Dairy - The Good, the Bad or The Ugly? Latest Studies On Heart Disease, Diabetes, Cancer, Obesity and Co. Plus: What Dairy Peptides Do For Your Heart, Gut, Brain, etc.

Do you take Liz Hurley's word and set all warnings about the "non-paleo-ness" of dairy in general and milk in particular at naught? Or do you put faith into the "got milk?" campaign? Personally, I'd suggest not to do one or the other. I'd rather suggest you join me and take a look at a selection of recent studies.

If you've been following the SuppVersity Facebook News and / or have read previous SuppVersity articles on milk and dairy, you will be aware that I am not exactly convinced that the mere existence of allergic reactions and the "fact" that "our ancestors did not drink milk before ..." *put your favorite guesstimate here* allows for the conclusion that we are "not meant" to consume cow's milk. I am nevertheless open to scientific arguments that would convince me that dairy is bad for me - it's just that I don't see this evidence outside of "western diet + dairy makes you fat and that makes you sick" contexts.

What I do see, though, are papers such as the one Sandra Abreu or the recent review by Flávia Galvão Cândido et al. - studies that tell us that the intake of milk is negatively associated with the clustering of cardiometabolic risk factors in adolescents (Abreu. 2013), and reviews which conclude that "the consumption of low-fat dairy products may be an important strategy to prevent and control T2DM [type 2 diabetes]" (Cândido. 2013).

The evidence that dairy is bad for us all is simply not there

But hey, ... let's tackle the evidence one by one. I mean, there is plenty of news-worthy material here and we don't want the fun to be over prematurely, do we? So, let's start with a brief sketch of what Sandra Abreu and her colleagues from the University of Porto base their assessment that the intake of milk, but not total dairy, yogurt, or cheese, is negatively associated with the clustering of cardiometabolic risk factors in Spanish adolescents - shall we?

No! Full-fat dairy is not bad for you: While most of the epidemiological studies with their hilariously unreliable food questionnaires appear to suggest that only low fat dairy was good for your heart, a recent study from the Harvard School of Public Health found a clever way to test the association more objectively. Instead of questioning their subjects, 2837 US adults aged 45 to 84 years, they tested the amount of certain phospholipids in their blood and found that "plasma phospholipid 15:0, a biomarker of dairy fat, was inversely associated with incident CVD [-19%] and CHD [-26%]." (de Oliveira Otto. 2013) The fact that other dairy related phospholipids were not associated (neither positive nor negative) with cardiovascular and coronary heart disease risk does yet, as the scientists rightly point out, warrant further investigation.

"To test th[e] hypothesis [that a higher dairy product intake is associated with lower cardiometabolic risk factor clustering in adolescents], a cross-sectional study was conducted with 494 adolescents aged 15 to 18 years from the Azorean Archipelago, Portugal. We measured fasting glucose, insulin, total cholesterol, high-density lipoprotein cholesterol, triglycerides, systolic blood pressure, body fat, and cardiorespiratory fitness. We also calculated homeostatic model assessment and total cholesterol/high-density lipoprotein cholesterol ratio. For each one of these variables, a z score was computed using age and sex. A cardiometabolic risk score (CMRS) was constructed by summing up the z scores of all individual risk factors. High risk was considered to exist when an individual had at least 1 SD from this score. Diet was evaluated using a food frequency questionnaire, and the intake of total dairy (included milk, yogurt, and cheese), milk, yogurt, and cheese was categorized as low (equal to or below the median of the total sample) or “appropriate” (above the median of the total sample). The association between dairy product intake and CMRS was evaluated using separate logistic regression, and the results were adjusted for confounders." (Abreu. 2013)

I know that sounds really sophisticated, but in the end, it's just standard procedure for cross-sectional studies like this - studies with one unfortunate downside: It's impossible to detect causal relationships. 

Figure 1: Dietary intake in the low and "adequate" dairy-, milk-, yogurt-intake groups (Abreu. 2013)

Keep that in mind, when you take a closer look at the data in Figure 2 which indicates that the average adolescent milk connoisseur of whom you can see in Figure 1 that he / she consumes significantly more energy on a daily basis has a significantly reduced cardiometabolic risk (predicted by cardiometabolic risk score; CMRS):

Figure 2: Cardiometabolic risk in "adequate" vs. low dairy, milk, yogurt and cheese consuming adolescents; adjusted for parental education , pubertal stage, low-energy reporter, energy intake, total fat , protein , and dietary fiber intake.

I personally was surprised to see a statistically significant protective effect only with milk - it's not that I had expected to see that for all forms of dairy, but based on previous studies I would have expected the fermented yogurt products to outperform conventional milk.

The negative effects of cheese on the other hand are by no means surprising. Food logs do after all include all types of "cheese" including the fake yellow vegetable oil based cheese analogues the kids shovel down with their pizzas, burgers and the rest of the fast food dirt. A high cheese intake has thus (unfortunately) become an indicator of low diet quality and the results of the study at hand hardly a credible marker that cheese is bad for you.

If 95% of your "dairy intake" comes from pizza, you are unlikely to see...

... any of the following benefits of dairy peptides, Blanca Hernández-Ledesma, María José García-Nebot, Samuel Fernández-Tomé, Lourdes Amigo, and Isidra Recio summarized in a soon-to-be-published review in the peer-reviewed scientific journal International Dairy Science:

• 

  Figure 3: Reduction of systolic blood pressure in mmHg per mg/kg of the said peptide you consume - mind the logarithmic scale(!); data calculated based on rodent studies summarized in Hernández-Ledesma (2014)

  Cardiovascular health effects due to the antihypertensive, anti-inflammatory, general antioxidant and hypocholesterolaemic properties of various dairy peptides
• Intestinal health effects due to the ability of dairy peptides to modulate and regenerate the gut mucosa, increase mineral absorption, exert local anti-inflammatory effects at the gastrointestinal level
• Antidiabesity effects that are related to both direct pro-insulinogenic effects of dairy peptides ant their ability to increase satiety. 
• Central nervous system relaxant and antinociceptive (pain-killing) effects
• Immune health which is promoted by antimicrobial and immunomodulatory peptides that are either already present in dairy or arise during the digestion process
• Anticancer effects that are mediated by the overall anti-inflammatory properties of certain dairy peptides, as well as direct anti-proliferative effects of dairy

Now, it goes without saying that you won't see the same effect from eating some goat kefir as Miguel et al. (2010) observed it, when they administered fraction 58-68 of goat casein to their lab rodents, but the data in Figure 3 can explain the well-established blood pressure lowering effects of dairy in general and the whey and casein induced BP reduction Figueroa et al. observed only recently in a study with obese women (Figueroa. 2013; see SuppVersity Facebook News).

