosamine to the development of insulin resistance (Baron. 1995; Rossetti. 1995; Shankar. 1998); and a compromised glucose metabolism would certainly not the best premise for a 10% longer life - right?

On the other hand, recent reviews have refuted the notion that glucosamine supplementation increases the risk of insulin resistance, because the necessary tissue levels to generate negative effects as they are displayed in Figure 2 would never be reached with oral supplement (Anderson. 2005). Moreover, Ristow himself mentions that two recent epidemiological studies on more than 77,000 individuals suggest that intake of glucosamine supplements is associated with reduced mortality in humans (Pocobelli. 2010; Bell. 2012) and says: "Unlike with our longer living mice, such an association is no definite proof of the effectiveness of glucosamine in humans, but the chances are good, and since unlike with most other potentially lifespan-extending drugs there are no known relevant side effects of glucosamine supplementation, I would tend to recommend this supplement" (from press release from the ETH Zurich).

References:

• Anderson, J. W., R. J. Nicolosi, and J. F. Borzelleca. "Glucosamine effects in humans: a review of effects on glucose metabolism, side effects, safety considerations and efficacy." Food and Chemical Toxicology 43.2 (2005): 187-201.
• Baron, A. D., et al. "Glucosamine induces insulin resistance in vivo by affecting GLUT 4 translocation in skeletal muscle. Implications for glucose toxicity." Journal of Clinical Investigation 96.6 (1995): 2792.
• Bell, Griffith A., et al. "Use of glucosamine and chondroitin in relation to mortality." European journal of epidemiology 27.8 (2012): 593-603.
• Pocobelli, Gaia, et al. "Total mortality risk in relation to use of less-common dietary supplements." The American journal of clinical nutrition 91.6 (2010): 1791-1800.
• Rossetti, Luciano, et al. "In vivo glucosamine infusion induces insulin resistance in normoglycemic but not in hyperglycemic conscious rats." Journal of Clinical Investigation 96.1 (1995): 132.
• Shankar, R. R., J-S. Zhu, and A. D. Baron. "Glucosamine infusion in rats mimics the β-cell dysfunction of non—insulin-dependent diabetes mellitus." Metabolism 47.5 (1998): 573-577.
• Weimer, Sandra et al. "D-Glucosamine supplementation extends lifespan of nematodes and of ageing mice." Nature Communications (2014), doi: 10.1038/ncomms4563 

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

Science Round Up Seconds: 2x10-15Min Of Tanning Per Week Equal 2,000IU Vitamin D3/Day. Low GI Diet Adds 9.4 Years to Your Life. Estrogen + Progestin = Bad Choice For ERT. 3g Salt/Day = 33% Lower Magnesium Retention

It has not always been this way, but these days our beauty ideal has at least one potentially healthy feat: The tan!

I don't know if you have been able to listen live to yesterday's in many ways "extraordinary" episode of the SuppVersity Science Round Up on Super Human Radio (click here to download the podcast), but if you were, you may have made the same observation I did: Whenever you feel that you got more than enough time to get a task done or, in this case, a list of topics discussed, you start loiter, to go on tangents and to end up in interesting, yet in the end "off-topic" discussions about all and sundry or "Gott und die Welt" as people in Germany woul say (literally translated: "God and the world").

Personally, I enjoyed the less packed format of yesterday's show, though. What about you? Shall we aim to discuss less news items in the future and thus have time to discuss those we picked in more detail or do you prefer the classic "short" over the long version?

This show is for you, so tell us what you want! We could also have a "motto show" once a months - something like "what's the news about fat burners" or "low carb dieting, what does the latest science say", ... I am doing this show for two reasons. Reason #1: I want to spread the word about the latest scientific studies and #2 I want you and other people to enjoy the show.

Now, it should be obvious that #1 and #2 are not independent from each other. In other words, I will reach more people if you like the show and I don't have to force you to listen to my painful accent ;-) So ... "where do you want to go", not today, but maybe next Thursday?

