Ever Wondered Why the Fat Keeps Falling Off When You Embark on Intermittent Fasting Regimens? Calories, Bro!

Whether it’s a mere reduction in energy intake or carbohydrate fasting, both lead to significant reductions in energy intake beyond the weekly dieting goal set by the scientists. What’s going on in these two studies in overweight women?

I know that 99% of the SuppVersity readers will be smart enough not to believe that calories don’t count. Accordingly, it may be news, but probably not very surprising for most of you to hear that a recent (re-)analysis of food logs from two intermittent fasting studies underlines how effective intermittent fasting really is when it comes to reducing people’s energy intake. In previous studies researchers have already been able to show that the vast majority of dieters do not overeat and consume more than the ~1500kcal/d you may be missing on a fasting day.

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A group of British researchers has now readdressed the issue. In their latest paper in “Food Science and Nutrition” (Harvey 2018) they assessed the initially wanted to quantify the “extent of compensatory overeating on unrestricted days” by reanalyzing subjects food logs from two randomised trials of comparisons of IER and CER (Harvie et al., 2010, 2013).

With the first study being conducted in young overweight women and the second one spanning larger age-group, both studies target similar populations, the “fasting” protocols were different, though. with ~650kcal on two fasting days per week in Harvie 2010, and two low-carb days per week in Harvie 2013. Here’s how the scientists summarize the protocols themselves (Harvey 2018):

  • Study 1 tested a 2 day IER in 53 premenopausal women with overweight or obesity (BMI 24–45 kg/m2) over six months. The IER was designed to provide an overall 25% energy restriction below estimated energy requirements and involved two consecutive days each week of 70% energy restriction below estimated energy requirements, and five relatively unrestricted days /week designed to meet 93% of their estimated daily energy requirements calculated using the Schofield Equation (Schofield, 1985). Restricted days in Study 1 provided 2,700 kJ and 50 g protein and comprised of 1.136 L (2 pints) of semi-skimmed milk, four 80 g portions of vegetables, one portion of fruit, a salty low energy drink, and an over the counter multivitamin and mineral supplement.

    Normal eating days advised a Mediterranean‐type diet (30% of energy from fat; [7% saturated, 15% monounsaturated and 7% polyunsaturated fatty acids], 45% low glycaemic load carbohydrate and 25% protein). Participants were advised on maximal quantities of protein, carbohydrate, and fat on these days and weekly guidance for treat foods (3 per week) and alcohol (14 units/week) to prevent over-consumption. Seven-day food diaries were completed after 1 and 6 months on the diets and were checked for completeness with participants and analyzed using Compeat Nutritional Analysis System (Carlson Bengston Consultants, London, UK).

If someone tries to tell you that intermittent fasting will – just like exercise – make you even more susceptible to overeating, show them the results of Buthani’s 2013 study  on the “effect of exercising while fasting on eating behaviour and food intake”.

How does the magic happen? If we are honest, we have to admit that we don’t even understand why the overeating that is a commonly observed in rodent studies (in almost all of them the rodents don’t overeat to an overcompensation level btw) doesn’t occur in humans… or, as in these particular studies, in overweight women. When it comes to rationalizing the “carry over effect”, which has likewise been observed by Klempel et al. (5% with alternate day fasting in | Klempel 2010) , does in fact seem to conflict with both common sense and previous short-term fasting studies conducted in laboratory settings amongst subjects not attempting to lose weight… and that’s exactly where an often-ignored argument is coming in: at least, when you’re still significantly overweight, every step in the right direction is going to make it easier to continue on the track.

In part that’s certainly due to behavioural aspects of following an IER as part of a weight loss programme, of which Harvey et al. explain that “[a]necdotal reports from subjects in the two reported trials suggest IER can make individuals more aware of their habitual food intakes and habits, increase awareness of appetite and hunger, and provide assurance that they can function adequately during restricted days without the need for extra energy on surrounding days” (Harvey 2018). That it’s (mainly) a behavioural/learning component would be supported by data from Bhutani et al. (2013) reported increased restrained eating and decreases in uncontrolled eating amongst overweight subjects undertaking alternate day energy restriction (75%).

Before you start celebrating, though, I have to warn you: the targeted weekly calorie deficit in the studies at hand was relatively small and as Harvey et al. point out it is well possible that a similar phenomenon “may not occur if IER diets are presented as spells of severe restriction and spells of feasting as is the case with many commercial IER diets” (Harvey 2018).

  • Study 2 tested two different versions of a 2-day IER for 3 months of weight loss and 1 month of weight maintenance (with one restricted day per week) amongst 75 pre and postmenopausal women with overweight or obesity (BMI 24–45 kg/m2). One IER was designed to provide an overall 25% energy restriction below estimated energy requirements and involved two consecutive days of energy and carbohydrate restriction each week (energy restricted low carbohydrate IER, 2,500–2,717 kJ/day, <50 g carbohydrate/day). Each restricted day allowed approximately 250 g of protein foods, three servings of low‐fat dairy foods, four 80 g portions of low‐carbohydrate vegetables and one portion of low‐carbohydrate fruit, at least 1,170 ml of other low‐energy fluids, and an over the counter multivitamin and mineral supplement.

    The five unrestricted days were as above with advice on maximal portions of foods and treats to ensure participants did not overconsume. The other two day IER regimen tested was similar, but allowed unlimited lean meat, fish, eggs, tofu and unsaturated fats on restricted days (ad libitum low carbohydrate IER). Seven-day food diaries were collected and checked for completeness with each participant at 1, 3 and 4 months and were analyzed via Wisp (Tinuviel Software, Anglesey, Wales).

Aside from 7-day food logs, the scientists also had data available that would allow them to classify the subjects into two groups: those that fasted flexibly, i.e. on different days and those that stuck to a certain weekly schedule… and what shall I say:

Here’s where the interesting stuff starts!

Instead of negative effects on adherence and thus reduced fat loss, a comparison of the two groups across studies revealed a significant positive effect of using a more flexible regimen with less than 50% of restricted days on the same 2 days each week: 

“When studies were combined percentage weight loss at 3 months was −5.8 (−6.7 to −4.7) % in the consistent group and −7.4 (−8.7 to −6.2) % in the non‐consistent group (p = .09)” (Harvey 2018)

With the overall large standard deviations, the inter-group difference didn’t reach statistical significance – if we take the relative difference of the means, i.e. 1.6% that’s more than some people manage to lose in total over a three months period and certainly note-worthy (see bottom line for thoughts on why this was the case).

Intermittent fasting is when undereating triggers further undereating!

Ya, I know. It sounds stupid, but the above, i.e. the observation that intermittent fasting does not just fail to trigger energy overconsumption on the following day, but rather

“a spontaneous reduction in energy intake below [subjects’] baseline reported intakes and the prescribed isoenergetic diet during all unrestricted days including the days immediately before and after restricted days” (Harvey 2018)

is a consistent result that was observed across of both of Harvie’s previously cited studies. Now, we are dealing with self-reported food intakes and would have to confirm that in future studies with tighter dietary control. For the time being, however, the (in both studies) significant advantage over a control diet does yet clearly support the notion that all subjects managed to reduce their food intake ~4%-6% below their reported baseline energy intake (Table 1).

Table 1: Energy intake at baseline and on the different unrestricted days of intermittent energy restriction in Study 1 (n = 44) and Study 2 (n = 67) in (kJ/day | Harvey 2018)

In that, a closer analysis of the data in Table 1 informs us that the subjects in study 1 (young, overweight women) were actually restricting their energy intake by 19% on the unrestricted days… voluntarily (they were supposed to eat 7,728 kJ, but ended up with only 6,250 kJ/day). Similar results have been observed in study 2, where only the carbohydrate intake was restricted:

“In Study 2 the mean (95% CI) recommended intake during unrestricted days for both groups was 7,546 (7,399–7,691) kJ, whereas the actual mean intakes were comparable between the energy restricted low carbohydrate IER 5,775 (5,243–6,243) kJ/day and the energy restricted ad lib low carbohydrate IER 6,427 (5,907–6,945) kJ/day (p > .05). The combined groups in Study 2 had a 19% energy restriction below the recommended intake on these days” (Harvey 2018). 

As the uuthors . rightly point out, the “overall energy restriction across the whole week including restricted and unrestricted days in Study 1 and 2 was [thus] 39% below estimated energy requirements, rather than the planned 25% energy prescription” (Harvey 2018)… and again: that happened in response to an intervention of which many well-paid experts will still try to tell you that it’s ‘just going to make you overeat’.

Neither on the day before (pre-) nor after (post-)compensatory mechanisms were observed

Figure 1: IF will not make you overeat – the opposite is the case.

In fact, GEE regression analyses of the data from the days immediately before and after fasting days  clearly indicate that neither in study 1, where data were available on 44 subjects for 59 days immediately following (after) and 59 days immediately before a restricted day (before) and for 177 other unrestricted days (other), nor in study 2, where data were available on 67 subjects for 166 days immediately after and 73 immediately before a restricted day and for 632 other unrestricted days not including days adjacent to a restricted day, showed significant differences in energy intake on the day immediately before and/or after the two restricted days compared with the ‘other’ unrestricted days (p = .46).

Which weekdays you’re fasting on, doesn’t seem to matter, either; after adjusting for the day of the week the scientists found no significant difference across the months that food diaries were completed (p = .38), and no significant difference between days of the week (p = .09). Moreover, there were no statistical significant differences in energy intake between “before” and “other” unrestricted days (p = .98), after adjusting for the day of the week and no significant difference between days of the week (p = .08) nor between months (p = .78 | all p-values from study 1, but generally the same results in study 2).

Cyclic Dieting (2:2 ON/OFF) Drops 12.3 vs. 8kg of Body Fat in 16 Weeks, Maintains REE During + Fat Loss Post Dieting | more

Bottom line: The first thing the re-analysis of the studies does for us is to confirm the notion that intermittent fasting is not a trigger of overeating in the average overweight woman (young and older).

The second thing it the paper at hand suggests is that being flexible in terms of when to take those fasting days seems to be an (albeit non-significant) advantage – an observation that seems only logical, but it will allow you to be more socially compatibel by, for example, post-poning your fasting day from Wednesday to Thursday if the former is a friends birthday and you’d have the choice between falling off the dieting wagon, and/or being the social pariah “on that funky diet, where you don’t eat for X days of the week”.

In conjunction with the excellent and (for many people) pain/hunger-free results (at least in the latter phases of the studies at hand, the subjects no longer complained about hunger on the fasting days), the two previously mentioned study outcomes alone would make intermittent fasting worth trying – the fact that it seems to inspire people (in this case overweight women) to reconsider their overall food intake and/or get used to eating less (could also be that this is a downstream effect of increased metabolic health), so that they reduce their food intake by another -14% beyond what’s prescribed by their diet, however, should convince even true skeptics that dieting two days a week could be a feasible, realistic long-term weight loss strategy that’s worth trying out | Comment!

