ONLINE DRIVERS MEDIA

Yes, coconut oil does contain MCTs, but it is not as some people believe pure MCT. Only ~50% of the fat in coconut oil is actually in MCT form. If you want pure MCTs you have to resort to specific MCT supplements / oils.

The mechanisms by which medium-chain triglycerides (MCTs) may help you to lose fat are manifold. They are not only hard to store for your body. They also counteract fat deposition in adipocytes by increasing thermogenesis and satiety.

MCTs contain 8 to 12 carbon atoms and include caprylic acid (C8:0, octanoic acid), capric acid (C10:0, decanoic acid), and lauric acid (C12:0, dodecanoic acid). Foods high in MCTs include coconut oil (58%), palm kernel oil (54%), desiccated coconut (37%), and raw coconut meat (19% of total energy) (USDA). Average intakes of 1.35 g/day (0.7% of total energy intake | USDA. 2008) MCTs have been reported in the United States and 0.2 g/day in Japan | Kasai. 2003).
MCT is cleaved into glycerol and medium-chain fatty acids in the gut lumen.5 The medium chain length makes a smaller, more soluble molecule compared with a longchain fatty acid, giving it a preferential absorption and metabolic route in the body. As the authors of the latest meta-analysis of the effects of MCTs on body weight say:

"[t]his physicochemical nature of medium-chain fatty acids allows them to pass into the portal vein on route to the liver to be rapidly metabolized via b oxidation with no requirement of reesterification in intestinal cells, incorporation into chylomicrons, or the rate limiting enzyme carnitine acyltransferase for intramitochondrial transport. In comparison, long-chain fatty acids have a slower route, being re-esterified in the small intestine and transported by chylomicrons via the lymphatic and vascular system before being oxidized for energy or stored. Thus, rapid metabolism of MCTs reduces their opportunity of adipose tissue uptake." (Mumme. 2015)

Several human intervention studies have been conducted investigating the weight-reducing potential of MCT, with mixed results. In their latest meta-analysis, Mumme et al. set out to separate the wheat from the chaff in order to answer the question whether MCTs, specifically C8:0 and C10:0, provide significant weight loss benefits and/or trigger changes in body composition compared to "regular" long-chain fatty acids (LCT).

Figure 1: Meta-analysis for changes in body weight (in kilograms) in randomized control trials that compared dietary medium-chain triglycerides (MCTs) with a longer-chain triglyceride (control) shows a favorable effect of MCT intervention on body weight. *Oleic acid as control. **Myristic acid as control. #Body mass index < 23. ##Body mass index > 23. IV inverse variance. SD standard deviation (Mumme. 2015).

The researchers primary outcome measures were body mass, waist and hip circumference, total body fat, and subcutaneous and visceral fat. Secondary outcomes were blood lipids, including triglycerides (TG), total cholesterol, high-density lipoprotein (HDL) cholesterol, and LDL cholesterol. Of the latter the foremost values are those that are of greatest interest and among them the body mass shows a measurable, albeit not earth-shattering reduction in almost all trials. Only the in the 2001 study by Matsuo et al. there was an increase in body weight in response to an MCT supplement that contained almost no medium chain triglycerides.

Figure 2: Meta-analysis for changes in total body fat, total subcutaneous fat, and visceral fat (Mumme. 2015).

In view of the fact that the most relevant obesity parameters, i.e. the waist and hip circumferences and body fat percentages (Figure 2) dropped in all studies that investigated this parameter and considering the fact that there were no significant deterioration - rather improvements - in blood lipids, it appears warranted to assume that the replacement (!), but not the addition, of 2g/day MCTs (1% of the energy) to 54 g/day MCTs (20% of the total energy intake)  over a duration of 4 to 16 weeks leads to measurable and potentially health relevant weight loss, compared to bacon, butter & co, i.e. regular long chain fatty acids.
References:

• DeLany, James P., et al. "Differential oxidation of individual dietary fatty acids in humans." The American journal of clinical nutrition 72.4 (2000): 905-911.
• Hamman, Richard F., et al. "Effect of weight loss with lifestyle intervention on risk of diabetes." Diabetes care 29.9 (2006): 2102-2107.
• Kasai, Michio, et al. "Effect of dietary medium-and long-chain triacylglycerols (MLCT) on accumulation of body fat in healthy humans." Asia Pacific journal of clinical nutrition 12.2 (2003): 151-160.
• Mumme et al. "Effects of Medium-Chain Triglycerides on Weight Loss and Body Composition: A Meta-Analysis of Randomized Controlled Trials." EAT RIGHT - Research Review (2015).
• US Department of Agriculture. Nutrient Intakes From Food: Mean Amounts Counsumed per Individual, One Day, 2005-2006. Washington, DC: US Department of Agriculture, Agricultural Research Service; 2008.