I guess these were more than enough questions for a single installment of the Seconds now and you are starving for the news items that did not make it into yesterday's show. Well, let's see what we've got here, then:

Tan Yourself into the >75nmol Range For Vitamin D 

Actually it is obvious that it should be possible to use a tanning bed (in the study at hand a type 3 sunbed w/ 2,15% UVB: 280-320nm; note: as Tim informed me in the comment area most sunbeds in the EU have max. 1% UVB, so you better make sure what type you are using) to boost and keep your vitamin D levels in the >75nmol range, of which current research suggests that this is where the magic happens (click here learn more also about Vitamin D and my own skepticism towards the "vitamin D solves all your problems" hype).

Figure 1: Graphical outline of the cross over design (Lagunova. 2013)

The same thought obviously occurred to a group of scientists from Norway, where the latitude, respectively the incidence angle of radiation and the scattering of short wave radiation in the atmosphere allows for effective vitamin D synthesis only in the summer months from April to October. To find out how long you'd have to stay on the "Asitoaster" (an only in some cases inappropriate derogative German term for the "sunbed", which denotes that only the less educated lower class uses the regularly) the scientists recruited 31 healthy Oslo (59°N) residents. The men and women were 23-61 and only one of them had already 25OHD levels in the >75nmol/L range.

As the graphical outline (see figure 1) of the study protocol goes to show you, the 8 men and 23 women were assigned to two different groups. Both groups underwent both the tanning bed, as well as the vitamin D3 supplement intervention (cross over design) with the only difference being that one group started out taking 2,000IU vitamin D (Carlson's brand), while group II jumped right onto the tanning bed, ...

...well, actually no one "jumped right onto the tanning bed"

For both groups the tanning bed intervention had a similar built-in progression as you would expect it from any beginner workout: Starting with a weekly exposure of 2 x 1-1.3 SED (7 min; this is what even the most fairly skinned individuals can do), the subject slowly accustomed their body to the radiation by extending their stay on the tanning bed to 1.9 SED (10 min) in weeks 2 + 3 over 2.4 SED (13 min; warning: according to Fitzpatrick et al. "light tanned" people with a greater risk of developing skin cancer can get a sunburn from this dose already; Fitzpatrick. 1995) in weeks 4 + 5 to a maximal exposure of 2.8 SED (15 min) in weeks 6-10.

Figure 2: Serum vitamin D (25OHD) levels during the supplementation / tanning bed phase in the two arms of the study (Lagunova. 2013)

As the data in figure 2 goes to show you, both protocols were equally effective in building and + or maintaining vitamin D levels in the >75nmol/L range.

In case you missed yesterday's "True or False" click here to learn whether or not you have to take your D3 supps with fatty foods.

For "the average" study participant that was a >40% increase over baseline, for the 9 volunteers who began with baseline vitamin D levels below the 50nmol/L margin, the increase was correspondingly higher.

The scientists do therefore have good reason to head the manuscript of their soon-to-be-published study with the following statement about what the study adds to our knowledge about the relative efficiency of supplemental and natural vitamin D sources, with respect to efficiency to increase serum 25-hydroxyvitamin:

"Two weekly whole body UV exposures to a total dose of 4.8 SED for 5 weeks to a total dose of  23.8 SED are equal to 2000 IU/d of oral vitamin D supplementation for 30 days and enough to achieve and maintain serum 25(OH)D concentrations above 75 nmol/L in ~ 55% of the cases." (Lagunova. 2013).

In the end, it does therefore not appear to matter, whether you take the natural or supplemental approach to keep your vitamin D levels in the upper tertile of the (revised) normal range - personally I would yet prefer the ultra-natural route (at least for the summer months).

---

Bottom line: There is little to add to the title of another recently published study "Make Vitamin D While the Sun Shines, Take Supplements When It Doesn't". Although,... when I come to thing about it, I guess there still is one thing to add: Don't be too cheap to test where you're at!