References:

  • Bhutani, Surabhi, et al. “Effect of exercising while fasting on eating behaviors and food intake.” Journal of the International Society of Sports Nutrition 10.1 (2013): 50.
  • Harvey, Jennifer, et al. “Intermittent energy restriction for weight loss: Spontaneous reduction of energy intake on unrestricted days.” Food Science & Nutrition 6.3 (2018): 674-680.
  • Harvie, Michelle N., et al. “The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women.” International journal of obesity 35.5 (2011): 714.
  • Harvie, Michelle, et al. “The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women.” British Journal of Nutrition 110.8 (2013): 1534-1547.
  • Klempel, Monica C., et al. “Dietary and physical activity adaptations to alternate day modified fasting: implications for optimal weight loss.” Nutrition journal 9.1 (2010): 35.

Ever Wondered Why the Fat Keeps Falling Off When You Embark on Intermittent Fasting Regimens? Calories, Bro! syndicated from http://suppversity.blogspot.com

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35g Pre-Bed Casein Protein, 1st Fair, Isocaloric High Protein (1.8g/kg) Comparison: No Extra Muscle Gain in Young Men

Using casein protein pre-bed can be useful but probably only for those of you who use it to up their total protein intake.

“Once Upon a Time…” It may sound like it, but it is a fact when I tell you that there was a time when bodybuilders got up at night to consume a protein shake. That’s not just the exact opposite of today’s lean gains physique athletes, it is also PM protein ingestion taken to the extreme. An extreme of which a bunch of studies investigating the effects of the ingestion of slow-digesting casein protein before bed suggests that – even if it works – it may be an unnecessary sleep-impairing hassle.

High-protein diets are much safer than some ‘experts’ say, but there are things to consider…

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Satiety: Casein > Whey? Wrong!

Protein Timing DOES Matter!

High Protein not a Health Threat

For those who don’t want to go to such extremes, a recent study by Jordan M. Joy (Joy 2018) could be of interest, the intent of authors from Texas was, after all, to conduct …

“[…] the first longitudinal isonitrogenous, isocaloric, nighttime casein supplementation study investigating the impact on body weight (BW) and composition as well as strength and muscle hypertrophy when an impactful resistance training stimulus occurs earlier in the day” (Joy 2018).

Previous studies have focused on the beneficial effects of additional protein intakes pre-bed. Now, these studies were useful to establish that …

  • protein is digested and absorbed during sleep,  
  • muscle and other tissues respond to hyperaminoacidemia during sleep by increasing muscle protein synthesis (MPS) when prior resistance exercise occurs in the evening 

In 2015, Snijders et al. (2015) conducted a study that supports both hypotheses. Over the course of 12-weeks, fourty-four young men (22 ± 1 y) were randomly assigned to a progressive, 12-wk resistance exercise training program. One group consumed a protein supplement containing 27.5 g of protein, 15 g of carbohydrate, and 0.1 g of fat every night before sleep. The other group received a noncaloric placebo… unfair? Well, I cannot deny that, but that’s what you call a “proof of principle” study.

Figure 1: Predicted resting energy expenditure (REE, kJ/d) for 50 min the morning after night-time consumption of a single serving of whey protein (WP), casein protein (CP), maltodextrin (CHO) and a non-energetic placebo (PLA | Madzimam 2014).

Won’t PM protein make you fat? The authors of the paper at hand already foresaw that you’d ask that and reference studies Ormsbee’s group at the Florida State University conducted between 2014 and 2016 (Madzima 2014; Kinsey 2015 & 2016). While Madzima et al. (2014) were able to show a significant increase in resting energy expenditure of young, healthy, normal-weight men on the morning after ingesting ~30g of whey, casein, or carbohydrates compared to placebo (see Figure 1), it took another 2 years for a follow-up study to make it from the drawing board through data-analysis and peer-review into the August issue of Nutrients.

Said study confirms: There are no detrimental effects of pre-bed casein on glucose metabolism, resting energy expenditure, and appetite – even if the study subjects are hyperinsulemic obese men… that’s good news in terms of fat gain, but bad news when it comes to the notion that the increased energy expenditure reported by Madzima et al. could help obese individuals lose weight… why? Well, as I wrote before: in the obese subjects of Kinsey 2016, it simply didn’t occur.

Accordingly, the previous study/-ies left us with the important question whether any improvements in protein synthesis and lean mass were more than the mere result of the fact that the supplement group consumes 1.9g/kg and the control group only 1.3g/kg protein per day. Exactly this is where Joy et al.’s new study is coming in.

As discussed in the context of different studies, protein timing is a thing… one that probably matters much less than the average gymrat believes. For pre-bed-protein the situation does, however, look different than it does for the legendary post-workout window of opportunity, for which – in science-terms – a ton of research on its importance (or non-importance) for gains exists. For the previously hinted at reasons, this cannot be said of the pre-bed protein research where there’s exactly one (the study at hand) fair comparison of post-workout vs. pre-bed protein…

Wait… post-workout vs. pre-bed that’s unfair, too, isn’t it?

It certainly depends on whether you are with Schoenfeld and Aragon when it comes to the (non-)importance of protein timing if you consider it a “fair” comparison if you have one group of healthy, recreationally active, 18–25-year-old males who have been engaged in regular exercise for the previous 1–3 years at a frequency of 2–5 days per week on night-time vs. post-exercise protein?

Figure 2: The study subjects consumed 1.8 g protein/kg BW inclusive of the casein supplement, and the remainder of calories were provided as 35% fat and 65% carbohydrate – the result is a macronutrient ratio of 28/52/20%.

A lot of strengths and one small weakness: DXA, body impedance and ultrasonography-determined (Logiq e, General Electric Corporation, Boston, MA) CSA of the rectus femoris and combined muscle thickness (MT) of the vastus lateralis and vastus intermedius = reliable data on potential benefits of pre-bed protein supplementation; trained (albeit only “recreationally”) subjects = no newbie gains messing with the results; high standardization in terms of strength/performance testing = reliable data on potential performance benefits of pre-bed protein; reasonable, yet intense workout program (see Table 1) as one will see it done by trainees in the real-world = high probability to see similar results in real-world strength/hypertrophy training; dietary standardization, including a standardized total protein and total energy intake = any putative effect will actually be due to timing…

That’s a pretty long list of strengths, isn’t it? Well, there is also one shortcoming, namely the fact that only 13 subjects completed the entire 10 weeks study. In spite of that, the study at hand is a good example of the often falsely neglected ‘null-result’ studies that add important information to our understanding of optimal training and nutrition for body composition and performance.

In that, the term “post-exercise”-protein may be misleading, because Joy et al. had both groups consume 25g of whey protein immediately after their workouts. In the literal sense – that’s the “post-exercise”-protein. The crucial timing difference, on the other hand, was introduced with 30g of micellar casein which were consumed (a) on top of the 25g of whey at (b) different timepoints. I’ve briefly corresponded with the authors about the casein timing issue because unlike pre-bed administration, the idea of having casein sometime later in the day is pretty vague. Here’s what Jordon Joy told me:

“For the day-time-group, they drank the casein at least 3 hours removed from exercise. Could have been before or after (usually depending on their training time) and they could not have it within 6 hours before bed” (Joy, private communication).

This is interesting as it introduces the possibility that the subjects in the day-time-group came to the gym with elevated amino acid levels. After all, Lacroix et al. were able to show that the serum amino acid levels remain elevated for 5+h in response to the ingestion of a micellar casein protein (Lacroix 2006) – a practice of which Tipton et al. show that it is at least as effective as the ingestion of protein after workouts (unlike in the study at hand, Tipton et al. used whey protein administered immediately before and after workouts in elderly subjects, though – the elevation of amino acids was thus significantly higher and age-related reductions in MPS may figure, as well | Tipton 2006). With that being said, the authors told me that the majority consumed the casein after workouts. 
Weeks 1–5
Monday
Tuesday
Thursday
Friday
Lower Hypertrophy
Upper Hypertrophy
Lower Strength
Upper Strength
Leg Press
5 × 6–15
Bench Press
5 × 6–15
Leg Press
5 × 1–5
Bench Press
5 × 1–5
SS Box Squat
4 × 6–15
Decline Press
3 × 6–15
Hack Squat
3 × 1–5
DB Press
3 × 3–8
Hyperextension
3 × 6–15
Incline Flye
3 × 6–15
Lunge
3 × 3–8
Shoulder Press
3 × 3–8
1-Leg Extension
3 × 6–15
Machine Shoulder Press
3 × 6–15
1-Leg Extension
3 × 6–15
Chest Supported Row
3 × 3–8
2-Leg Curl
3 × 6–15
Lateral Raise
3 × 6–15
2-Leg Curl
3 × 6–15
Pulldown
3 × 3–8
Calf Press
3 × 6–15
Low Cable Row
5 × 6–15
Leg Raise
3 × 10–20
YTWL
3 × 6
1-Tricep Extension
3 × 6–15
Pulldown
3 × 6–15
2-Bicep Curl
3 × 6–15
1-Cable High Row
3 × 6–15
Cable Abdominal Crunch
3 × 10–20
2-Rear Delt Flye
3 × 6–15
Weeks 6–10
Monday
Tuesday
Thursday
Friday
Lower Hypertrophy
Upper Hypertrophy
Lower Strength
Upper Strength
Leg Press
5 × 6–15
Bench Press
5 × 6–15
Leg Press
5 × 1–5
Bench Press
5 × 1–5
Front Squat
4 × 6–15
Incline Press
3 × 6–15
SS Box Squat
3 × 1–5
Pause Press
3 × 1–5
V-Squat Good Morning
3 × 6–15
Decline DB Press
3 × 6–15
DB Lunge
3 × 3–8
DB Shoulder Press
3 × 3–8
1-Leg Extension
3 × 6–15
Shoulder Press
3 × 6–15
1-Leg Extension
3 × 6–15
Cable Low Row
3 × 3–8
2-Leg Curl
3 × 6–15
Cable+DB Lateral Raise
3 × 6–15
2-Leg Curl
3 × 6–15
Pulldown
3 × 3–8
Calf Press
3 × 6–15
Chest Supported Row
5 × 6–15
Leg Raise
3 × 10–20
YTWL
3 × 6
1-Supine Tricep Extension
3 × 6–15
Pulldown
3 × 6–15
2-Preacher Curl
3 × 6–15
1-Cable High Row
3 × 6–15
Abdominal Crunch
3 × 10–20
2-Rear Delt Flye
3 × 6–15
Table 1: Overview of the workout program Joy et al. prescribed (Joy 2018).