What now? Wait 3 minutes or off to the bench for an alternate set of bench presses or pulls ?

Traditional strength training with 80% of one-repetition maximum (1RM) utilizes 2- to 5-minute rest periods between sets. These long rest periods minimize decreases in volume and intensity, but result in long workouts. Performing upper-body exercises during lower-body rest intervals may decrease workout duration, but may affect workout performance.

The above is how Anthony B. Ciccone, Lee E. Brown, Jared W. Coburn, Andrew J. Galpin kick off their latest paper in the venerable Journal of Strength and Conditioning Research (Publish Ahead of Print).
The purpose of the corresponding study was to compare the effects of traditional to those of alternating whole body strength training on squat performance. To this ends, Ciccone et al. recruites 20 youn men, who had to perform two workouts:

• The traditional set workout (TS) consisted of four sets of squats at 80% of 1RM on a force plate with 3-minutes rest between sets. 
• The alternating set workout (AS) also consisted of four sets of squats at 80% of 1RM but with bench press, and bench pull exercises performed between squat sets 1, 2 & 3 with between-exercise rest of 50 seconds, resulting in approximately 3-minutes rest between squat sets. 

For both workouts, sets 1-3 were performed for four repetitions, while set four was performed to concentric failure. The total number of completed repetitions, the peak ground reaction force (GRF), peak power, (PP), and average power (AP) of every squat repetition were recorded and averaged for each set.

Figure 1: Maximal # of reps on last set and average power in the classic vs. alternating condition (Ciccone. 2014)

Interestingly, there was no significant interaction for GRF, PP, or AP. Only, the volume-equated AP was ca. 5% greater during the TS condition (989 ± 183) than the AS condition (937 ± 176). A more pronounced difference which was yet still within the margin of one standard deviation (in this case 2.2. reps) was observed for the fourth squat set to failure, where the TS condition resulted in 15% more reps to failure (7.5 ± 2.2) than the AS condition (6.5 ± 2.2). Reason enough for Ciccone et al. to suggest that:

1. Individuals who aim to optimize squat AP should refrain from performing more than three AS sets per exercise.
2. Those who aim to maximize squat repetitions to failure should refrain from performing upper body multi-joint exercises during squat rest intervals.

Certainly a sound advice, but in the end, we all live in a world where time is a precious gem and some people give a fuck about average power and the number of reps until they fail.
References:

• Ahtianen, Juha P., et al. "Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men." The Journal of Strength & Conditioning Research 19.3 (2005): 572-582.
• Ciccone AB, et al. "Effects of Traditional Versus Alternating Whole-body Strength Training on Squat Performance." J Strength Cond Res. (2014) Jun 17. Ahead of print.
• de Salles, Belmiro Freitas, et al. "Rest interval between sets in strength training." Sports Medicine 39.9 (2009): 765-777.

Its nice to be lean, but is it really worth ruining your health? I dont think so, but everyone is the architect of his / her own future.

I want to say in advance that youd better not read this article if you belong to the ever-increasing number of carbophobs (people who are afraid of carbohydrates) who have been so indoctrinated by the confusing information on the Internet that they are willing to close their eyes to all objective data.

In view of the fact that you kept reading, I assume that you (a) dont belong to this group of blockheads or are (b) a blockhead who is about to scroll down to the comment section to start raving about how bad carbohydrates are, pointing out that "you just have to eat a ketogenic diet to live happily ever after" - spare me this bullshit, please!
Its scaremongering bullshit like that due to which more and more non-athletes develop what Can Zhao et al. describe in their latest paper in the peer-reviewed scientific Journal of Sport and Health Science as "exercise-associated menstrual dysfunction" aka EAMD (Zhao. 2014).

For those who have read the SuppVersity Athlete Triad Series, its no news that menstrual irregularities and amenorrhea in female athletes is closely linked to the imbalance between energy intake and exercise-associated energy requirement (Williams. 2001). Accordingly Zhao et al. wanted to investigate, ...

"[...]whether carbohydrate supplements can reverse EAMD and protect against exercise-induced impairment in ovary as an important part of HPO axis regulation and rebalances the energy intake and energy expenditure to support the reproductive function" (Zhao. 2014).