Bottom line: You can't expect dairy to fully protect you against diabesity, cancer and a leaky, you can't expect it to lean you out in days, and you can't expect it to build muscle overnight, but you can expect general health benefits not detriments from incorporating a variety of fermented and unfermented dairy products into your diet - as long as you ain't lactose intolerant.

"Are Camels the Better Cows? Cancer, CVD, Allergies,Infections & More - Camel Milk Prevents or Fixes All These Ailments" | more

One thing you should keep in mind, though, is the unfortunate fact that the amount of "non-dairy" cheese, cream and other products is increasing by the day. Especially the former, the fake yellow vegetable oil based cheese analogues is something you want to avoid. The same goes for many of low fat products. While much of the "magic" is in the peptides, most of the commercially available "diet" products contain tons of sugar and all sorts of questionable additive to make up for the loss of color, taste and texture that's brought about by the removal of the fat. And lastly all products that extend the shelf-life to "eternity" by adding questionable preservatives.

References

• Abreu, S., Moreira, P., Moreira, C., Mota, J., Moreira-Silva, I., Santos, P. C., & Santos, R. (2013). Intake of milk, but not total dairy, yogurt, or cheese, is negatively associated with the clustering of cardiometabolic risk factors in adolescents. Nutrition Research.
• Cândido, F.G., Ton, T. S., & Alfenas, R. D. C. G. (2013). Dairy products consumption versus type 2 diabetes prevention and treatment; a review of recent findings from human studies. Nutr Hosp, 28(5), 1384-1395.
• de Oliveira Otto, M. C., Nettleton, J. A., Lemaitre, R. N., Steffen, L. M., Kromhout, D., Rich, S. S., ... & Mozaffarian, D. (2013). Biomarkers of dairy fatty acids and risk of cardiovascular disease in the multi‐ethnic study of atherosclerosis. Journal of the American Heart Association, 2(4), e000092.
• Figueroa, A., Wong, A., Kinsey, A., Kalfon, R., Eddy, W., & Ormsbee, M. J. (2013). Effects of Milk Proteins and Combined Exercise Training on Aortic Hemodynamics and Arterial Stiffness in Young Obese Women With High Blood Pressure. American Journal of Hypertension, hpt224. 
• Freedman, B. J. (1980). Sulphur dioxide in foods and beverages: its use as a preservative and its effect on asthma. British Journal of Diseases of the Chest, 74, 128-134.
• Hernández-Ledesma, B., García-Nebot, M.J., Fernández-Tomé, S., Amigo, L.,
  Recio, I., Dairy protein hydrolysates: Peptides for health benefits, International Dairy Journal(2014), ahead of print
• Iammarino, M., Di Taranto, A., Palermo, C., & Muscarella, M. (2011). Survey of benzoic acid in cheeses: contribution to the estimation of an admissible maximum limit. Food Additives and Contaminants: Part B, 4(4), 231-237.

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.

Organic vs. Conventional: The Overlooked Low Cadmium Advantage. Almost 50% Lower Cd Levels and Half-Lifes of 10-30 Years May Be Another Reason to Buy Organic

Eating organic is not so much about what you get extra (vitamins etc.), but rather about paying more for getting less. Less pesticides and, as recent studies show, significantly less cadmium.

In view of the hype around organic produce, it would appear as if this was a bogus question, but previous studies were not able to confirm any of the huge claims you will read all over the internet. The only established benefit so far - and that's certainly not one you should underestimate - appears to be a relative lack of pesticides.

Only recently scientists have compared a broad variety of organic and conventially grown crops and found that organically grown crops do tend to have a notably lower cadmium content, as well. According to  conventionally grown crops – on average, about 48 % lower (this estimate takes into account 87 previously reported comparisons).

Learn more about the effects of your diet on your health at the SuppVersity

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Dairy Protein Satiety Shoot-Out: Casein vs. Whey

How Much Carbs Before Fat is Unhealthy?

5 Tips to Improve & Maintain Insulin Sensitivity

Carbohydrate Shortage in Paleo Land

In view of the fact that the heavy metal cadmium (Cd) is emerging as a major cause of vascular disorders, various common cancers, kidney disease, osteoporosis and other health disorders, even in populations that do not have occupational exposure to this toxin(2–4), this is significant news.

With the exception of smokers, who are constantly exposed to significant amounts of cadmium, green vegetables, root vegetables, tubers, grains, organ meats and shellfish are the major sources of this toxin. Any reduction of the Cd levels in these foods may thus have significant beneficial health implications, since once Cd gets into your body, it cannot be excreted again.

Scientists estimate the half-life of cadmium in the human body to be 10–30 years (Suwazono. 2009)! Thus every nanogram you don't consume counts!

While cadmium can induce oxidative stress throughout the body, and interference with some of the physiological roles of Zn (as in DNA repair), the evidence that dietary (not smoke) exposure to cadmium has significant health effects is yet scarce.

There is something you can do to reduce cadmium absorption: Iron deficiency increases the efficiency of dietary Cd absorption and will put you at increased risk of toxicity. In addition to a correction of any existing iron deficiency, Zn and Mg may lessen the absorption of dietary Cd to some degree (Gallagher. 2011; McCarty. 2012)

This is partly due to the fact, though, that our ability to measure the chronic effects of very low doses of a certain toxic substance are very limited. In a recent review, McCarthy et al. (2014) list the following hitherto published studies:

• 

  Table 1: Whether there are more or less antioxidants in organic produce depends on the antioxidant you're looking at (Barański. 2014)

  Japanese researchers have long speculated about an involvement of cadmium exposure in the development of breast cancer and researchers from all around the world have speculated based on elevated urinary Cd concentrations that it may be responsible for 27-68% of the breast cancer cases (McElroy. 2006; Gallagher. 2010; Nagata. 2013).
• Recent multivariate-adjusted analyses of the National Health and Nutrition Survey cohort have concluded that Cd exposure may be responsible for 28 % of the myocardial infarction cases and 17 % of the total CVD and cerebrovascular disease cases (Everett. 2008; Agarwal. 2011). And data from the prospective Strong Heart Study (focusing on Native Americans) suggest that Cd exposure may account for 16, 23 and 28 % of the coronary disease, stroke and heart failure cases, respectively (Tellez-Plaza. 2013).