Even if we assumed that this form of pre-workout (slow digesting) protein supplementation was relevant, it is thus unlikely to have had an effect in the study at hand. Accordingly, any beneficial/detrimental inter-group differences should – as the authors planned – be a consequence of nighttime protein ingestion in response to a realistic hypertrophy + strength workout (see Table 1) in what you can describe as otherwise “optimal” protein-anabolic conditions.

Figure 3: Changes in body composition over the 10-week study in the nighttime and daytime protein group (Joy 2018).

The scientists’ data analyses using repeated measures ANOVA with Bonferroni post-hoc (alpha was set at p < 0.05), do yet show: there is no such effect. In fact, if anything, the daytime protein administration seems to have a non-significant edge when it comes to the extent of the significant main effect of time (p < 0.05).

No effect was observed for the weekly averages of DOMS and RPE, either. Things look only marginally different for the performance measures. No significant inter-group differences… with one exception: The peak force (PF) during vertical jumps decreased by − 249 ± 386N while it increased by 445 ± 602 N in the daytime supplementation arm of the study.

In 2012 a study by Res et al. rekindled the interest in pre-bed casein | more.

Bottom line: Within the limits of this (small-scale N=13) 10-week study the timed ingestion of micellar casein before bed doesn’t offer significant advantages in terms of either changes in body composition or performance markers. In fact, the “daytime administration” group seems to have seen greater benefits from the workouts… non-significantly greater, that is. Eventually, the study at hand does, therefore, confirm the notion that timing doesn’t really matter as long as a high enough protein intake (here: 1.8 g protein/kg body weight) is achieved.

This doesn’t mean that the issue is settled once and for all, though. In fact, an even longer-term and (more importantly) larger-scale follow-up would be great… maybe one in which Joy et al. investigate a hypothesis they present in the discussion of the results: “[…] it could be possible for DT casein consumption to create an ‘elevated baseline’ for hyperaminoacidemia, thereby reducing the absolute amount of dietary protein necessary to maximize protein synthesis in meals consumed during the 6–7 h postprandial period following casein supplementation”. To me, that sounds logical and it should be possible to test it by repeated pre-post-meal blood draws and subsequent analyses of the amino acid content of the subjects’ blood – ideally, obviously, these results would be corroborated by concomitant changes in muscle protein synthesis in after meals | Comment!

References:

  • Joy, Jordan M., et al. “Daytime and nighttime casein supplements similarly increase muscle size and strength in response to resistance training earlier in the day: a preliminary investigation.” Journal of the International Society of Sports Nutrition 15.1 (2018): 24.
  • Kinsey, Amber W., and Michael J. Ormsbee. “The health impact of nighttime eating: old and new perspectives.” Nutrients 7.4 (2015): 2648-2662.
  • Kinsey, Amber W., et al. “The effect of casein protein prior to sleep on fat metabolism in obese men.” Nutrients 8.8 (2016): 452.
  • Lacroix, Magali, et al. “Compared with casein or total milk protein, digestion of milk soluble proteins is too rapid to sustain the anabolic postprandial amino acid requirement–.” The American journal of clinical nutrition 84.5 (2006): 1070-1079.
  • Madzima, Takudzwa A., et al. “Night-time consumption of protein or carbohydrate results in increased morning resting energy expenditure in active college-aged men.” British journal of nutrition 111.1 (2014): 71-77.
  • Snijders T, Res PT, Smeets JS, van Vliet S, van Kranenburg J, Maase K, Kies AK, Verdijk LB, van Loon LJ. Protein ingestion before sleep increases muscle mass and strength gains during prolonged resistance-type exercise training in healthy young men. J Nutr. 2015;145:1178–84.
  • Tipton, Kevin D., et al. “Stimulation of net muscle protein synthesis by whey protein ingestion before and after exercise.” American Journal of Physiology-Endocrinology and Metabolism 292.1 (2007): E71-E76.

35g Pre-Bed Casein Protein, 1st Fair, Isocaloric High Protein (1.8g/kg) Comparison: No Extra Muscle Gain in Young Men syndicated from http://suppversity.blogspot.com

β2-Agonists Build Muscle: Low Dose Terbutaline Adds 1kg (DXA) in 4 Weeks – With and Without Resistance Training

Who would have thought that? Asthma-sprays probably beat the crap out of good old clenbuterol tabs when it comes to building muscle – even if you don’t train!

Have you ever wondered why so many poor athletes suffer from asthma? Well, if you read my old article about the effects of clenbuterol on myostatin it may long have dawned on you that this could be due to the muscle-building effects of β2-agonists – doping on prescription, so to say.

A couple of days ago, a group of Danish researchers confirmed your suspicions. They’d investigated if inhaled beta2‐agonist, terbutaline, alters body composition and metabolic rate with and without concurrent exercise training in healthy young men.

Learn more about Clen– / Albuterol and safer ways to get jacked at the SuppVersity


Albuterol Can Improve Glucose Metabolism

The Myostatin <> Clenbuterol Connection

Higenamine Useful “OTC Clenbuterol”?

Out of question: β2-Agonists = Doping Agents

Battle the Rope to Get Ripped & Strong

Up Your Squat by 25% With Sodium Bicarbonate

In the corresponding 4-week RCT, sixty‐seven participants completed subjects received what was not even a “therapeutic” dosage (daily terbutaline, 8×0.5 mg) or placebo treatment without concurrent training (habitual; n=23), with resistance (n=23) or endurance (n=21) training three times weekly (Jessen 2018).

  • Participants in the endurance training group performed a high-intensity training program three times weekly on indoor spinning bikes. All training sessions were supervised by an instructor and consisted of 10 min warm-up followed by three blocks of exercise at ~85% of maximum heart rate for 10 min with 30 s of all-out sprinting at the end of each 10-min block.
  • Participants in the resistance training group performed a full-body programme three times weekly. All training sessions were supervised by an instructor and consisted of eight exercises until failure. Resistance was adjusted continually so failure occurred at ~10-12 repetitions.

    The training program was progressive, as each exercise consisted of two sets in the first week, three sets in the second and third week, and four sets in the fourth week. The training program consisted of leg press, bench press, knee extensions, military press, lunges, lat pulldowns, laying leg curl, and low row. Each set was separated by two minutes recovery.

  • Participants in the habitual group did not perform any specific training, but were habitually active in some cases, such as bicycle transportation to and from work, soccer matches, or light running. All participants were physically active less than 4 h weekly.

Before and after the interventions, participant’s body composition was determined by dual‐energy X‐ray absorptiometry, and resting metabolic rate and substrate oxidation by indirect calorimetry.

Serum concentrations of terbutaline after oral administration of 10 mg and inhaled administration of 4 mg in 12 healthy trained men (Dyreborg 2016).

Inhalation may be the preferable method (compared to oral): As Jessen et al. point out, their study is the first of the handful of studies in which beta2-agonists have been shown to be potent anabolic agents in humans that used inhaled vs. orally ingested beta2-agonists – and that despite the fact that inhaled product have a higher systemic bioavailability as compared to oral ingestion(Dyreborg 2016).

Wrt both doping and side effects, it is also worth remembering that the study at hand proves that the dosage one needs to see (at least in the short term) significant results “was more than four times lower than the oral doses administered by Hostrup et al.” (Jessen 2018)

The results in Figure 1 speak for themselves: While ‘doing cardio’ stopped the muscle gains in its tracks, both the resistance training and the sedentary groups gained ~1kg of lean body mass. In that, the scientists found no effects on metabolic rate, fat oxidation or body fat — “[t]his was unexpected, as oral treatment with terbutaline has been shown to reduce fat mass16, and other beta2-agonists did increase fat oxidation acutely” (Jessen 2018).

Figure 1: Changes in lean mass (kg, left) and body fat percentage (right) after 4 weeks on only “near‐therapeutic” dosages of the beta-2-agonist terbutaline (8×0.5 mg) | DXA data (Jessen. 2018).

Overall impressive results, but still… we should not forget that we are talking about young healthy men with 2-5 h physical activity per week, and an average maximal oxygen consumption (VO2max) of 40-60 ml/min/kg – that’s not exactly what you’d see in pro-athletes… accordingly, future studies won’t just have to test the effects of higher dosages of terbutaline, but also if “real” athletes benefit to a similar extent. I guess, in this context, it is worth highlighting, again, that …

“[…] the dose administered in the present study is higher than that normally prescribed to asthmatics, the dose is within the limit of what many elite athletes may use in association with training sessions as prophylactic treatment” (Jessen 2018).

Accordingly, the authors of the study at hand are right to point out that “present study should be a point of caution for clinicians who are treating elite athletes as terbutaline inhalation in doses of 4 mg, and presumably above, may potentiate training adaptations to resistance training” (Jessen 2018) – I guess none of the athletes would mind, though?!

If you look at the individual gainz, resistance training does no longer seem so useless as the non-significant inter-group difference in gains would suggest – does it (Jessen 2018)?

Mechanism = myostatin inhibition!? As I’ve discussed in the previously cited article about the anti-myostatin effects of clenbuterol beta-2-agonists may work by loosening the muscle-building brakes. Whether that was the case for terbutaline in the study at hand cannot be said in the absence of corresponding bio-assays. This, as well as possible desensitization effects, will have to be investigated in future studies.

Against that background, it is not really surprising that they work their performance-enhancing magic only in strength athletes, in endurance athletes, where they are commonly abused, they even seem to impair the intended training effects (Hostrup 2018) | Comment on Facebook!

References:

  • Dyreborg, Anders, et al. “Pharmacokinetics of oral and inhaled terbutaline after exercise in trained men.” Frontiers in pharmacology 7 (2016): 150.
  • Jessen, S. , Onslev, J. , Lemminger, A. , Backer, V. , Bangsbo, J. and Hostrup, M. (2018), “Hypertrophic effect of inhaled beta2‐agonist with and without concurrent exercise training: a randomized controlled trial.” Scand J Med Sci Sports. Accepted Author Manuscript. doi:10.1111/sms.13221
  • Hostrup, Morten, et al. “Chronic β2‐adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men.” The Journal of physiology 596.2 (2018): 231-252.

β2-Agonists Build Muscle: Low Dose Terbutaline Adds 1kg (DXA) in 4 Weeks – With and Without Resistance Training syndicated from http://suppversity.blogspot.com

Hair Loss: Nutrient Deficiencies, Supps, Herbal Shampoo Ingredients, and Egg Yolk Hair Masks for Alopecia | Plus: Carcinogens & Endocrine Disruptors in Your Shampoos

While women will (comparatively) rarely go completely bald, they have the same problems with thinning hair as men do… and diet (from nutrient deficiency to excess – esp. vitamin A + D) are primary drivers of hair loss in both, men and women; and that despite the fact that deficiencies of both retinol and 25OHD contribute to hair loss, too (Rushton 2002; Guo 2017).