Now the bad news is that they did this in rodents. 45 healthy mature 2-month-old female Spraguee Dawley rats, to be precise. This sounds idiotic, but in view of the fact that the experimental procedure required that "subjects" are sacrificed in the course of the study its quite reasonable to use rodents, not ladies.

Figure 1:  Treadmill running schedules show the specific timeline and various treatments of each groups (Zhao. 2014)

Figure 1 shows a graphical overview of the study protocol which involved an identical initial exercise period in the course of which the speed of the treadmill was continuously increased for six weeks.

At the end of this initial 6-week study period, the female rats, the ovary epithelial cells of the rodents showed significant abnormalities. At the end of week 9, the follicular cells of the rodents in group E contained swollen mitochondria with broken cristae.

Similar exercise-induced mitochondrial damages were also observed in the EAMD rats with post-exercise rest. In the rodents in group O and G, however, Zhao et al. observed a significant recovery of exercise-induced mitochondria impairment. They showed significant reduction of swollen endoplasmic reticulum and Golgi complex, and increases in abundant organelles, irrespective of whether they had been fed a 30% glucose or 30% oligosaccharide diet.

Normalization of organ changes and hormones w/out increase in energy intake

In contrast to the previously hinted at prejudices, the addition of simple sugars to the rodent diet did not lead to an increase in energy intake - in spite of the fact that the goal was a 30% increase in energy intake from glucose / oligosaccharide supplements, the total energy intake was not higher than in the non-exercised control group (see Figure 2).

Figure 2: Changes in energy intakes in each group throughout 9 weeks study (Zhao. 2014).

In conjunction with the significant improvement in GnRH, LH, FSH and estrogen its thus more than unlikely that a comparable increase in "sugar" intake in human females would trigger the increase in body fat many women fear so much that they are willing to run around tired and infertile for years, although most of them know that reducing the exercise volume and normalizing their eating behavior would solve the problem once and for all.

Figure 3: Relative levels (% of control) of GnRH, FSH, LH, E2 and Progesterone (P) after 9 weeks (Zhao. 2014)

Interestingly, the saccharide polymers (oligosaccharides), which are also commonly found on the plasma membrane of animal cells, where they can play a role in cell–cell recognition, did a slightly better job than glucose, when it comes to the restoration of normal hormone levels (see Figure 3).
Reference:

• Qiang, Xu, Chao YongLie, and Wan QianBing. "Health benefit application of functional oligosaccharides." Carbohydrate Polymers 77.3 (2009): 435-441. 
• Tomten, S. E., and A. T. Høstmark. "Energy balance in weight stable athletes with and without menstrual disorders." Scandinavian journal of medicine & science in sports 16.2 (2006): 127-133. 
• Williams, Nancy I., et al. "Longitudinal Changes in Reproductive Hormones and Menstrual Cyclicity in Cynomolgus Monkeys during Strenuous Exercise Training: Abrupt Transition to Exercise-Induced Amenorrhea 1." Endocrinology 142.6 (2001): 2381-2389. 
• Zhao, Can, et al. "Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science (2014).

NEMS devices are usually marketed as "ab trainers" - do you own one?

Convenience above everything! Although I personally believe that this mantra is to blame for most of the modern health issues, scientists from the Department of Biomedical Engineering and Institute for Convergence Study of Bio-Medical Wellness at the Yonsei University in Korea have now been able to demonstrate that you can counter part of the negative side effects of our post-modern convenience culture quite conveniently.

Plug an NMES device into your convenient outlet, attach it to your biceps, sit down conveniently in front of your television screen and have the device train your muscles.
You dont believe that this works? Well, basically this is what the seven healthy male subjects who were recruited for the study did at the laboratory. The participants were trained two times per week (three subjects: Mondays and Thursdays; and four subjects: Tuesdays and Fridays) for 12 weeks. Each exercise session was performed for 30 min with no rest interval.

You could do this in front of your TV at home (image from Son. 2014)

"During the training, the subject was required to maintain a shoulder joint angle of 90° in the sagittal plane. The electrical stimulation (pulse width: 200?s; and frequency: 20 Hz (Dreibati et al., 2010)) was delivered through a pair of 5 × 5 cm gelcoated electrodes attached to the region of the biceps brachii muscle belly. The magnitude of the stimulation was determined as the subjects maximum comfortable current level, but no more than 80 mA, with complete elbowflexion from the fully extended state; the mean value was 57.00 (SD 4.28) mA." (Son. 2014)

I am not sure if this hurts, but based on my experience with a friends NMES ab trainer, I suppose it did... not convenient, ok, but still better than actually moving for most of the the members of the convenience generation, Id guess - And I mean, you cant argue with results, right?