In spite of the fact that the epdidemiological evidence is not exactly abundant and disregarding the null results of case-control studies attempting to correlate dietary Cd intake with disease risk McCarthy et al. conclude that "if one focuses on urinary Cd concentrations when surveying Cd epidemiology, the hazard of Cd stands out crystal-clear" (McCarthy. 2014).

Organic or conventional? Learn more in my previous article about he different pesticide levels.

Bottom line: In view of the fact that vitamin content of organically grown produce is not necessarily higher (depends on the crop) and considering the fact that Baranski et al. found that organically grown crops do not have a lower content of lead or arsenic, two other mineral contaminants linked to health risks, when compared with conventionally grown crops, the lower cadmium along with the lower pesticide content I wrote about previously, remain the major scientifically verified advantages of organically grown produce.

That's obviously less than the internet gossip would suggest, but still enough to have anyone who is seriously concerned about his health can afford them choose organic over conventional produce | Comment on Facebook!

References:

• Agarwal, Shikhar, et al. "Heavy metals and cardiovascular disease: results from the National Health and Nutrition Examination Survey (NHANES) 1999-2006." Angiology 62.5 (2011): 422-429.
• Barański, Marcin, et al. "Higher antioxidant and lower cadmium concentrations and lower incidence of pesticide residues in organically grown crops: a systematic literature review and meta-analyses." British Journal of Nutrition 112.05 (2014): 794-811.
• Everett, Charles J., and Ivar L. Frithsen. "Association of urinary cadmium and myocardial infarction." Environmental research 106.2 (2008): 284-286.
• Gallagher, Carolyn M., John J. Chen, and John S. Kovach. "Environmental cadmium and breast cancer risk." Aging (Albany NY) 2.11 (2010): 804. 
• Gallagher, Carolyn M., John J. Chen, and John S. Kovach. "The relationship between body iron stores and blood and urine cadmium concentrations in US never-smoking, non-pregnant women aged 20–49 years." Environmental research 111.5 (2011): 702-707.
• McCarty, Mark F. "Zinc and multi-mineral supplementation should mitigate the pathogenic impact of cadmium exposure." Medical hypotheses 79.5 (2012): 642-648.
• McCarty, Mark F., and James J. DiNicolantonio. "Are organically grown foods safer and more healthful than conventionally grown foods?." British Journal of Nutrition 112.10 (2014): 1589-1591.
• McElroy, Jane A., et al. "Cadmium exposure and breast cancer risk." Journal of the National Cancer Institute 98.12 (2006): 869-873. 
• Nagata, Chisato, et al. "Cadmium exposure and the risk of breast cancer in Japanese women." Breast cancer research and treatment 138.1 (2013): 235-239.
• Suwazono, Yasushi, et al. "Biological half-life of cadmium in the urine of inhabitants after cessation of cadmium exposure." Biomarkers 14.2 (2009): 77-81.
• Tellez-Plaza, Maria, et al. "Cadmium exposure and incident cardiovascular disease." Epidemiology 24.3 (2013): 421-429.

Intermittent Thoughts on Intermittent Fasting - Finally Getting Started - Setting Yourself Up For Success!

Image 1: Socrates unquestionably did not look like he knew anything about intermittent fasting or physical culture, but he knew a lot about how to unlock the potential of his students.

In the last parts of the series you have learned so much about the biochemical underpinnings of how your diet and exercise regimen can change the way you look, feel and perform that you should by now have a general idea of why people, like Duong, "all of a sudden" drop tons of body fat, without having to resort to the still much-heralded combination of low-intensity-steady state "cardio" sessions and frequent low-fat high carb mini-meals. You should, however, also have grasped the idea that copying Duong's or Adelfo's regimen probably won't get you where you want to be. My intention thus is (and has always been) to teach you all the stuff you will need to find your own way... just as children will not learn to read if you just read books to them, you will never be able to constantly progress unless you totally surrender yourself to the advice of a highly paid personal trainer who babysits you 24/7 or - and I would assume that this is the way more desirable alternative - learn how to do his job on your own. In this installment of the Intermittent Thoughts and probably a few follow ups, I am thus going to "think" about how you can decide on the necessary steps you have to achieve your personal goals.

Do you want to know how to set yourself up for failure?

If I wanted to make it easy for me, I would follow the example of many health and fitness authors and provide you with a 3-10 item list of how you can "set yourself up for failure". This is easy, because you do not even have to know what works. It is enough to now what does not work. Yet even though there are much more things that don't work, than things that do work,  the word(s) "overeating" or even "constant overeating" would be totally misplaced on the list of "don'ts" of a skinny person who insists to do an intermittent fast and still wants to gain weight. Without "constant overeating" in the restricted feeding windows this is not going to happen.

Image 2: The new "MyPlate" is probably the most prominent example of moribund one-diet-fits-them all solutions (even if it was not intrinsically flawed, as well)

As you may notice, it gets pretty difficult for me, not to set you up for failure, even if I am providing advice that would be spot on for 90% of my readers. This is why I will not give you any answers, at all, but ask questions. I will ask questions that will enable you (based on the information of the future installments and concrete examples I will weave into future Intermittent Thoughts) to come up with the answers yourself - in didactics, this is referred to as a "socratic dialogue" (Rose. 2001), where the lecturer is trying to ilicit information from students through a direct line of reasoning... I suspect that this may sound counter-intuitive, after all it sounds as if it implied that you already know what the answers would be. That, however, is not the case. Socrates made his pupils discover for themselves things they could know - and that is fundamentally different from inquiring about things you do know.

Who are You and what do You want to achieve?

As I am doing it at the beginning of each semester with my real world students, the first thing I will ask you to do is to introduce yourself. What relevant information would you have to provide? Are you being fed up of being the fat or skinny kid, the girl or guy who is always just "a friend", the last one to be picked when you are playing football with peers, the pre-diabetic who got scared, when the doctor told him that if he did not start jogging and eating "healthy" *haha* whole grains will sooner or later be injecting insulin? If you do not have an answer to this question, yet, chances are you won't be able to help yourself make a change - and if you do not want to change, why are you even contemplating an intermittent fast?

Image 3: Are you sure "getting skinny" is really what you want, former fat kid?