Additional news and follow ups

• Can you add 9.4 years to your live by following a low GI diet? Maybe... at least if the recent data from a rodent study that was conducted at the School of Medicine of the Deakin University in Geelong (Australia) would translate to human beings (Nankervis. 2013). Especially in those of us (or the others) who still live on the garbage that's called food, when it's part of the standard American diet, I am yet pretty confident that it would.
  
  Over the course of their 24-months experiment the scientists had provided their mice with either the normal rodent chow or (GI 70) or a low GI alternative (GI 27), did a whole series and tests and waited for the animals to pass away.

  

  Figure 3: Relative telomere length of the mice and diet composition (Nankervis. 2013)

  Much to my personal surprise this one set-screw (=low GI diet) was potent enough to extend the average lifespan by 12%.
  
  

  

  I doubt it's a coincidence that the purported telomerase activator Astragalus is also a potent anti-diabetic and anti-inflamatory - in the end glycemia and inflammation are the determinants of longevity, telomerase length only an indicator (learn more)

  If we take into consideration that the life-expectancy of the average American is 78.7 years (CDC. 2013), this would mean that he / she would live almost 10 years longer if he simply stayed away from all the processed junk to reduce the average GI of his / her diet to the sub 30pts region.
  
  And while it is probably not even necessary to say that this increased life-expectancy went hand in hand with improved glucose tolerance up into the old age and an "impressive [...] amelioration of oxidative damage to DNA in white blood cells." (Nankervis. 2013), it is imho important to point out that this longevity bonus came in the absence of improved telomere lengths in quadriceps muscle and/or the reactivation of telomerase.
  

  ---

  Bottom line: Contrary to overpriced and from a science perspective highly questionable "telomerase promoters"  a simple reduction of the sugary onslaught on your metabolism will not just improve some exotic markers of which we still don't know exactly how they figure in the aging process, but actually extend the life of a relatively complex species. How beneficial a similar dietary protocol would be in humans

• 

  Pre- or post-menopausal, Drinking coffee, tea or cacao could protect you from breast cancer (learn more)

  Estrogen therapy for women -- Everyone who's following the SuppVersity Facebook news closely, will probably remember my recent post on the latest scientific spin-off from the Women's Health Initiative (WHI) dataset which suggests that the combination treatment of estrogen + artificial progesterone (=progestin) was associated with a 55%+ higher risk of breast cancer. Even more when the drug treatment was initiated in the early phase of menopause (Chlebowski. 2013). Against that background.
  
  And as if that was not enough, the same wicked drug cocktail (equine estrogen + progestin) has also been shown to increase the risk of dementia, although you would expect that ERT (estrogen replacement therapy) should do the opposite (Shumaker. 2003).
  
  Way before the publication of the troublesome data from the large scale WHI study, the perspective on HRT for women has been changing, with the current concept suggesting that estrogen plus progestin use increases breast cancer risk and the effect on risk may be greater in women who initiate therapy closer to menopause, broadly increases breast cancer risk with the increase in risk not limited to hormone receptor–positive cancer, interferes with breast cancer mammographic detection resulting in cancers diagnosed at more advanced stage and increases breast cancer mortality. Estrogen only use on the other hand is currently understood to reduce breast cancer risk and does not interfere with breast cancer detection by mammography (cf. Chlebowsky. 2012).
  

  ---

  Bottom line: If you consider hormone therapy ladies, don't let your Dr. tell you that the "new" (when he went to medical school) estrogen + progestin drugs were the way to go.

• 

  Figure 4: Relative magnesium absorption and retention in black and white girls (11–15 y old) after 3 weeks on a high sodium diet (3.8 g/d); neither calcium intake nor vitamin D levels influenced the detrimental effects of the high sodium diet (Palacios. 2013)

  Too much NaCl or too little Mg is that the question? It actually could be the question, after all a recent study from the School of Public Health at the University of Puerto Rico would suggest that magnesium deficiency, which is in and out of itself associated with most if not all the bad things salt is usually blamed can come about much easier if you consume a high salt diet.
  