I’ve written extensively about “conventional alternative” treatments (alternative = avoiding 5-AR inhibitors that block the conversion to DHT and not paying for a transplant) roughly a year ago in “Hair Loss: Finasteride, Laser Light or Minoxidil – What Will Really Help Men & Women Regrow Lost Scalp Hair?” (re-read it).

In view of the fact that this is still one of the more popular articles and considering the interest many of you showed in a recent Facebook post of mine that included the list of nutrient deficiencies, ailments, and behaviors that may cause hair loss (Table 1) on Facebook, I decided to re-address the issue. This time with a focus on the former, i.e. dietary and behavioral factors that promote hair loss and potential ways to address them while avoiding increasing your exposure to carcinogenic endocrine disruptors from cosmetics.

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

Potassium vs. Diet-Inducded Insulin Resis.

In the Lime Light: The Ill Effects of Low K Intakes

Bad News: Most Americans are Sign. K Deficient

Lean, Healthy … Correlates of High Hair Potassium

Eating a High Protein Diet? Better Watch K!

Potassium Bicarbonate = Anabolic!?

To begin with, let’s briefly readdress why you may be losing your hair in the first place. As Rajesh Rajput Rajendrasingh points out in Chapter 71 of “Practical Aspects of Hair Transplantation in Asians” (Haber 2018), …

“[… h]air loss is a derangement or disregulation [sic!] of the hair growth cycles in the body caused by multiple factors acting in tandem. There is a role of genetic predisposition. However, the outcome is influenced by environmental factors, pollution, stress, lifestyle, aging, diet, scalp care, and hygiene” (Rajendrasingh 2018).

Now, genetics and aging are (as of now) factors you can neither tweak (safely) nor avoid. The rest of the factors, however, may be addressed and could (no guarantees, here) allow/force your body to (re-)start replacing the 100% natural loss of hair with new hair, again (that’s the way it’s supposed to work – and no, science indicates, the cells rarely die, they just stop to reproduce hair).

Table 1: Tabular overview of various factors that may cause hair loss – apart from androgenetic alopecia, where the mechanism does not involve DHT as a mediator of hair loss (Rajendrasingh 2018).

Thus, “[t]reating hair loss is more about how to retain hair, strengthen the roots, promote hair growth, and stimulate the hair cycles to continue rather than fighting hair fall” (Rajendrasingh 2018).
This is particularly important because research indicates that usually less than 10% of the roots are affected in any given growth cycle, and thus it takes a few years for baldness to become apparent – even if your hair is already falling out without being subsequently replaced.

You will read all sorts of things about the (sex)hormonal origin(s) of hair loss, don’t believe it! While both testosterone and estrogen have been shown to inhibit hair growth in the petri dish, epidemiological evidence shows that only DHT, not estrogen or testosterone levels are elevated in people with increased hair loss (in men | Kische 2017).

I’ve previously addressed low-dose 2% and 5% topical minoxidil applications, the use of medicated shampoos, and LLLT in last year’s article (re-read it). This article is sort of a follow-up that will focus on diet (antioxidants, vitamins, and minerals) and selected supplements.

Table 2: Too much of a good thing – Side effects of excessive use of supplements that could help w/ hair loss (Guo 2017).

Obviously, the first stop on your journey to stopping hair loss is to make sure you avoid deficiencies in zinc, vitamin A, C, E, and D and check for typical triggers such as thyroid dysfunction or medication you may be taking for other reasons. Other reasons to address are…

  • potential toxins in your diet/environment – Since a toxin-free environment is required for the cells to divide, minimizing your exposure to agents that are known to cause hair loss – these include heavy metals, such as thallium and mercury, for which industrial and mechanical workers are at most risk for exposure, dietary supplements, such as vitamin A, insecticides, such as boric acid, and other more specific agents, such as colchicine, arsenic, excess selenium, botulinum toxin, Podostroma cornu-damae, and the synthetic opioid MT-45 (Yu 2018).
  • lack of catalysts required to facilitate metabolic processes required for hair growth – The former include some of the previously mentioned nutrients, i.e. trace elements such as iron, calcium, zinc, and magnesium that form the structure of the hair, but also amino acids, the building blocks for the hair, as well as vitamins (here in the broader sense) such as biotin (largely overrated according to Patel 2017), B-complex, vitamin C, and omega 3. All these vitamins, minerals, and nutrients, if

Talking in-depth and in an evidence-based fashion about the former would go way beyond the scope of this review – my advice thus is:

Reconsider the amounts of vitamin A (retinol in its various forms) and selenium you’re supplementing with and stay away from processed junk food and known sources of heavy metals.

You want to keep the above in mind also when it comes to supplements. Even the “holy health grail”, vitamin D (the hype supplement of the decade) has been shown to promote hair loss when taken in excessive amounts (Carlberg 1996). More doesn’t help more!

The magic (peptide) is in the yolk: I am pretty sure you’ve seen women use egg-based “hair masks” in YouTube videos before, too. Be honest, did you laugh about such stupidity? Well, in this case, you may be the stupid one: It is both logic (hair mostly grows in a precocial bird) as well as scientifically proven that the yolk of chicken eggs contains a key hair growth factor. Nakamuro et al. (2018) were able to show that the VEGF stimulation and effects on human hair follicle dermal papilla cell growth are significant enough to be observed even if the eggs are not massaged into your scalp, but simply eaten … well, certain peptides from the yolk, that is (note: in different but related contexts, i.e. healing burn wounds egg yolk has been used topically successfully | Yenilmez 2015).

Egg yolk peptides may facilitate hair (re-)growth in women. Female pattern hair loss patients were orally administered placebo or HGP-containing capsule (2x125mg) for 24 weeks. (A) Changes in Savin scale. (B) Number of subjects with improved hair growth; that is, number of decreased Savin scale subjects. (C) Photographs of subject scalp before and at 24 weeks after administering egg yolk peptide. (D) Hair density measured by phototrichogram (Nakamura 2018).

In their study, there were significant improvements in hair growth in both mice and humans who were fed a diet containing 0.1% of egg yolk peptides (mice) and 2x125mg of egg yolk peptides in supplemental form.

Next to the surprisingly visible results in the photo in the figure to the left, the paper that has been published ahead of print in the Journal of Medicinal Food shows that the water-soluble egg yolk peptides induce VEGF expression through insulin growth factor-1 receptor activation-induced hypoxia-inducible factor-1α transcription pathway… “Wait, IGF1?” If you are now thinking about the eggs vs. egg-white study showing 40% increased gains with whole eggs vs. egg whites, you are probably a similar science geek as I am… or simply remember my article from last year ;-).

What could help, though, is a supplementation protocol outlined by Rajendrasingh et al. in the previously cited chapter in “Practical Aspects of Hair Transplantation in Asians” (Haber 2018). It takes into consideration that ‘anti-hair loss supplements’ heavily compete for absorption and is thus a three-day protocol that avoids the simultaneous provision of agents such as iron and calcium, of which 30-40% are lost when they are administered together:

Table 3: Cyclical vitamin therapy for hair loss management as suggested in Rajendrasingh 2018.

In this context, it is worth mentioning that scientists dabbling in the field explicitly warn people not to consume multi-vitamins – especially the high(er)-dosed ones that are marketed to athletes might do more harm than good. Moreover, Rajendrasingh et al. (2018) advise that the “addition [of] topical application of biomimetic peptide[s] is advised every morning to promote hair growth [see infobox on egg], and topical minoxidil 2% in females and 5% in males is advised every night” to get the most from the previously outlined stack. Moreover, ketoconazole 2% shampoo is recommended once every 3 days and regular pH balanced shampoo twice a week or up to every day as desired. Plus: The optional use of LLLT hair growth for 20 min once a week may yield even better results.

Do not laugh about “alkaline diets” – They imply switching to healthier food options and that will promote both your health and performance!

Why’s high protein a problem? You will probably have spotted it right away in Table 1 – fad-diets and high protein diets promote hair loss… supposedly! The explanation Rajendrasingh (2018) give, is not 100% convincing, though. He writes: “High protein diet leads to acidic blood pH which requires reabsorption of calcium to neutralize the acidity, leading to indirect calcium deficiency and hair loss”. Furthermore, there is research suggesting that blood androgen levels will increase after high meat and fat meals – this could, in fact, promote hair loss in susceptible individuals.

Even if I don’t think that that high protein (esp. meat) intake is the most common cause of hair loss, the solution Rajendrasingh offers, i.e. to “rotate the source of protein to include beans, dals, chickpeas, soy, mushrooms, milk, yogurt, egg, fish, and some meat” is good advice, anyway – low protein intakes will, after all, also promote hair loss, because protein is your #1 (and only) natural source of the previously listed amino acids that are required or facilitative for/to hair growth.

As far as individual dietary factors are concerned, the list of potentially useful nutrients (vitamins, minerals, etc.) includes…

  • vitamins: biotin (vitamin B7) for hair growth and dry skin; nicotinamide (vitamin B3) for its anti-inflammatory purposes; cyanocobalamin ’cause it prevents anemia; pyridoxine HCl (B6) which prevents anemia and water retention, vitamin C as an antioxidant, and prerequisite for collagen synthesis; vitamin A (moderate amounts) and vitamin E as antioxidants and cell-protecting agents; folic acid (B9) to help prevents anemia and facilitate DNA synthesis, and vitamin D (moderate amounts of <2,000 IU/d) to promote calcium metabolism
  • amino acids: l-histidine, tyrosine and lysine, which are required for/seem to improve hair growth; l-ornithine which promotes DNA and protein synthesis, as well as arginine, which is involved in rapid cell division, repair, and endothelial stability; taurine (2 aminoethanesulfonic acid), which has potent detoxing (in the real-science sense 😉 effects; glycine, which is an important precursor to biosynthesis of various proteins, as well as the sulfur proteins l-selenomethionine/sodium selenate and sulfur-methylsulfonylmethane 
  • Zinc is one of the candidates for totally overrated supps. Its benefits in T2DM are a result of increased insulin, not improved sensitivity.

    minerals: ranging from iron (preferably Ferrous fumarate), calcium and magnesium, over manganese, iodine, molybdenum to chromium, zinc, and (specifically important for the morons many people in the fitness industry are) copper, which (just as iron) can be depleted if you supplement with zinc like crazy (and NO you are not fat because you’re zinc deficient, the opposite may be the case!)