Outside of the realm or professional athletics, the issue we are approaching right now is something that is commonly overlooked by many trainees and oftentimes not accordingly valued by their trainers (if they have any) - it is the complex interrelation of personal motivation and goals. Let's assume you were the "fat kid" all your life. Is you goal actually to "get skinny"? Probably not. And in case it is - just stop eating. If you take in enough fluid, and maybe a protein shake with some olive oil from time to time, you will probably live long enough to see a skinny image of yourself in the mirror, someday. Will this provide the social acceptance you have been longing for, all these years? I don't think so. It would rather have you descend deeper into the social abyss...

Why are you here? What is it that motivates you to "study" at the SuppVersity?

The first step in setting yourself up for success is thus to set an appropriate long term goal. I know that each and every one of you will tell me that he is "freakin' motivated" and "ready to do whatever it takes" to achieve his/her goals... so!? Then give me the elevator pitch of what you want to achieve... if it took you longer than 2 seconds to put your main goals into a single sentence, I must tell you that you have not yet taken the first and most fundamental step to set yourself up for success. Even the slightest doubts on your part as far as your goal is concerned will eventually become major obstacles on journey to a "new" or "better" you. That does not mean that your goals cannot change in the course of your journey (it is very likely that they will and in most cases it is even necessary), but if you were not sure, whether you want to go to Canada or to the South Pole, don't you think it would be better to stay at home, then?

Figure 1: Initial motivation (as assessed by the MPAM-R questionaire on a 7-point Likert scale) of male and female trainees going to a commercial gym and correlation (r-values) with adherence to the exercise program (adapted from Ryan. 1997)

Maybe it will help you if we take a look at what others set out to achieve. In a 1997 study, Richard M. Ryan and his coworkers at the Universities of Rochester and Southern Utah conducted a study where they asked 66 male and 89 female gym-goers for their personal motives and correlated this information on initial motivation with the subjects adherence to their respective exercise programs. The results are quite interesting, because although physical fitness and appearance were ranked highest, they showed the least correlation with the individuals adherence to the exercise program. In the case of "appearance" - my often-cited "I just want to look good naked" - there was even no (statistical significant) correlation at all. In other words, it did not matter how bad people wanted to improve their physical appearance - if this was their main motive to go to the gym. It did not help them to stay on track. Or as the scientists put it:

The implications of these findings [...] suggest that body-related motives are not, on average, sufficient to sustain regular exercise regimens, and thus should not be made the most salient justification for engaging in exercise.

Image 4: For Arnold (you know he is my favorite ;-) "the pump is like cumming ... like having sex with a woman" ... well, we all know how much he enjoys both, and it was the former joy, the one from the pump, him on track and made him succeed (still from video).

The scientists suggest that trainers & trainees would be better off if they emphasized "the inherent enjoyment associated with physical activity and/or the growth of competences that exercise promotes". Now, think about yourself and the people surrounding you. Think about the "losers" and the ones who had success. Do you see a pattern? Think about their faces when they come to the gym. Think about how they approach the weight stack. Think about what they say and how they respond, when you ask them: "What do you train today?" Do you see the pattern? Think of Arnold

Your muscle get a real a tight feeling [...] that's the pump [...] it feels different, it feels fantastic [...] it is as having sex with a women [...] I am cumming day and night ... it's terrific, I am in heaven (if you don't believe he said that, watch the video)

Do you see the pattern? Think of the fat lady that was holding on to the inclined treadmill, trampling away sweating, when you were doing your HIIT on the stair-master. Do you see a pattern?

Well, obviously both Arnold and the lady wanted to improve their physique. For the Governator, however, it was a necessary consequence of his life-style, a life-style that was based on doing what he loved to do. For the lady you saw on the treadmill, on the other hand, it was something alien - a physique "those other all have", something "nature has given those skinny anorexic chicks", something she "can work for as hard as she wants, but will never achieve". Be honest with yourself: Who are you? Arnold or the lady on the stairmaster?

Did I just hear you say that "it is not my fault, Dr. Andro!"?

Image 5: "Good" or "bad" this DNA helix is a part of your setup for success. Trust me - a few pathologic exceptions aside - it will only hinder your success if you lull yourselves into believing that it does.

From the fact that you did not head right to the gym to jerk... ahh I mean pump off ;-) I gather that you are not on the extreme "arnold'esque" side of the continuum - in other words: Things have not worked out the way you intended in the past, have they? You know what? That's your advantage! Thusly you save yourself at least a few of the 1001 mistakes that lurk on the way that lies between the "old" you and the "new" one... which reminds me: Do you already have your elevator pitch ready? What? You still "just want to look good naked"? Well, that is fine with me. Just be aware that even if you went to bed tonight, woke up the next morning, stood before the mirror in your bedroom and ... finally looked good naked, it will probably only take few weeks to restore your looks to your old "inner self", which obviously would not have changed, when the beauty fairy struck you with her magic wand in that fateful night.

You need to realize that whatever the central aspect of your motivational elevator pitch is going to be ...

• looking good naked (how do you define that?)
• never being called "skinny bitch/bastard", again (are you sure that is only an issue of how you look?)
• not being the fat guy/girl, any more (what do you think will change, then?)
• eventually get rid of the constant fatigue (could the fatigue be the result of trying to achieve unrealistic aims?)
• adding +20lbs of lean muscle to my frame (what will you have achieved then? will this be enough? or are you going to want more?)
• losing -50lbs of fat (is it just the figure on the scale you are looking for?)
• getting off your diabetes drugs (do you have an idea why you maneuvered yourself into this situation in the first place?)
• living into your 100s (do you just want to live long or is this more about good health into the old age?)
• and so on and so forth

 ... chances are, you would already be there, or at least on your way to achieve them, if there was not this one person that was standing in your way: YOU! No excuses! Taking responsibility for where you are at now, regardless of which "bad advice" you have been following or "how bad your genes" may be - your status quo is the foundation on which you are going to reinvent yourself - not just your training or your "diet". If that works out, patience and perseverance will be the only thing it will take you to eventually arrive, where you see yourselves in your elevator pitch.

Homework for the next installment: Post your elevator pitch

Figure 2: Robb Wolf once mentioned the "performance - health - longevity triple point" in one of his numerous insightful blogposts on his webpage. In essence the figure above expands on his idea: You obviously cannot max out on all of the items. Notwithstanding, all of them are attached to the very same life-style foundation and the practical overemphasis of any of them may have pathological consequence (Adonis complex, depression, drug addiction, obesity, anorexia, ...).