  As the data in figure 4 goes to show you, the amount of magnesium that's actually retained (not the amount you absorb!) is reduced by 33%, when the salt intake approaches the 4g/day mark. With a dietary intake of ca. 230mg/day (RDA for 11-15y old girls) the participants were "grams away" of a daily intake level that would require the body to get rid of excess magnesium.
  

  ---

  Bottom line: If you don't eat processed foods, you are not really at risk of getting too much NaCl or too little magnesium. Plus, as an aspiring physical culturist you lose tons salt, but almost no magnesium (the NaCl:Mg ratio in sweat is >682:1; cf. Montain. 2007) with your sweat, but don't we all have friends and family who are still pretty "average"? Well, in that case you already have a present for them: 1-2lbs of cheap magnesium citrate powder... but beware, never use this as a birthday, anniversary or Valentin's present for your significant other ;-)

Actually I could go on forever with notes on stuff Carl and I have been talking about, but you would not be interested in it anyways, right? Plus, let's be honest if you have listened to the podcast, read and digested the Seconds it's about time for some Intermittent SuppVersity Fasting. You know the whole thing about the cyclicity of life? This is not much different with the latest science news: If you were not forced to be without them for some time, you would lose sight of how extraordinary the daily SuppVersity news actually are ;-)

References:

• CDC. FastStats - Life Expectancy. March 04 2013. < http://www.cdc.gov/nchs/fastats/lifexpec.htm > retrieved on April 11, 2013. 
• Chlebowski RT, Manson JE, Anderson GL, Cauley JA, Aragaki AK, Stefanick ML, Lane DS, Johnson KC, Wactawski-Wende J, Chen C, Qi L, Yasmeen S, Newcomb PA, Prentice RL. Estrogen Plus Progestin and Breast Cancer Incidence and Mortality in the Women's Health Initiative Observational Study. J Natl Cancer Inst. 2013 Mar 29.
• Chlebowski RT, Anderson GL. Changing concepts: Menopausal hormone therapy and breast cancer. J Natl Cancer Inst. 2012 Apr 4;104(7):517-27.
• Fitzpatrick TB, Cesarini JP, Young A, Kollias N, Pathak MA. Reported in Fitzpatrick TB, Bolognia JL. Human melanin pigmentation: Role in pathogenesis of cutaneous melanoma. In: Zeise L, Chedekel MR, Fitzpatrick B, eds. Melanin: Its Role in Human Photoprotection. Overland Park, KS: Val-denmarPublishing Co; 1995: 177-182.
• Lagunova Z, Porojnicu AC, Aksnes L, Holick MF, Iani V, Bruland OS, Moan J. Effect of vitamin D supplementation and ultraviolet B exposure on serum 25-hydroxyvitamin D concentrations in healthy volunteers: a randomized, crossover clinical trial. Br J Dermatol. 2013 Apr 1.
• 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.
• Nankervis SA, Mitchell JM, Charchar FJ, McGlynn MA, Lewandowski PA. Consumption of a low glycaemic index diet in late life extends lifespan of Balb/c mice with differential effects on DNA damage.  Longevity & Healthspan. 2013; 2(4).
• Palacios C, Wigertz K, Braun M, Martin BR, McCabe GP, McCabe L, Pratt JH, Peacock M, Weaver CM. Magnesium retention from metabolic-balance studies in female adolescents: impact of race, dietary salt, and calcium. Am J Clin Nutr. 2013 Apr 3.
• Pittaway JK, Ahuja KD, Beckett JM, Bird ML, Robertson IK, Ball MJ. Make Vitamin D While the Sun Shines, Take Supplements When It Doesn't: A Longitudinal, Observational Study of Older Adults in Tasmania, Australia. PLoS One. 2013;8(3):e59063. 
• Shumaker SA, Legault C, Rapp SR, Thal L, Wallace RB, Ockene JK, Hendrix SL, Jones BN 3rd, Assaf AR, Jackson RD, Kotchen JM, Wassertheil-Smoller S, Wactawski-Wende J; WHIMS Investigators. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA. 2003 May 28;289(20):2651-62.