  • others: potentially useful are also the fatty acid gamma-linolenic acid (GLA) for its anti-inflammatory prowess; para-aminobenzoic acid (PABA), which prevents premature graying of hair; inositol, which prevents hair thinning in women, in particular; green apple extract (probably the pectin), as well as all the proanthocyanidins, flavonoid, and catechins in berries, tea, etc. 

Saw palmetto, which is also on the original list of potential supplement candidates in Rajendrasingh (2018) is a natural 5-AR inhibitor of which I am still not sure if they are a good idea (at least not as a default therapy).

Figure 1: First rule of controlling hair loss – Get your dietary ducks in a row.

An important part of getting your nutritional ducks in a row (see Figure 1) is also proper hydration of both, your whole body and – maybe in this particular case even more importantly – your scalp! The latter may easily dry out in response to the use of inappropriate shampoos and/or hair styling products! As far as the former is concerned, there’s, by the way, an interesting rodent study showing highly beneficial effects of mineral-rich spring water in SKH-1 hairless mice who are almost non-response to conventional treatment with (e.g.) minoxidil (Begum 2017).

Can you wash your hair too often? No, but you can style them to death…

If you wash your hair thrice a day, I would start investigating OCD issues, but as far as hair loss is concerned, there’s currently no evidence that washing your hair daily (or even more frequently) would trigger hair loss – assuming you use a pH neutral (non-alkaline) shampoo, ideally without sulfates, that won’t dry out your scalp (more about shampoos in Draelos 2010).

Caffeine penetrates the skin and open follicles are important for the time-course of penetration, human study shows putting caffeine shampoo right on the skin of hairy chests for 2 minutes (Otberg 2007).

Caffeine-based anti-hair-loss shampoos!? In case you’ve previously tried caffeine-based shampoos to no avail, you will also be interested to hear that you probably didn’t leave them on/in your hair long enough.

If you look at the absorption data from Otberg et al. (2007 | figure on the left) it becomes clear that the absorption is significant, however, it occurred when the scientists smeared the caffeine shampoo right onto the skin and left it there for 2 minutes. Moreover, anything that would seal the follicles (like too much sebum) would at least slow down, if not impair the absorption kinetics.

What you do want to avoid, though, are (almost) boiling hot water, using a really hot hair-dryer, and – mostly for women and hipsters – tieing your strands back so tightly that they will pull on your skin and (ab)using so much hair gel, hairspray and other stuff that’s keeping your scalp from breathing that your hair follicles are suffocating.

No hot water, no hot hair-dryers, no hair pulling hair hairdos – check ✓

Speaking of suffocating, while the previously mentioned ketoconazole 2% shampoo seems to have some independent anti-inflammatory effects on the dermis beneath your more or less full scalp hair, it does also kill  Malassezia spp. and Staphylococcus spp., both examples of fungi, and bacteria which are (naturally) growing on your skin, and have both been implicated in the induction of the micro-inflammatory processes that are at the heart of several types of male/female hair loss (Pierard-Franchimont 1998; Gaber 2015).

Table 4: Contrary to some claims you may have read online, anti-dandruff shampoos prevent/reduce hair loss and don’t promote them. In that, the more expensive ketoconazole shampoos (Nizoral) are slightly more effective than the cheap zinc pyithione (Head & Shoulders) based products (Piérard‐Franchimont 2002)

The influence of the microbiome is yet not just restricted to local effects. In fact, studies like Nair et al. (2017) indicate that calming down the pro-inflammatory effects of the microbiome with a broad-spectrum antibiotic cocktail (ampicillin, neomycin, metronidozole, vancomycin) protects mice from autoimmune alopecia. If it’s just the previously mentioned Staphylococcus species that are a problem is yet still a matter of ongoing research and, as in other related areas, the whole “microbiome and hair loss”-research is still pretty much in its infancy – and that’s despite papers such as Chen, et al. (2016) which claim that “[t]he gut microbiome is required for the development of alopecia areata” as early as in their title.

Table 5: Plants commonly used in herbal shampoos (Arora 2011).

Before this research is not available you may want to look into ditching your chemically loaded P&G + Co. shampoos with natural ingredients as they have been listed in a recently published review by Arora et al. (2011 | see Table 5) – don’t assume, though, that those are natural and hence without potential side effects; as far as their allergenicity are concerned some may even be worse than the “chemicals” in commercial shampoos.

Moreover, many of the commercially available “herbal shampoos” are everything but exclusively herbal-based. In fact, some of them even contain particularly unhealthy substances such as…

  • sodium lauryl sulphate and related compounds – SAS is one of the most commonly used detergent. While it is recognized as Generally Recognized As Safe (GRAS), a study done at the Medical College of Georgia has shown that shampoos with SLS could retard healing of wounds in surface of cornea and can cause cataract in adults. Furthermore, SLS will build up in heart, liver, lungs and brain can cause major problem in these areas – to this ends, it does yet have to be ingested in significant amounts. Similar effects have been observed for other sulphate-containing groups (Chiu 2015).

    Skin contact to SAS will lead to generally less severe side effects such as flaky, rough skin roughness and – you almost guessed it – corroded hair follicles with an impaired ability to grow hair. Decyl polyglucoside may be a viable alternative (Vozmediano 2000).

  • cocamidopropyl betaine –  While it is often used in ‘no tears shampoos’ for children, it seems to be responsible for many of the allergic reactions in response to both shampoos and shower gels – especially in kids (Militello 2006). 
  • diethanolamine or DEA – While DEA including the formerly widely used cocamide DEA seems to disappear from the market slowly, it is sill used in many shampoos – probably because it is still considered GRAS (offically), despite the fact that, in laboratory experiments, exposure to high doses of DEA-related ingredients has been shown to cause liver cancers and recancerous changes in skin and thyroid, as well as to “cause mild to moderate skin and eye irritation” (Udebuani 2015) – you shouldn’t forget the qualifier “in high doses”, though.
  • disodium ethylenediamine tetraacetic acid (EDTA) – Has mostly case reports to support its allergic potential. If you react with dermatitis to a shampoo, it may still be worth checking the label for the acronym “EDTA”.
  • formaldehyde and formaldehyde releasing substances (also disguised as Quaternium – 15) – Is another potential allergenic substance that has long been one of the favorite preservatives of the average shampoo producer, because it has the nice side effect of altering hair keratin to reduce the frizziness and give a smoothness effect. Unfortunately, formaldehyde is a known carcinogen, which can cause allergic reactions of skin, eye and nose irritation, and lung cancer during dermal exposure (Chiu 2015).
  • parabens – Methylparabens and propylparabens are the most common preservatives found in the cosmetic industries that are used to control microbial growth to extend the shelf life… and they accumulate in cancerous breast tissue (Chiu 2015) – coincidence? Well, let’s say that almost all major consumer good brands have either already pulled it from their formulas or are about to do that very soon. Smart move, ’cause research indicates that their bioavailability is probably higher when applied topical vs. being ingested orally.
  • polyethylene glycol (PEG) – Is, just like parabens, one of the substances producers even use to market their products… as “PEG-free”, obviously. Just like parabens PEG is absorbed through intact skin and demonstrated penetration of substances across biological barriers; it can alter and reduce the skin’s natural moisture factor causing accelerated aging as well as increasing permeability of substances including harmful ingredients. As Chiu et al. point out, though, that …

    “[…a]part from the potential concerns, there are no sufficient evidence showing systemic toxicity of acute dermal exposure [accordingly, from] the safety assessment, PEG is considered safe for use in personal care products, but there has been concerns with the contamination of 1,4-dioxane and ethylene oxide during the manufacturing process” (Chiu 2015).

    Said 1,4-doixane is, as you probably guessed it, another carcinogen, and ethylene oxide is classified as a developmental neurotoxicant. Ever since the Organic Consumers Association have found traces of contaminations in the PEG containing hygiene products – ever since, producers are pulling PEGs from their products

  • phthalates and silicon – While phthalates have been shown to possess developmental and reproductive toxicity and hormonal disturbances particularly in males (Heudorf 2007), the “wise” FDA does not recognize that phthalates pose a safety risk. The same goes for silicones such as dimethicone, where the scientific data on its toxicity is allegedly less convincing than for phthalates and many of the previously mentioned agents.

If you cannot find a shampoo without any of these (for “cosmetics”, in general, the list can be extended endlessly, by the way, but those appear to be the major culprits in shampoos), you can simply use the info from Table 5 to produce your own hair care products… ok, I know, “too inconvenient” – in that our hair care choices mirror our dietary choices, where we also gravitate towards convenient, cheap products even though, by now, we should know that this won’t just support the food industry, but also and even more so the pharma companies that produce and sell drugs to battle metabolic syndrome we develop in response to these foods :-/

#SVClassic: Hair Loss: Finasteride, Laser Light or Minoxidil – What Will Really Help Men & Women Regrow Lost Scalp Hair? | more

Ok, I am “eating healthy”, still losing hair – What can I do? If you have the previously mentioned ‘dietary ducks’ in a row, there are a handful of specialty supplements with (usually sponsored) scientific backup. Zanzottera et al (2017), for example, describe a fatty acid + phytosterol supplement that prevents hair loss and promotes hair health in both women and men. The product comes in gel-caps and contains borage, linseed, wheat germ (all three >25 and <50%), and saw palmetto (>10 and <25%) as well as phytosterols (0.5-5%) from pine and rye extract. A brief look at the photos in the corresponding paper does yet show IMHO disappointing results (those I wouldn’t be willing to pay for).

Rather than to waste time and money on these or related products, it would thus make sense to revisit my previous article on actually proven (but in all cases less convenient) treatment modalities such as the previously mentioned daily application of minoxidil (in dry hair!) and/or the regular use of LLLT… or coffee! Seriously, only recently Alonso and Anesi published a study showing that a spray that applies a coffee extract (+Larrea divaricata) locally can help with both hair loss and dandruff (Alonso 2018) – don’t forget you got to keep it on for >2 minutes, though. Ah… and it may also help that each cup of coffee you use to rinse your hair is a cup less you’ll drink and thus risk impairing the absorption of iron from your diet. Low iron is, after all, one of the #1 reasons women, especially women who don’t live within the iron-fortified cereal world of North America (iron deficiency < 10% vs. 40%-60% in Africa, Asia and the Eastern Mediterranean | Stoltzfus 2003) or exercise regularly (among women with >3h of mostly aerobic work per week ~30% are deficient | Sinclair 2015), tend to lose hair | Comment on Facebook!