As a  "homework" I want you to fine-tune and post your elevator pitch in the comment section of this post. Not only will you thusly make yourself accountable for what you will feel, look and perform in a few weeks or months from now, you will also help me tailor the next parts of this series, which are going to deal with the actual "programming of success" by making appropriate life-style interventions, to your goals. So don't miss out on this chance and give the world a preview of what the characteristic feature(s) of the "new you" is going to be.

And don't forget, where you came from. Maybe you've just been straying around, because your present elevator pitch incorporates two or more of the partly diametrically opposed extremes in figure 2? Think about it. Have you ever seen an Olympic athlete partying 5 days à week, who goes to bed at 4am has pizza for "breakfast" at 4pm and improves the world record at 8pm? Probably not. So incorporating diametrically opposed extremes into your elevator pitch is about as much a no-go as having none at all, remember that before you go public - I mean, what would the world think if your plan to have french fries instead of the pizza and them perform a new world record fails?

The Healthy Taste of Olive Oil. Would the Flavor Be Enough to Induce At Least Some of Its Health & Satiety Effects? Plus: Cholesterol Control - Pomace vs. Refined Olive Oil

What about an EVOO perfume, then?

I know, it sounds crazy, but in view of what you've learned in previous articles here at the SuppVersity about sweet taste receptors (learn more) and their far-reaching influence on our metabolism, it does not appear to far-fetched to assume that there is a receptor that "tastes" the flavor-active compounds of olive oil that's responsible for some of its beneficial health effects - right?

I guess, Sabine Frank and almost a dozen of other scientists from Germany and Austria must have had a similar idea, when they came up with the research question of their most recent study.

Olive oil flavored yoghurt?! Really?

I suppose, olive oil flavored, or, more specifically, low-fat yogurt mixed with a fat-free aroma extract from olive oil may not sound appealing to the average Western customer, but it would certainly deserve the label "functional food":

Figure 1: Only the olive oil enhanced yogurt will also enhance the activity of the frontal operculum (Frank. 2013)

As you can see in Figure 1, it's a functional food that has a statistically highly significant effect on the cerebral blood flow in the frontal operculum 30 and 120 min after a meal: This and the increased activity in the anterior insula of which the scientists found that it correlated positively with the postprandial change in bloos glucose change in the 11 healthy male subjects of the study, clearly suggest: The taste of olive oil alone has significant effects on the blood flow in parts of the brain that are involved in the control of energy intake and metabolic rate.

"What is the "frontal opercular" and why would I care about its blood supply?"

If the subheading to this paragraphs describes what you are thinking right now, it's about time to take a look at the little information we have about the frontal operculum:

• 

  Suggested read: "Pimp My Olive Oil! When Virgin is not Phenol-Rich Enough: The Pharmacokinetics of Phenol-Enriched Virgin Olive Oil." | read more

  We know from previous studies that the frontal operculum (FP) is sensitive to food intake.
• The study at hand shows that the FP does not care about caloric values (the yogurts were isocaloric).
• In task-related studies, the frontal operculum as part of the primary taste cortex, has shown pronounced activation to visual food cues and anticipation of food intake.
• The activation of the frontal operculum appears to control the "this smells good" or "this looks good, I must have it" response that makes weight loss so difficult.
• There is a telling relation between the sensitivity of the frontal operculum and the BMI of a person (Batterink. 2010; Yokum. 2011)
• Earlier fMRI studies showed that oral delivery of a drop of fat leads to an immediate increase in insular and frontal opercular activity, which suggests that there are "fat taste receptors" somewhere in the oral cavity or digestive tract that are wired to the the frontal perculum (Small. 2012).

Now, in context of the results of the study at hand, it is obviously the last of these points, which is particularly interesting. The discovery Frank et al. made would after all suggest that we can get satisfactory "fat effect" without the fat - simply by having the right "aroma."

Figure 2: Modulating effect of the minor components of pomace olive oil (POMACE) on lipid composition in 10 healthy young men (Cabello-Moruno. 2013) - severs as illustration for the importance of the "non-fat" components for our health.

Frank et al. also point out that the fact that they measured the CBF not immediately but 30 min and 120 min after the consumption of the yogurt would make it quite unlikely that they had mistaken an acute aroma response for what they believe is the "association with fat" - in other words, the researchers believe that the ingestion of the olive oil flavor components "modifies later responses to achieve an appropriate sensory control." Effects just as we know them from glucose and artificial sweeteners which "prepare" the body to release insulin.

Per capita consumption of vegetable oils and fats in selected European countries in 2009 (Eurostat. 2011)

Bottom line: I guess it is too early to say, whether and what kind of applications the said olive oil extract could have in the future. What the study does however show is that focusing on macros and even micronutrients, only, is insufficient.

In fact, the "ideal" diet, with the perfect macros and 100% adherence could in the end turn out to produce inferior results to a "sub-optimal", but tasty diet with olive oil and other aromas triggering all-sorts of still to be elucidated beneficial downstream effects on our physiology and psychology.

Reference: 

• Batterink L, Yokum S, Stice E. Body mass correlates inversely with inhibitory control in response to food among adolescent girls: an fMRI study. Neuroimage 2010;52:1696–703.
• Cabello-Moruno R, Martinez-Force E, Montero E, Perona JS. Minor components of olive oil facilitate the triglyceride clearance from postprandial lipoproteins in a polarity-dependent manner in healthy men. Nutrition Research. Oct. 2013 [accepted manuscript]
• Small DM, Green BG. A proposed model of a flavor modality. In: Murray MM, Wallace MT, eds. The neural bases of multisensory processes. Boca Raton, FL: 2012
• Yokum S, Ng J, Stice E. Attentional bias to food images associated with elevated weight and future weight gain: an FMRI study. Obesity (Silver Spring) 2011;19:1775–83.

Intermittent Thoughts On Intermittent Fasting - Exercise (3/3): How Training Solves the AMPK/mTOR Antagonism.

Image 1: Just like Two-Face, a character from the Batman comic books, AMPK turns out to have two faces,... ah I mean isoforms the differential expression of which explain why exercise, contrary to starving yourself, maintains or even builds muscle mass while reducing your love handles (img batman.wikia.com).