SuppVersity Science Round Up Seconds: Wheat Gluten Hydrolysates Fail, Exposure to Air Pollutants During Workout Reduces Brain Benefits, Homocysteine, B-Vitamins, Cognitive Impairment and Mortality

Before the profound weight loss (A) you don't see any of the glucose sucking and fad burning brown fat depots (black spots in B) on the neck of the in (B) 'foermerly obese', now only 'overweight' subject (also take a look at how the visceral fat in the abdominal region in (A) is actually pushing the organs upwards; img Vijgen. 2012)

Those of you who have listened to yesterday's show will have noticed that despite its flow the number of things you can discuss in a 1h podcast is simply very limited, to say the least. This is also why these Friday posts are probably never going to be simple summaries of the SuppVersity Science Round Up of the day before. The same is true for today and still I decided not to use the allegedly lame logo I did for the first two installments, but provide you with some 'real science' evidence of the absence of brown adipose tissue on the obese and it's magical reappearance after shedding 100lbs+ subsequent to a gastric bypass operation, instead (see image on the right).

Assuming that you have no idea what this "evidence" is for, I would suspect that you missed the live show yesterday and also did not find the time to download and listen to the podcast, yet -- right? Well, you should either download and listen to the show now and digest the Seconds later, or you read the following paragraphs first and download the podcast later.

What is not an option, however, is to miss one or another - I mean you can hardly want to eat the seconds if you have not had the main dish yet... and after listening to the podcast, I cannot imagine you don't want at least some seconds. Apropos seconds, here are today's seconds...

• Wheat gluten hydrolysate is not the new goto protein supplement - certainly not for female distance runners and probably not for anyone else, either! These are the kinds of studies that really annoy me. Studies that start out with blatant statements like "WGH [Wheat gluten hydrolysate] has been reported to suppress post-exercise rises in serum creatine kinase in male distance runners" (Hirao. 2012).
  
  

  

  Figure 1: CK, AST, ALT response in the "success trial" with men. In women even the miniscule beneficial effect on CK was not there. No reason to even think about buying a gluten hydrolysate as you new go-to protein supplement with only 5.6g of leucine/100g (whey has 50% more) and almost no GSH replenishing cysteine in it (0.9g vs. 3g+ in whey, which is more than +200% more).

  Sentences like that make the null-results of the study they precede look like the exception to the rule and are still nothing but a concession to a bias (let's hope not due to the grant from Nisshin Pharma Inc. which was the manufacturer of the wheat gluten hydrolysate used in this study). A bias, due to which an isolated observation as the slightly blunted increase in CK is blown up as if a slightly lower CK level was what could turn a sedentary pencil pusher into the next Hussein Bolt (Aoki. 2012).
  
  So, even if you are not afraid of the evil in gluten (which I believe not everyone has to), I strongly caution against making the switch from a high EAA protein with ton's of GSH boosting cysteine in it like whey to a mediocre grain protein, which is a potential allergen and contains tons of glutamine your body will readily turn into glucose, once it passes through the portal veign into the liver (I bet a large part won't even make it into systemic circulation).
  
  And as far as the purported "gender difference" goes the study at hand tries to blame the null result on (Hiriao. 2012), I suspect that it is rather the indisputable difference between the long-distance running at a continuous pace the women in the study at hand did, versus the totally different strains the guys in the previous study were exposed to during a soccer training + mini-match, which made the difference.
• Working out next to a street takes away some of the beneficial cognitive effects due to ultrafine particulate matter (UFPM) exposure. "Working out in the fresh air will promote weight loss more than working out inside." You heard me state that in one of the previous installments of the SuppVersity Science Round Up on Super Human Radio. Now this is still correct and based on sientific evidence, but at least as far as the cognitive benefits are concerned, working out outside does also have its downsides - at least for those of you who live in the inner city area.
  
  

  

  You better watch what you breath while you run.