References:

  • Alonso, María Rosario, and Claudia Anesini. “Clinical Evidence of Increase in Hair Growth and Decrease in Hair Loss without Adverse Reactions Promoted by the Commercial Lotion ECOHAIR®.” Skin pharmacology and physiology 30.1 (2017): 46-54.
  • Arora, Pooja, Arun Nanda, and Maninder Karan. “Shampoos based on synthetic ingredients vis-a-vis shampoos based on herbal ingredients: a review.” International Journal of Pharmaceutical Sciences Review and Research 7.1 (2011): 41-46.
  • Begum, Rahima, et al. “Hair Growth Promoting Effects of Mineral-rich Spring Water in SKH-1 Hairless Mice.” 한국물학회지 Vol 6.1 (2017).
  • Carlberg, Carsten. “The concept of multiple vitamin D signaling pathways.” J. Investig. Dermatol. Symp. Proc. Vol. 1. 1996.
  • Chen, J. C., et al. “470 The gut microbiome is required for the development of alopecia areata.” Journal of Investigative Dermatology 136.5 (2016): S83.
  • Draelos, Zoe D. “Essentials of hair care often neglected: Hair cleansing.” International journal of trichology 2.1 (2010): 24.
  • Gaber, Hisham Diab, Ahmed M. Mohamed, and Reham M. Abdel Gaber. “Presence of Alternaria in Scalp of Patients with Alopecia Areata: Triggering Factor or Coexistence?.” Journal of Life Sciences 9 (2015): 341-345.
  • Haber, Robert. Practical Aspects of Hair Transplantation in Asians. Springer, 2018.
  • Heudorf, Ursel, Volker Mersch-Sundermann, and Jürgen Angerer. “Phthalates: toxicology and exposure.” International journal of hygiene and environmental health 210.5 (2007): 623-634.
  • Johnstone, Murray A., and Daniel M. Albert. “Prostaglandin-induced hair growth.” Survey of ophthalmology 47 (2002): S185-S202.
  • Militello, Giuseppe, Sharon E. Jacob, and Glen H. Crawford. “Allergic contact dermatitis in children.” Current opinion in pediatrics 18.4 (2006): 385-390.
  • Nair, L., Z. Dai, and A. M. Christiano. “649 Gut microbiota plays a role in the development of alopecia areata.” Journal of Investigative Dermatology 137.5 (2017): S112.
  • Otberg, N., et al. “Follicular penetration of topically applied caffeine via a shampoo formulation.” Skin pharmacology and physiology 20.4 (2007): 195-198.
  • Patel, Deepa P., Shane M. Swink, and Leslie Castelo-Soccio. “A review of the use of biotin for hair loss.” Skin appendage disorders 3.3 (2017): 166-169.
  • Pierard-Franchimont, C., et al. “Ketoconazole shampoo: effect of long-term use in androgenic alopecia.” Dermatology 196.4 (1998): 474-477.
  • Piérard‐Franchimont, C., et al. “Nudging hair shedding by antidandruff shampoos. A comparison of 1% ketoconazole, 1% piroctone olamine and 1% zinc pyrithione formulations.” International journal of cosmetic science 24.5 (2002): 249-256.
  • Rajendrasingh, Rajesh Rajput. “Nutritional Correction for Hair Loss, Thinning of Hair, and Achieving New Hair Regrowth.” Practical Aspects of Hair Transplantation in Asians. Springer, Tokyo, 2018. 667-685.
  • Rushton, D. H. “Nutritional factors and hair loss.” Clinical and experimental dermatology 27.5 (2002): 396-404.
  • Sinclair, Lisa M., and Pamela Sue Hinton. “Prevalence of iron deficiency with and without anemia in recreationally active men and women.” Journal of the American Dietetic Association 105.6 (2005): 975-978.
  • Stoltzfus, Rebecca J. “Iron deficiency: global prevalence and consequences.” Food and nutrition bulletin 24.4_suppl2 (2003): S99-S103.
  • Udebuani, A. C., et al. “Possible Health Implications Associated with Cosmetics: A.” Science 3.5-1 (2015): 58-63.
  • Vozmediano, J. M., et al. “Evaluation of the irritant capacity of decyl polyglucoside.” International journal of cosmetic science 22.1 (2000): 73-82.
  • Yenilmez, E., et al. “Chitosan gel formulations containing egg yolk oil and epidermal growth factor for dermal burn treatment.” Die Pharmazie-An International Journal of Pharmaceutical Sciences 70.2 (2015): 67-73.
  • Yu, Vicky, et al. “Alopecia and Associated Toxic Agents: A Systematic Review.” Skin Appendage Disorders (2018).
  • Zanzottera, F., et al. “Efficacy of a Nutritional Supplement, Standardized in Fatty Acids and Phytosterols, on Hair Loss and Hair Health in both Women and Men.” J Cosmo Trichol 3.121 (2017): 2.

Hair Loss: Nutrient Deficiencies, Supps, Herbal Shampoo Ingredients, and Egg Yolk Hair Masks for Alopecia | Plus: Carcinogens & Endocrine Disruptors in Your Shampoos syndicated from http://suppversity.blogspot.com

Want to HIIT it, but Hate Sprinting? 4-Minute-HIIT-Workout using Burpees, Mountain Climbers, Squats + Thrusts w/ 3-kg Dumbbells, and Jumping Jacks Works Almost as Well

Guys, you can benefit from bodyweight exercises, too – not just when traveling!

Running ain’t for everyone. I know that, … So, if you’ve sustained an injury that keeps you from all-out sprints, or you simply hate sprinting, altogether, it would appear as if high-intensity interval training (HIIT), the time saving and in several aspects, such as the effects on post-workout oxygen consumption, superior version of “cardio” was not for you. Wrong.

I belong to the group of people who are not really into sprinting, so, as mentioned before, I like using a rowing ergometer for my HIIT sessions and if that doesn’t sound appealing to you, either, what about some whole body + body weight exercises?

You can learn more about HIIT at the SuppVersity

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

The beauty of the workout Schaun et al. investigated for their latest paper in the Journal of Strength and Conditioning Research (Schaun 2018) is that …

  • Fast-paced weight lifting circuits yield both strength and fitness gains | more

    it can be easily done in a hotel room with minimal (or no) equipment, and takes only ~4 minutes (+4 min warm-up = 8 minutes vs. 30 minutes for MICT), and

  • it is almost as effective as sprinting in increasing the VT2_max, i.e. the point where you’ll have to stop training and is thus a true cardio training

and it is a strategy that may be valuable beyond the everyday AM workouts you are hopefully doing to stay in shape when you’re traveling – you must just have the guts to perform the 2x4x20s efforts of burpees, mountain climbers, squat and thrusts with 3-kg dumbbells, and jumping jacks at truly “maximum effort” (this workout produced quite outstanding results in McRae et al. (2012), already)

Speaking of staying in shape…

As the results of the study at hand show, both sprinting and MICT seem to be better suited for improving classic performance-related outcomes and body composition.

Table 1: Descriptive variables according to protocol performed in response to 16 weeks of training in healthy young adults; †Significantly different from pre (p < 0.001 | Schaun 2018)

As the data in Table 1 goes to show you, the pre-post differences in skinfold thickness and body fat % favor the classic sprint (HIIT-T) and medium-intensity steady state (MICT) training. This does not mean, however, that the body weight workout didn’t produce results in the (initially) N=55 young, healthy subjects who had been randomly assigned to one of the three protocols over a 16-week period.

Figure 1: VO2max increases (left) clearly favor the classics, the changes in the ventilatory threshold 2 (right), i.e. the point where you have to quit exercising because you’re fatigued, on the other hand, benefit more from whole-body + body-weight HIIT vs. classic medium-intensity cardio (no difference to sprinting | Schaun 2018).

Furthermore, it should be noted that the testing procedures used to quantify the performance effects illustrated in Figure 1 clearly favored HIIT-T and MICT as they were based on treadmill-based – confounding by a sport-specific training effect in either of the last-mentioned groups can thus not be excluded.

Eight HIIT Sessions on the Rowing Ergometer Cut Body Fat, Increase Adiponectin, VO2Max & Performance in National Level Rowers – Workmatched Classic ‘Cardio’ Does Nada. What does that tell you? You can and should stop sprinting if you hate it and try different modes of high-intensity interval training… including, if you want, whole body w/ body-weight training | more

So what does that mean for me or my clients? Well, I guess the most important take-home message is that a sequence of is a viable alternative to both, classic steady state medium- and sprint high-intensity interval training.

I would estimate the effects to be even more pronounced if there was a way to monitor one’s own efforts while training objectively – the MICT and HIIT-T group had the treadmill to tell them how fast they were going. This helps you keep accountable and may (via downstream effects on exercise intensity) alone explain the slight disadvantages of HIIT-MB.

I would thus support the scientists’ conclusion that “this training mode can [already] be suggested as a great possibility for training regimes aimed at health and physical fitness promotion […] despite the need for large-scale studies in nonlaboratory environments” (Schaun 2018) and the questionable applicability of this way of training to/in obese individuals, by the way | Comment on Facebook!

References:

  • McRae, Gill, et al. “Extremely low volume, whole-body aerobic–resistance training improves aerobic fitness and muscular endurance in females.” Applied Physiology, Nutrition, and Metabolism 37.6 (2012): 1124-1131.
  • Schaun, GZ, Pinto, SS, Silva, MR, Dolinski, DB, and Alberton, CL. Sixteen weeks of whole-body high-intensity interval training induce similar cardiorespiratory responses compared with traditional high-intensity interval training and moderate-intensity continuous training in healthy men. J Strength Cond Res XX(X): 000–000, 2018

Want to HIIT it, but Hate Sprinting? 4-Minute-HIIT-Workout using Burpees, Mountain Climbers, Squats + Thrusts w/ 3-kg Dumbbells, and Jumping Jacks Works Almost as Well syndicated from http://suppversity.blogspot.com

Protein-Timing & Fasting: Fasted Sprints & the Remarkable Muscle↑, Fat↓ Effect of Timing Whey With vs. Between Meals

Not sure what would happen to your sprints if you have whey before HITing it…

While more and more scientists and “evidence-based” trainers and fitness gurus, alike, keep repeating that “protein timing” – as heavily and feverishly as it is often debated on Facebook and elsewhere on the interwebs – is significantly less important than some gymrats still tend to believe (Schoenfeld 2013). The question “When do I take my whey shake?” is still a topic worth discussing. In particular, if an interesting new study – a systematic review, to be precise – seems to suggest that protein timing does, at least in protein supplementation studies, matter…

and what’s most exciting, it seems to matter for the one outcome of physical exercise and dietary discipline many gymrats consider the #1 on their priority list: improvements in body composition… or, as many call it, “getting ripped and jacked” 😉

Learn more about building muscle and strength while losing fat with http://www.suppversity.com


Acutely Increased Hormones Don’t Grow Muscle?