In the last installment of the Intermittent Thoughts on Intermittent Fasting series, we have revisited the idea of different training modalities, i.e. endurance and strength training, for the promotion of AMPK-related reductions in body fat and mTOR-dependent increases in muscle mass. We have also busted the long-standing myth of the "anabolic window of opportunity", which, upon closer examination, turned out to have the size of a barn door (>24h) that is unlocked with the key of exercise and nutrition sciences. Related findings showed that even in the absence of additional nutritional stimuli a single intense strength training session led to a profound and (>24h sustained) increase in mTOR phosphorylation in 24 untrained, young, healthy, male subjects (Vissing. 2011). In conjunction with the results of Burd et al. (Burd. 2011), who found that the beneficial effects of strength training on the subsequent response to protein feeding depend on exercise intensity and volume and last for >24h, these results further underline the synergistic effects the fasting, training, feeding cycle of classical intermittent fasting regimens had and still has on the health and physiqueof its practitioners.

Unfortunately, both the concept of "fat loss", as well as that of "muscle gain" are still largely associated with notion of what is commonly referred to as "energy balance". If you read my recent blogpost on the  "High(er) Reps for Fat Loss"-Myth, you will be aware of the fallacy behind the idea of "going to the gym to burn fat". And while more and more trainees (also thanks to the educational work of BodyRX Radio ;-) are getting the idea that you have already lost the fight against your love handles, when you go to the gym solely "to burn calories", the notion that you go to the gym to either "pump up" or "totally exhaust", "damage" and "break down" muscle tissue is similarly illusive. Contrary to what the more is more mentality of the western society may suggest, simple linear causality is nothing you will ever see as the underlying "reason" for the success of a given exercise regimen.

Gain muscle or lose fat? AMPK vs. mTOR and the unique effect of exercise
 

Image 2: "Immunocytochemistry/ Immunofluorescence - AMPK alpha 1 + AMPK alpha 2 (phospho S485 + S491) antibody (ab39400)" ... and if you do not understand this lingo, what you see here is nothing else but one of the unspecific markers for both isoforms of AMPK that is used in most of the studies (img abcam)

Regardless of whether you intend to lose fat, to build muscle or strength, the previous installments should have made it pretty clear that you will always be dealing with two-way processes, or I should say cycles. Now, interestingly enough, exercise, contrary to dieting or overeating, appears to have the unique quality of driving both at the same time - fat loss and protein synthesis, AMPK and mTOR. This works, and this is going to be the main message of this concise piece of the Intermittent Thoughts series, because the exercise induced muscular(!) AMPK-response differs from the one your brain and many other organs will exhibit, when you starve yourself during a diet. Actually we have been knowing for quite some time that the predominant isoform of AMPK that is expressed during exercise is AMPK-alpha2. Back in 2000, already, Wojtaszewski et al. found that "high" (in this case >70% of the individual VO2max) intensity exercise for 60min selectively increased AMPK-alpha2 activity almost threefold (Wojtaszewski 2011). Similar to the results of previously discussed studies, the increased AMPK levels returned to baseline within 3h after exercise-cessation.

Unfortunately, only few of the subsequent studies, which investigated the effects of different exercise regimen, used iso-form specific tests to determine which of the two AMPK isoforms was expressed consequent to the respective training protocols. According to the ground-laying work of Stapleton et al. (Stapleton. 1996) and supported by a study by Stephens et al., it is yet likely that the relative exercise-induced expression of AMPK-a1 in human muscle tissue is negligable.

Figure 2: AMPK-a2 expression (arbitrary units measured in the absence of AMP) and fat oxidation in g/min in 7 healthy individuals during 30 minutes cycling at 62.8% of VO2Max (data adapted from Stephens. 2002).

Moreover, the results of Stephens et al. underline that the exercise-induced increase in AMPK-alpha2 does not only increases fatty acid oxidation, but that both exhibit an excellent correlation with exercise induced glucose depletion (Stephens. 2002).

Figure 2: Glycogen content (mmol/kg) and phosphorylation of AMPK (arbitrary units) in human vastus lateralis muscle before (0 min) and at the cessation of 120 min of one-legged knee-extensor exercise, while consuming either a glucose containing drink or a placebo drink.  (data adapted from Thorbjorn. 2006)

It is thus not surprising that Thorbjorn et al. were able to show that the ingestion of 0.7 g of glucose/kg of body weight/hour did not only blunt the exercise induced AMPK-a2 response but also reduces its beneficial effects on fat oxidation by -47% (cf. figure 2)!

The results of older studies sometimes begin to shine in the light of novel findings 

Now, you probably knew all that before - after all we have been talking about this effect, its beneficial effects on fatty acid oxidation and glucose uptake, as well as its supposedly negative impact on protein synthesis in previous installments of this series. And in fact, these results begin to shine only, in the light of the results of a a recently published study by Mounier et al., who were able to show that only the increased expression of the alpha1 isoform of AMPK, but not AMPK-alpha2 does impair mTOR signalling. Against that background, the systemic antagonism of AMPK-alpha1 (expressed in liver, brain, and other organs) and mTORc1 mediated protein synthesis stands in stark contrast to the metabolically highly beneficial synergism of concomittant exercise-induced AMPK-alpha2 and mTORc1 expression.

To make a long story short: Exercise is unique in its ability to help you shed fat and build muscle "at the same time", because it activates a specific isoform of the "starvation sensor" AMPK, which does not block the concomitant increase in protein synthesis subsequent to the (likewise) exercise-induced increase in mTOR phosphorylation. On that note, my schedule forces me to end this abbreviated version of the Intermittent Thoughts, yet not without the promise that I am finally going to tie all the knots together in the next installments of this series.

Intermittent Thoughts On Intermittent Fasting - Exercise (2/3): Opening the "Anabolic Barn Door" With the Key of Exercise and Nutrition Science!

Image 1: The "anabolic window" turns out to be more of a barn door, which is unlocked by the key of exercise and nutrition science (Random House Books)

Looking back, the main take-aways from the last installment were the dependence of exercise performance on adequate and not so much constant energy supply, as discussed in the context of the Ramadan fasting soccer players, the increased AMPK response to fasted training on a hypercaloric diet, which would suggest that things like "fasted cardio" in the morning could well have it's place in an intermittent fasting regimen even when you are bulking (in order to ward off fat gains), and, last but not least, the differential AMPK- and p70S6K protein synthetic response of cyclists and powerlifters to unaccustomed training stimuli. Accordingly, a versatile training routine that is timed in a way that allows you to train fasted or semi-fasted training, i.e. having your first easily digestible high protein meal / supplement ~30min-1h before you hit the gym, will certainly help with lean gains and muscle-sparing fat loss.