  During a 12-week program the researchers from the Universiteit Brussel, the Hasselt University and the Royal Military Academy measured the improvements in physical performance, changes in serum markers and corresponding ultrafine particulate matter (UFPM) concentrations in the enviromnent in which their 15 previously untrained subjects conducted their aerobic training program thrice a week (Bos. 2012). What Bos et al. found was that the UFPM levels were signfificantly higher in the urban compared to the rural environment and that the higher UFPM exposures correlated with increases in leukocyte counts (p = 0.02), neutrophil counts (p = 0.04), and eNO levels (p = 0.002) that were exclusively observed in the group that trained in the urban environment.
  
  With the latter being markers of inflammation which exert their effects systemically, i.e. not just in the lung or musculature of which you may be thinking now, but also in the brain, it is no wonder that
  

  "reaction times on the Stroop task improved in the rural group (p = 0.001), but not in the urban group" (Bos. 2012). 

  What's comforting, though, is that the physical fitness did increase to a similar extend in both arms of the study.
• Homocysteine levels, mortality, cognitive impairment and which nutrients can offer some protection. I am not sure about what your impression is, but for whatever reason homocystein seems to be 'out of vogue' -- probably no room for it on the research agenda with all the hype surrounding vitamin D. It used to be all the rage in CVD risk research and today's news item is actually ain't about cardiovascular health, either.
  
  What the researchers from China and Taiwan actually were interested in was the correlation of high and low homocysteine levels with cognitive impairment and the corresponding nutrient intakes. In that Xiu et al. paid particular attention to the "B-vitamins" and found the following correlations between the mortality, cognitive status, homocystein levels and nutrient intake of their 1412 study participants (Xiu. 2012):
  

  • 

    Figure 2: Unadjusted mortality in the four quartiles of homocysteine levels (top); mortality according to homocysteine levels in subjects with different degrees of cognitive impairment (based on Xiu. 2012)

    if you go by the unadjusted data in figure 2, it's plain obvious that the all-cause mortality increases linearly from one quartile to the other 
  • this relation between plasma homocysteine levels and all mortality remained statistically significant after adjustments for age, sex, smoking status, BMI, physical function and general health were made
  • of the general foods, the scientists assessed, only regular fish intake had a statistically significant effect on homocysteine levels, with higher intakes being associated with lower homocysteine levels
  • of the b-vitamins choline was the only one with a significant association with plasma homocysteine levels (suggested read "Old School Supplement Choline Could Save Your Live and Liver!") 
  • neither betaine, nor vitamin B1, B2, B3 or B6 intakes did show statistically significant correlations with plasma homocysteine (not even "borderline significant; p > 0.15 for all, most way hither)
  • of the plasma markers, folate showed a highly significant correlation with homocysteine (14.4 nmol/L in the lowest HCY and 8.70 nnmol/L in the highest HCY group)
  • PLP, the active form of vitamin B6, came in close second with 70.3 nmol/l in the lowest HCY quantile and only 44.4 nmol / l in the highest quantile.
  Now, if you consider the fact that higher intakes of B-vitamins are probably not doing much to lower homocysteine levels int he elderly (at least not dose-dependently, when they are already getting enough) oddity #1, another look at the data in figure 2 will reveal oddity #2: The surprisingly high mortality in the lowest homocysteine quartiles in the patients with severe cognitive decline - how come? I mean, with low homocysteine they should not be at risk of having severe cognitive decline, anyway - right?
  