Protein vs. Carbs 4 Glycogen, BFR & Recovery …

Pre-Exhaustion Exhausts Your Growth Potential

Exercise not Intensity Variation for Max. Gains

Battle the Rope to Get Both, Ripped and Strong

Study Indicates Cut the Volume Make the Gains!

Now, while these results are somewhat surprising, they are not as counter-intuitive as the results of the 2nd study that made it into this “Meal-Timing & Fasting” special. The study I would like to begin with:

  • Sprinting fasted significantly increases time-to-exhaustion in trained cyclists (Terada 2018) — If anything you would probably have expected that going into a sprint-interval session fasted, after an overnight fast (SITFast) would maybe increase the initial performance, because of elevated stress hormones, but the reality of a recent RCT (N=20) from the University of Alberta shows “that SITFast compromises exercise intensity and volume but still can have a greater impact on the ability to sustain high-intensity aerobic endurance exercise compared to SITCHO” (ibid.).

    The scientists had investigated the effects of sprint interval training (SIT) and exercising in the fasted state. To this end, they compared the effects of SIT with exogenous carbohydrate supplementation (SITCHO) and SIT following overnight fast (SITFast) on aerobic capacity (peak oxygen consumption: VO2peak) and high-intensity aerobic endurance (time-to-exhaustion at 85% VO2peak [T85%]).

    Figure 1: Fasted and without carbs, cyclists can train harder, but they are more enduring at submaximal, yet high (85%) intensities (ibid.).

    “Twenty male cyclists were randomized to SITCHO and SITFast. Both groups performed 30-second all-out cycling followed by 4-minute active recovery 3 times per week for 4 weeks, with the number of sprint bouts progressing from 4 to 7. Peak power output (PPO) and total mechanical work were measured for each sprint interval bout. 

    The SITCHO group performed exercise sessions following breakfast and consumed carbohydrate drink during exercise, whereas the SITFast group performed exercise sessions following overnight fast and consumed water during exercise. 

    Before and after training, V̇ O2peak and T85% were assessed. Blood glucose, non-esterified fatty acids, insulin and glucagon concentrations were measured during T85%” (ibid.).

    What the scientists found was (a) the expected reduction in total work done, i.e. that the “[o]verall PPO and mechanical work were lower in SITFast than SITCHO (3664.9 vs. 3871.7 Joules/kg; p=0.021 and 10.6 vs. 9.9 Watts/kg; p=0.010, respectively)”, but also (b), i.e. that the baseline-adjusted post-training T85% was [significantly] longer in SITFast compared to SITCHO (19.7 ± 3.0 vs. 16.6 ± 3.0 minutes, ANCOVA p=0.038)” (ibid.).

    Plus the circulating energy substrates or hormones did not differ for the two conditions. Based on this and the previously mentioned results we can draw two conclusions:

    • Sprinting after an overnight fast (=AM fasted training) does not burn extra fat, but it burns less energy than doing cardio with a CHO supplement ⇉ for fat loss via sprint intervals, the additional CHOs – if accounted for in terms of 24h energy intake – are beneficial (’cause calories count 😉
    • Your high-intensity endurance (surprisingly) benefits from training fasted and without additional CHOs to replete the loss of liver (and minimal loss of muscle) glycogen ⇉ It’s yet hard to imagine a context in which this is actually relevant, though.
  • Having your protein with vs. between meals (as a snack) and thus extending the inter-meal fasting period may benefit your body composition (Hudson 2018) — I am pretty sure some of you will remember this from the @SuppVersity Facebook News a few months (if not a year ago), where I have already addressed the study results based on the abstract of what was either a poster presentation or a conference talk, I believe.

    For their paper, Hudson et al. (2018) used the PubMed, Scopus, Cochrane, and CINAHL databases to identify those papers that had been published up to 2017 that described “randomized controlled trials of parallel design that prescribed a protein supplement and measured changes in body composition for a period of 6 weeks or more” (Hudson 2018).

    The carefully monitored reviewing process brought up a total of 34 randomized controlled trials with 59 intervention groups and their analysis showed that the subjects saw the following trends in changes body composition according to ingestion pattern:

    • Those who consumed whey with meals were less likely to gain total body weight (56% did), more likely to increase lean mass (94% did) and highly more likely to lose fat mass (87% did).
    • Those subjects participating in studies, where the whey was consumed in-between meals were more likely to see increases in total body weight (72% did), less likely to see increases in lean mass (90% did) and less likely to see reductions in body fat (59% did).
  • Based on these observations, Hudson et al. conclude that: “Concurrently with resistance training, consuming protein supplements with meals, rather than between meals, may more effectively promote weight control and reduce fat mass without influencing improvements in lean mass” (Hudson 2008).
    Figure 2: No differences in lean mass, but a “consistent” increase in body mass only in the inter-meal group, which also failed o see consistent decreases in body fat; consistent increases/decreases were defined as relative changes +/-  67-100% with ↑ indicating consistent increases and ↓ consistent decreases (Hudson 2018).

    According to the researchers’ definition of “consistency” (67% to 100% change from baseline in either direction), though, both groups saw consistent increases in lean mass. The difference that they observed is thus related, mostly, to the effects on body fat, which was non-consistent in the inter-meal studies while it was highly consistent in the with-meal studies.

    As the authors point out, their deliberate exclusion of energy controlled studies doesn’t allow us to say that this is a mechanistic effect beyond the mere reduction in energy intake on the main meals that may not occur when whey is consumed between meals. Bad news? Honestly, I’d say the opposite is the case: after all, this is the real-world, where perfect dietary adherence is the exception, not the rule.

    If it’s not a decrease in total energy intake what’s the advantage of not “snacking” whey… if this advantage actually exists?

    As previously highlighted, we cannot exclude that the effect was a mere result of reduced energy intake on the main meals. Nevertheless, there are at least half a dozen of potential other reasons that facilitate the higher rate of body composition improvements of the whey-with-meal studies (most from the excellent discussion of the results by Hudson et al.):

    • Whey = non-satiating snack – The whey shake that had to be consumed in-between meals may be seen as a mandatory snack of which previous studies show that they promote weight gain – especially if the snacks came in the non-satiating form of liquids (and yes, whey may be more satiating than coke, but let’s be honest, it won’t keep you satiated for long unless you spike it with something like xanthan to increase its viscosity | learn more about advantages of using xanthan).
    • Whey = possible replacement of regular dessert or simply reduction in meal size – Consuming the whey shake with the meal, on the other hand, may have the consequence that participants consume the (usually sweet) beverage instead of a dessert, instead of soda, or – because the spike in insulin, GLP1 and GIP gives them a temporary satiety boost – simply by consuming less on breakfast, lunch, and dinner, when co-consuming the whey protein shake.

    The exact mechanism, and whether and how significant any potential effects will actually be when you don’t compare highly heterogeneous studies, but rather conduct a head-to-head (or shake-to-shake?) comparison of the effects of protein timing (i.e. ingesting whey with vs. in-between meals) should now be explored in an experimental follow-up study.

Hitting it After Weights – There are Downsides, but Systemically Impaired Strength & Size Gains are a Myth, Human RCT from 2016 Clearly Indicates | more

Bottom line: There are two things we should not forget. The first is something you can say about almost every scientific paper. Even if it is a systematic review and thus draws on available evidence from multiple experiments, its generalizability is never 100%. There are always exceptions to the rule and outliers. So, if you realize that you start snacking Snickers when you skip your inter-meal whey shakes, I would highly doubt that the body composition advantages will persist. In a similar vein, you must not forget that the endurance improvements with fasted sprinting will, to a large extent, depend on your ability to burn fat as fuel. If the latter is low, I would rather expect “bunking” (having to stop running early, because you are close to going hypoglycemic) than running “forever”.

If you keep the previous caveats in mind and pay attention to the way your body, behavior, and quality of life(!) are affected by them, fasted sprints and whey with vs. whey in-between meals are two science-based ‘bio-hacks’ you may want to give a try | Comment!

References:
  • Joshua L Hudson, Robert E Bergia, Wayne W Campbell; Effects of protein supplements consumed with meals, versus between meals, on resistance training–induced body composition changes in adults: a systematic review, Nutrition Reviews, (2018) – Ahead of Print at https://doi.org/10.1093/nutrit/nuy012.
  • Schoenfeld, Brad Jon, Alan Albert Aragon, and James W. Krieger. “The effect of protein timing on muscle strength and hypertrophy: a meta-analysis.” Journal of the International Society of Sports Nutrition 10.1 (2013): 53.
  • Terada, T., et al. “Overnight fasting compromises exercise intensity and volume during sprint interval training but improves high-intensity aerobic endurance.” The Journal of sports medicine and physical fitness (2018).

Protein-Timing & Fasting: Fasted Sprints & the Remarkable Muscle↑, Fat↓ Effect of Timing Whey With vs. Between Meals syndicated from http://suppversity.blogspot.com

Eat Your Fish Oil and Digest it, Too (Unoxidized!) | DHA:EPA Ratio of 1:1 Minimizes Oxidation, Maximizes Uptake | Plus: Fishes that Come Close are Sardines, Rainbow Trout, …

The often-heard “the more DHA, the better”-rule is – like so much you’ll read about fish oil online – not the evidence-based truth it seems to be. Some extra EPA may keep the oil from getting oxidized before you even absorb it.

No, I am not a fish oil fanboy, that’s for sure. But how can you be if your chances to get already oxidized fish oil are 100% if you buy any of the US TOP-sellers (and assume that it’s not different in Europe). Speaking of which: There’s new research allowing us to add two new and potentially important criteria to the inofficial SuppVersity-“How to buy and use your fish oil” guide.

The corresponding research comes from an international team of researchers and was first published in 2017. It is thus not exactly revolutionarily new but in view of the fact that I haven’t seen the results being addressed anywhere before still SuppVersity newsworthy (Dasilva 2017).

You can learn more about omega-3 & co. at the SuppVersity

Fish Oil Makes You Rancid?

POPs in Fish Oils are Toxic!

N3/N6 Ratio Doesn’t Matter

MUFA & Fish Oil Don’t Match

Fish Oil Doesn’t Help Lose Weight

Rancid Fish Bad 4 Health

In the paper, the authors followed up on their own research showing that increasing the proportion of DHA in marine lipid supplements significantly reduces associated health benefits (in terms of lipidomic biomarkers of oxidative stress and inflammation) compared with balanced EPA:DHA supplementation (Dasilva 2015). In conjunction with evidence suggesting that these difference may be brought about during the digestive process, where the rate of oxidation and subsequently impaired uptake may be a function of the ratio of DHA:EPA.