How to train if someone "just wants to look good naked"?

While the observations of the Coffey study (Coffey. 2005) did underline the importance of versatility, or, I should say constant "novelty", or at least modification of the training stimuli, they did not really provide any clues on how someone, who "just wants to look good naked" (and I assume this applies to the majority of non-athletes, today) should train to transform his formerly at best non-obese physique to the cover-model'ish look everybody is aspiring these days.

Figure 1: Study design of the Vissing study with its 10-week preconditioning phase for the strength and endurance training groups (generated based on information from Vissing. 2011)

In regard to this question, a similar, yet more recent study on non-athletes comes to mind. In the course of the latter, K. Vissing and his colleagues from Aarhus, Denmark, and Geelong, Australia, took a closer look at the response of the "AMPK/mTOR seesaw" to either endurance or strength training (Vissing. 2011) after a comparatively brief per-conditioning period of 10 weeks (cf. illustration 1) - a scenario of which we can expect more reliable results than from its "highly trained recreational athletes" counterpart from the Coffey study, where the participants have been focusing on training for their respective sport (cycling or powerlifting) for years. Accordingly, Vissing et al. expected to see that...

[...] mTORC1 signaling would be selectively activated by SE [strength training], whereas AMPK signaling would be activated by both types of exercise but to a relatively higher degree after EE [endurance exercise] compared with SE [...]

Thus, their research hypothesis was in accordance with the publicly accepted idea that only strength training builds muscle (obviously the role of mTOR-activation in this process is widely unknown in the general public), while endurance exercise would be the better form to train if one wanted to lose fat - as a diligent reader of the SuppVersity, you will obviously be aware that the reduction in adipose tissue you will hopefully observe, when you are dieting, is primarily a result of the depletion of muscular (and hepatic) ATP stores, which brings the AMPK energy emergency police on the scene which will concomitantly tell your muscles to suck up all extra (i.e. more than your brain needs) glycogen from your blood stream and kick your adipocytes' asses, so that they release some of their fatty energy reserves as metabolic firewood for your mitochondria.

I hope you remember "The 'hungry' side of neuronal AMPK activation", i.e. the differential effects of AMPK phosphorylation in reaction to energy shortage in muscle or liver tissue vs. its effects in the brain. If not, I suggest you (re-)read the respective passage in "AMPK III/III: Natural Rythmicity for Maximum Fat & Minimal Muscle Loss", as a thorough understanding of this difference if of utmost importance if you want to be able to compare and interpret the data from various studies correctly.

The Coffey study (discussed in the last installment) did however show that this assumption, i.e. both endurance, as well as strength training will always increase AMPK, does not hold true, when we are talking about highly trained athletes - neither in the cyclists nor in the powerlifters from the Coffey study did engaging in their respective discipline produce statistically significant increases in AMPK phosphorylation.

Figure 2: AMPK phosphorylation (0, 2.5, 5 and 22h post) and approximate area under the respective curces (small graph) during post-exercise recovery from single-bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training (data calculated based on Vissing. 2011)

Conversely, in the Vissing study, AMPK phosphorilation did transiently increase in both the strength and endurance trained groups immediately post (at 0h) exercise (cf. figure 2). However, with the subsequent drop of the phosphorylated AMPK (pAMPK) below the values of the control groups, the estimated area under the curve (AUC; I simply used weighed averages for the calculation), i.e. the absolute AMPK phosphorylation over the whole 22h post-exercise window, for which the scientists have data (cf. figure 2, right), was -12% and -17% lower in the strength training group than in the control and endurance group, respectively.  

Without the AMPK elevation of an intermittent fast (or calorie reduction), it is thus unlikely that strength training alone is going to trigger significant AMPK responses.

Interestingly, the scientists state that the protein expression "of any of the reported signaling proteins" was "not altered" by the 10 weeks of pre-training, which would indicate that, contrary to years of competitive endurance exercise (cf. cyclists in illustration 1 in previous installment), 10 weeks with three weekly sessions of combined steady-state and interval exercises on stationary bikes do not blunt AMPK phosphorylation in response to 120 min of bicycle exercise at 60% of the individual VO2 max.

The induction of mTOR phosphorylation is and will remain the real strength of strength training

Likewise, the protein synthetic response (as evidenced by mTOR and p70S6K expression) did not change in response to a 10-week pre-conditioning phase comprising 30 leg workouts (3 exercises; 3-5 sets; 10 reps in the first 15 sessions, 4-6 reps in the last 15 sessions). Interestingly, and contrary to the often heard assertion that mTOR phosphorylation would be a strength training exclusive, figure 3 shows that there is still a minor, yet over the course of the post-exercise period, non-negligible increase in mTOR phosphorylation in the endurance trained subjects, whose 45min cycling session effectively blunted the mTOR dephosphorylisation the control group, who, just like all of the previously (before the preconditioning) 22 untrained healthy male subjects (79.1 kg; 182 cm; 23.3 years), fasted for the first 5h "post exercise" (their exercise consisted of sitting on the couch, doing nothing ;-).

Figure 3: mTOR phosphorylation (0, 2.5, 5 and 22h post) and approximate area under the respective curces (small graph) during post-exercise recovery from single-bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training (data calculated based on Vissing. 2011)

Even without looking at the data in figure 3 it should be obvious that the meager increase in mTOR phosphorylation in the endurance group cannot compete with what we see in the strength trained subjects, whose p-mTOR ( = phosphorylated mTOR) levels skyrocket in the post exercise phase, peaking at +218% (control: 56%; endurance: 130%) not immediately or maybe 1h post exercise but 5h after. Thus, the purported "anabolic window" of 1-2h after a workout turns out to be a barn door, in the real world - a barn door which is wide open right in the middle of your intermittent fasting feeding window!

Strength training = opening the "anabolic barn door"

Yet, while we do now know how to unlock the barn door, we still do not know if there ain't a way to push it open even further / faster, and how to keep it wide open for as long as possible. In this context, a study by Burd et al. from Steward Phillips group at the Department of Kinesiology of  McMaster University in Hamilton, Ontario (Burd. 2011) could provide further clues into the "optimal" way(s) to push the "anabolic barn door" open, as wide as possible.