  Actually if you follow this rationale you can almost answer the question yourself. If you have low homocysteine and severe cognitive decline, the severe cognitive decline can hardly be from high homocysteine levels, so it must have another obviously pathological reason, or as the scientists have it
  

  "The joint effects of the 2 variables [homocysteine and cognitive decline] were most pronounced with severe cognitive impairment where mortality HRs ranged from 5- to 18-fold across a wide range of homocysteine concentrations. The findings with hypohomocysteinemia provide some insight into what might be an optimal range for this analyte in peripheral blood and tissues. The low concentrations may be seen with severe illness and malnutrition, and our study population comprises the health-vulnerable aged. For these reasons, we adjusted these associations for BMI (using the World Health Organization chronic energy deficiency category of, 18.5 kg/m 2 ), and we excluded those who died in the first year of follow-up. The findings were unchanged. Because mortality among the very old may have skewed the joint effects, these are presented for those ≤75 years and over, but again with similar findings." (

  A sarcastic person would now probably say: "We all have to go some time!" and just wave his hands at these results. True! And I am the last to advice you to become over-anxious. Yet in the mean time it would appear prudent to make sure to get your homocysteine levels checked from time to time, not to forget that choline is a b-vitamin as well and not to fall for the idea that you cannot overdose on B-vitamins - I don't have to remind you of the negative effects, specifically folic acid supplementation can have on all sorts of cancer (e.g. breast cancer, where a high folic acid intake from foods and supplements is associated with a +30% risk of cancerous growth; cf. Kim. 2006).

In case you are looking for the post on "ammonia accumulation brain-fog, toxicity, liver 'pathologies' and workout performance", yeah it was on the list, but I decided it would be a shame to tackle that within a short two paragraph seconds items. Don't worry I am not going to forget about it, after all its in my humble opinion one of the main reasons the diets and workout regimen of the many ambitious physical culturists fail. If you are still looking for more and have not listened to the podcast, yet, this would be the right moment to download the file from the Super Human Radio Network server (click here to download), otherwise the latest short news on the SuppVersity Facebook Wall may offer some diversion ;-)

References:

• Aoki K, Kohmura Y, Suzuki Y, Koikawa N, Yoshimura M, Aoba Y, Fukushi N, Sakuraba K, Nagaoka I, Sawaki K. Post-training consumption of wheat gluten hydrolysate suppresses the delayed onset of muscle injury in soccer players. Exp Ther Med. 2012 Jun;3(6):969-972. Epub 2012 Apr 3.
• Bos I, De Boever P, Vanparijs J, Pattyn N, Panis LI, Meeusen R. Subclinical Effects of Aerobic Training in Urban Environment. Med Sci Sports Exerc. 2012 Oct 15.
• Cankurtaran M, Yesil Y, Kuyumcu ME, Oztürk ZA, Yavuz BB, Halil M, Ulger Z, Cankurtaran ES, Arıoğul S. Altered Levels of Homocysteine and Serum Natural Antioxidants Links Oxidative Damage to Alzheimer's Disease. J Alzheimers Dis. 2012 Oct 29.
• Guest PC, Urday S, Ma D, Stelzhammer V, Harris LW, Amess B, Pietsch S, Oheim C, Ozanne SE, Bahn S. Proteomic analysis of the maternal protein restriction rat model for schizophrenia: Identification of translational changes in hormonal signalling pathways and glutamate neurotransmission. Proteomics. 2012 Oct 16.
• Hirao T, Koikawa N, Aoki K, Sakuraba K, Shimmura Y, Suzuki Y, Sawaki K. Female distance runners show a different response to post-workout consumption of wheat gluten hydrolysate compared to their male counterparts. Exp Ther Med. 2012 Apr;3(4):641-644.
• Kim YI. Does a high folate intake increase the risk of breast cancer? Nutr Rev. 2006 Oct;64(10 Pt 1):468-75.
• Vijgen GH, Bouvy ND, Teule GJ, Brans B, Hoeks J, Schrauwen P, van Marken Lichtenbelt WD. Increase in brown adipose tissue activity after weight loss in morbidly obese subjects. J Clin Endocrinol Metab. 2012 Jul;97(7):E1229-33. Epub 2012 Apr 24.
• Xiu LL, Lee MS, Wahlqvist ML, Chia-Yu Chen R, Huang YC, Chen KJ, Li D. Low and high homocysteine are associated with mortality independent of B group vitamins but interactive with cognitive status in a free-living elderly cohort. Nutr Res. 2012. Ahead of print.