The scientists starting hypothesis was thus that EPA and DHA molecules “might have differential resistance to oxidation during gastric digestion, and the oxidation level achieved could be inversely correlated with intestinal absorption and, hence, with the resultant health benefits” (Dasilva 2017).

Figure 1: TIM system, simulating the upper gastrointestinal tract for fat digestion studies (Domoto 2013). In the study I grabbed this illustration from, it was used to demonstrate and quantify the improved absorption of phospholipid- vs. triglyceride bound omega-3s I wrote about as early as in 2012 (read the #SVClassic)

To really get to the bottom of the underlying mechanisms, the scientists decided to test their hypothesis by investigating the degree of oxidation in the stomach, and the levels of bioaccessible lipids, of varying molar proportions of DHA and EPA (2:1, 1:1, and 1:2) using the well-established dynamic gastrointestinal tract model TIM-1.

Tumor-free status according to age. Description of the results in the text.

Less surprising but noteworthy: Fish oil is more potent than plant sources of omega-3s when it comes to the prevention of breast cancer, a recent study from the University of Guelph and the McGill University shows. While we are dealing with rodent data, it is newsworthy that the scientists were able to assess the potency of ALA (plant omega-3) vs. DHA+EPA (as in fish oil) for the first time. Their estimates show “that ALA was 1/8 as potent as EPA+DHA” (Liu 2018).

As usual, though, it makes sense to look beyond the abstract and at the data in the Figure on the left!

The mice receiving 7% safflower + 3% fish oil (FO) developed the virally programmed tumor significantly later than those on either 7% safflower + 3% flax (3%FS) or the control diet with 10% safflower, but the higher dosed (more omega-3, but in form of ALA vs. DHA/EPA) 10% flaxseed diet (10%FS) outperformed them all. That doesn’t change the overall conclusion that – gram by gram – fish oil is more important, but it highlights that ALA, the plant form of omega-3s, is a pretty potent anti-tumor agent, as well.

TIM-1 (see Figure 1) was particularly designed to simulate the upper gastrointestinal tract for fat digestion studies (Guerra 2012; Verwei 2016).

Figure 2: Graphical abstract of the study design (Dasilva 2017).

Figure 2 illustrates the methodology at the most basic level. With TIM-1 being designed to adequately simulate the human digestion process, the scientists obviously had to prepare “test meals”… what? Yeah, the artificial digestive tract is meant to test the absorption of fats from real-world(-ish) food matrices. Accordingly, the scientists mixed a commercial rodent chow (caloric composition: 22% from protein, 66% from carbohydrate, and 12% from fat) with either soybean oil as a control (source of ω-6 LA), or with different proportions of the two main ω-3 FA from fish oils (1:1, 2:1, or 1:2 EPA:DHA) – and surprise, unlike the products in the previously mentioned study, the commercial fish oils had a peroxide value of below the 5 meq O2/Kg of oil cut-off, the 2.84 mg tocopherol/g oil (see “How much vitamin E do you need to consume with PUFAs” | read it) added an extra protective effect.

DHA/EPA and total fatty acid composition of the test diets.

The study used the regular triglyceride-bound versions of EPA & DHA: It is not irrelevant to say that the scientists used the cheap(er) triglyceride-bound forms of DHA and EPA you will find in almost every regular fish oil capsule/bottle. Why’s that relevant? As previously hinted at, the phospholipid (PL) versions are better absorbed – the results could thus have been different and, since few people actually use krill oil and other sources of PL-bound DHA & EPA, less practically relevant.

Moreover, the scientists blended regularly available commercially fish oils from AFAMPES 121 EPA (AFAMSA, Vigo-Spain), EnerZona Omega 3 RX (ENERZONA, Milano-Italy) and Oligen liquid DHA 80% (IFIGEN-EQUIP 98, Barcelona-Spain) – another factor that adds to the real-world relevance of the study at hand… speaking of “real-world” the natural ratio of DHA/EPA ratio in Atlantic salmon is 2:1,… you can find better choices like rainbow trout & others in the bottom line.

As a control, the authors used plain cold pressing unrefined organic soybean oil from Biolasi S.L. (Ordizia, Guipuzcoa-Spain). All diets were high in PUFAs, and delivered approximately 42% of calories from fat (34% from PUFAs of the supplements and 8% from the chow), 43% from carbohydrates and 14% from proteins (the figure in the red box has some details about the individual fatty acid composition if you’re interested in that).

Figure 3: Concentrations of conjugate dienes (CD) and conjugate trienes (CT) evolution during the in vitro stomach digestion in TIM-1 for supplements 1:1, 2:1, 1:2 DHA:EPA, and soybean oil (Dasilva 2017).

Again, the “diets” were not fed to rodents or human beings but digested in the artificial gut from Figure 1, in which the scientists observed a really significant increase in the formation of conjugate dienes and trienes (Figure 3), which signify increased peroxide levels only with the 2:1 oil – exactly those oils supplement companies are going to seel most expensively. The difference between 1:2 and 1:1, i.e. the medium- vs. lowest-price fish oils you will see on the virtual and real shelves (obviously you also pay for brand names, but in general the high DHA fish oils are simply the most expensive ones), on the other hand, wasn’t statistically significant, though.

Figure 4: Lipid metabolism of 1:1 EPA*:DHA and 1:1 EPA:DHA* (TOP). of 2:1 EPA*:DHA and 2:1 EPA:DHA* (middle) and 1:2 EPA*:DHA and 1:2 EPA:DHA* (bototm). Data are expressed as percentage of each lipid class by total lipids. | Please mind that I used the DHA:EPA ratio in previous graphs and throughout the article, i.e. 2:1 EPA:DHA = 1:2 DHA:EPA.

In view of the fact the researchers also found a tendency toward higher amounts of bioaccessible lipids at all-time points in jejunal dialysates for the soybean and 1:1 EPA:DHA diets, compared with the 2:2 and 1:2 diets (differences were significant at 1-2 h, when jejunal absorption principally occurs), it will not be a total surprise to hear that…

  • with 2:1 DHA:EPA, the uptake was maximally reduced, i.e. by 21-23% at 2-6h, 
  • with 1:2 DHA:EPA there was still a relatively high reduction of 18-14%, and 
  • with the 1:1 DHA:EPA the intestinal cells the scientists fed left only 8-5% of the N3s. 

In relative terms that means that you lose 3x more DHA + EPA from the 2:1 DHA:EPA mixture compared to the balanced one. Unfortunately, the study at hand cannot answer a far more important question for sure:

How bad is the oxidation and potential incorporation into blood lipids and cell walls, really?

What the scientists were able to show is that the uptake of oxidized DHA and EPA is generally reduced by -19% and -15% over 6h. This, however, doesn’t tell us anything about the biological/health effects of the slightly differential rates of incorporation/occurrence of oxidized DHA and EPA in trigs, phospholipids, fatty acids and diglycerides as depicted in Figure 4 and downstream effects on cell walls inflammation, etc.. Without the answer to these questions, it is not possible to tell if you just have to take more fish oil to make up for the increased loss, of the corresponding increase in the amount of oxidized PUFAs in your blood and cells wiill do more harm than good.

Current evidence seems to suggests: The less oxidized junk omega-3s you have in your blood and, even more importantly, your cell membranes, the better.

We can thus still not say how “bad” the non-balanced fish oils are – or, as the scientists have it “by which [mechanisms] the oxidative stability of the PUFAs may be correlated with their metabolic fate” and downstream effects on cell integrity and metabolic health, in general – but we can say for sure that “the balanced 1:1 diet showed the lower oxidation level and minor metabolite changes after oxidation” (Dasilva 2017).

Table 1: DHA, EPA and their ratio in fish products (USDA 2005).

Why haven’t I heard about this before? I guess that’s because the whole omega-3 hype is heavily pushed by the industry whose margins are maximized if they manage to con you into buying highly purified high DHA, low EPA products. If there’s no financial interest involved, science news rarely make it to the mainstream media outlets… even if they deal with one of everybody’s darlings like fish oil or vitamin D… well, whatever the reasons may be, unless you need DHA-only for whatever funky science- and not marketing based reason, you will hopefully buy the medium-priced fish oils with a ratio of DHA:EPA of roughly 1:1 to make yourself, not the fish oil manufacturers happy and, obviously, “to eat your fish oil and digest and absorb it, too” 😉

Speaking of eating: The currently available research suggests that you are more likely to see significant health-benefits from consuming (fatty) fish vs. fish oils or other omega-3 supplements, anyway. Against that background you may be interested to hear that wild rainbow trout, sablefish, sardines, or flatfishes (ratio 1.1) come very close to the ‘magic ratio’ – according to USDA data (Table 1), the Atlantic wolffish is yet unique with it’s 1.0 DHA/EPA (with natural variations of ±20% it’s not necessarily ‘the best’ or significantly better than a whole host of fish in the tabular overview on the right, though) | Comment!

References:

  • Dasilva, Gabriel, et al. “Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation.” The Journal of nutritional biochemistry 26.11 (2015): 1385-1392.
  • Dasilva, G., et al. “Relative levels of dietary EPA and DHA impact gastric oxidation and essential fatty acid uptake.” The Journal of Nutritional Biochemistry (2017).
  • Domoto, Nobuhiko, et al. “The bioaccessibility of eicosapentaenoic acid was higher from phospholipid food products than from mono‐and triacylglycerol food products in a dynamic gastrointestinal model.” Food science & nutrition 1.6 (2013): 409-415.
  • Guerra, Aurélie, et al. “Relevance and challenges in modeling human gastric and small intestinal digestion.” Trends in biotechnology 30.11 (2012): 591-600.
  • Liu, et al. “Marine fish oil is more potent than plant-based n-3 polyunsaturated fatty acids in the prevention of mammary tumors.” Journal of Nutritional Biochemistry 55 (2018) 41–52.
  • Verwei, Miriam, et al. “Evaluation of two dynamic in vitro models simulating fasted and fed state conditions in the upper gastrointestinal tract (TIM-1 and tiny-TIM) for investigating the bioaccessibility of pharmaceutical compounds from oral dosage forms.” International journal of pharmaceutics 498.1-2 (2016): 178-186.
  • USDA. “The Report of the Dietary Guidelines Advisory Committee on Dietary Guidelines for Americans, 2005 > Appendix G2: Original Food Guide Pyramid Patterns and Description of USDA Analyses; Addendum A: EPA and DHA Content of Fish Species” (2005). 

Eat Your Fish Oil and Digest it, Too (Unoxidized!) | DHA:EPA Ratio of 1:1 Minimizes Oxidation, Maximizes Uptake | Plus: Fishes that Come Close are Sardines, Rainbow Trout, … syndicated from http://suppversity.blogspot.com