After all that has been said about the over-expression of mTOR in our current society in the previous installments, it should be said that the problem does not lie with mTOR itself, as it is not the latter which inhibits AMPK, but the energy abundance that triggers the mTOR response in our western obesity scenario. This chronic nutritionally induced suppression of AMPK is something we need to distinguish from both the training-induced increase in mTOR phosphorylation and the temporary and strategically used dietary stimuli that are so characteristic of intermittent fasting.

Figure 4: If we disregard the nutritional component, the training induced "anabolic barn door" does not only coincide with the feeding window, it would also keep you nicely "anabolic" in the course of the fasting period.

In figure 4, I have extrapolated the missing two hours to complete a 24 hour intermittent fasting period, in the course of which you would do your training session early in the morning, head towards the gym at 8:00am, change your clothes, warm up, training for about an hour and break the fast at 10:00am. Thereafter, you would have a pretty long feeding window of about 6 hours, to then begin another fast... in that, your meal pattern would differ profoundly from the one of the study subjects, because the latter had to fast for the first 5 hours post exercise, so that the mTOR response was not augmented and the study results distorted by meal ingestion (afterwards they were allowed to eat whatever they wanted until 22:00pm and had to report back for the 8:30am blood draw (mTOR still +89% elevated) on the next morning. Due to these differences it is difficult to predict how your overall (i.e. exercise + food induced) mTOR response would look like on the above regimen.

Will the "anabolic barn door" stay open in the course of the fast and thusly prevent muscle breakdown?

This is where the data from the Burd study comes into play (Burd. 2011). In their study, Bird et al. had measured the fractional protein synthesis rate in response to feeding (15g of whey protein) and feeding and exercise (unilateral leg raises) at different intensities, i.e. 90% 1RM to failure, 30% 1RM with matched work-load and 30% 1RM to failure. What they found was that

regardless of condition, rates of mixed muscle protein and sarcoplasmic protein synthesis were similarly stimulated at FED and EX-FED (Burd. 2011)

- an observation, the scientist attribute to the fact that the sarcoplasmic constituents of the muscle may be more susceptible to hydration flux, so that the results may not adequately represent the "actual" protein synthetic response.Thusly, the researchers rely in their interpretation of the data mainly on the myofibrillar protein synthesis rate (cf. figure 5).

Figure 5: Changes (% per hour) in absolute myofibrillar protein synthesis (adapted from Burd. 2011)

As you would expect and actually can see in figure 5, the latter did respond to the additional exercise stimulus. Pumping away at 30% of your 1RM max without going to failure, is yet not enough to augment the statistically hardly significant increase in fractional protein synthesis that was triggered by protein ingestion, alone. It takes some effort, or, in other words, heavy weights and training to failure to trigger elevations in AKT phosphorylation (90% 1RM to failure) or mTOR phosphorylation (30% 1RM to failure) to get that done (note: neither of the two, i.e. protein kinase B = AKT or mTOR was significantly elevated by feeding, alone).

[...] protein ingestion stimulated rates of myofibrillar protein synthesis above fasting rates by 0.016 ± 0.002%/h and the response was enhanced 24 h after resistance exercise, but only in the 90FAIL and 30FAIL conditions, by 0.038 ± 0.012 and 0.041 ± 0.010, respectively. Phosphorylation of protein kinase B on Ser473 was greater than FED at EX-FED only in 90FAIL, whereas phosphorylation of mammalian target of rapamycin on Ser2448 was significantly increased at EX-FED above FED only in the 30FAIL condition.(Burd. 2011)

Moreover, and this may be of even greater importance in the context of exercising on an intermittent fast, muscle protein synthesis stayed elevated way beyond what is usually considered the <4h "anabolic window".

Our results suggest that resistance exercise performed until failure confers a sensitizing effect on human skeletal muscle for at least 24 h that is specific to the myofibrillar protein fraction. (Burd. 2011)

While this is obviously important for everyone who wants to accrue as much muscle muss as possible, any elevations in protein synthesis will also help a dieter to keep is hardly earned muscle, because in essence our muscles are continuously build up and broken down  - proteolysis, i.e. the breakdown of muscle tissue, and protein synthesis are going hand in hand and it is the ratio of one to the other, which decides whether we are in an "anabolic" (synthesis > breakdown) or catabolic (breakdown > synthesis) state. Consequently, any elevation in protein synthesis will ameliorate muscle loss - no matter how proteolytic a dieter may become during the fasting phase.

It takes >24h for the barn door to close itself - use this time to get rid of fat, not muscle

Fine, we unlocked the "anabolic barn door", it stays open for "at least 24h"... blah blah... wtf! how does all that translate from the metaphorical into the real world of intermittent fasting? Well, the answer is pretty simple, as hundreds of trainees have been practicing exactly that with extreme success over the past couple of months:

1. fast until min. 1h before your training
2. spike your protein synthesis with a protein shake (~20g of whey), EAAs (~10g) or BCAAs (~8g)
3. train semi-fasted and heavy
4. feast within a 5-8h window
5. repeat the same litany again

Now, the sheer size of the barn door, ahm... sorry, the long-lasting anabolic and thusly anti-catabolic effect of intense strength training should allow you to either skip or replace "3. train semi-fasted and heavy" with "3. passive or active recovery" (in that case you also do not want to ingest the protein shake / EAA / BCAA) or even some "3. semi-fasted cardio" (see notes in red box) if you feel that your conditioning or weight loss will benefit from that, every other day without running the risk of either gaining too much fat weight.

Image 2: Your "anabolic barn" is huge enough to accommodate one or two steady state, low intensity or high intensity "cardio" sessions per week.

If you want to incorporate "cardio" training into your routine, the pre-conditioning protocol from the Vissing study could actually be a very good, since diversified, regimen. In that, you would cycle between doing "standard" steady state conditioning work, longer medium-intensity interval training and short, but intense HIIT sessions. The result would be a very complete "cardio" protocol, of which the Vissing study showed that it will help you ramp up your AMPK levels pretty profoundly, even if you are only sitting on one of those cycle ergometers pedaling away jovially at 60% of your VO2 max. And in case you are now concerned about possibly shutting the barn door - look at figure 3 again, the mTOR response to this kind of exercise may not be earth-shattering, but a plus of 25% @5h post exercise is better than what you would get if you just lay around lazily, as the control group in the Vessing study did.

With these insights into why that of which you already knew that it works actually works, I conclude this week's installment of the Intermittent Thoughts and hope that I did not bore you so much that you do not come back next Sunday for another installment of this series ;-)