Figure 1: Maximal force and muscle thickness before and after the NMES training (Son. 2014)

I must admit I was quite impressed with the 8% increase in muscle size and the 23% increase in performance. Ok, the study doesnt tell us anything about the training experience of the subjects, but even if they were noobs thats more than Id expected to see from two weekly sessions of NMES.
Reference:

• Jongsang Son, Dongyeop Lee, Youngho Kim, Effects of involuntary eccentric contraction training by neuromuscular electrical stimulation on the enhancement of muscle strength, Clinical Biomechanics, Available online 10 June 2014.

Taking vitamin D pills on their own may be less effective than taking them with a meal containing 30% of the calories from fat - at least for older men & women and high doses of vitamin D3

This is science. Only 6 months ago, I wrote in an article about the effects of fat on the absorption and bioavailability of fat soluble vitamins that vitamin D would be the fat soluble vitamin with the lowest dependence on the co-administration of fat. Rather than the amount, it appeared as if the change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was rather associated with the types of fat, i.e. MUFA = increased absorption vs. PUFA = decreased absorption (Niramitmahapanya. 2011).

Now, half a year later, it appears as if another, previously overlooked variables would force me to reformulate previous recommendations: Age and dosage!
In contrast to previous studies, Bess Dawson- Hughes and colleagues investigated the influence of fat on the absorption of vitamin D3 in older, not young men and women. In that, inclusion criteria for the study were

• no use of not more than 400 IU vitamin D or 1,000 mg calcium per day,
• serum 25(OH)D level in the range 20 to 29.5 ng/mL (49.9 to 73.6 nmol/L),and
• a body mass index in the range 20 to 29.5 (normal weight)

Subjects with kidney problems, hypercalcemia, general issues with malabsorption, Crohn’s disease, disorders of bone metabolism, kidney stones, cancer and those who were using proton pump in hibitors, lipid-lowering medications, fish oil, or flaxseed oil, hormones, osteoporosis medications, or high-dose thiazide diuretic therapy were equally excluded as those subjects who attended tanning salons, regularly.
This was yet not the only difference. Next to the subjects age, the amount of vitamin D3 in the capsules the subjects received differed, as well. While previous studies that reported little to no effect of fat on the absorption of vitamin D3 used small(er) amounts of vitamin D, like 1,000, 2,000 or 5,000 IU per serving, Dawson-Hughes et al. used a single serving of 50,000 IU(!) and thus more than 10x higher dosages than previous studies.

Figure 1: Composition of the test breakfast, lunch, and dinner meals, expressed as % of total energy the 50 healthy older adults consumed in the study at hand (Dawson-Hughes. 2014)

Alongside said vitamin D3 super-dose all 50 subjects ingested one out of three randomly selected meals that were either fat free or contained 30% of the total calories in form of dietary fat - albeit at two different PUFA:MUFA ratios (see Figure 1)

"[The m]eals were provided by the metabolic kitchen and consisted of real food. For example, breakfast consisted of egg whites flavored with small amounts of onion and tomato, fruit, toast, and cranberry juice. The groups were balanced for energy by adjusting the amount of sugar in the cranberry juice (diet or regular juice or a mixture of the two). Protein and fiber were balanced across all groups. MUFA:PUFA was manipulated by adding varying amounts of MUFA (olive oil) and PUFA (corn oil) to achieve a ratio of 1:4 in the low and 4:1 in the high MUFA:PUFA diets. The boxed lunch and the dinner provided to the study subjects on the test day had fat/protein/carbohydrate content similar to that of the test breakfast meals.

Importantly, the subjects were required to (a) eat all of the food provided and (b) refrain from pigging out on anything that was not on the menu for the study day.

Figure 2: Serum vitamin D3 levels in subjects after consuming fat-free or -containing meals (Dawson-Hughes. 2014)

What the scientists found, when they analyzed the vitamin D response of the subjects depending on (a) the fat content and (b) the type of the fat, Dawson-Hughes et al. found:

• In analyses of vitamin D absorption at baseline and the three follow-up time points, there was a significant interaction of fat-free vs fat-containing meal group with time (P < 0.001). As shown in [figure 2], there was no significant difference in plasma vitamin D-3 levels at baseline, but the fat-containing meal group had significantly higher plasma vitamin D-3 concentrations than the fat-free meal group at each time point thereafter.
  
  At 12 hours, the fat-containing vs fat-free meal mean difference in plasma D-3 concentration was 26.9 ng/mL (95% CI 9.6 to 44.1 ng/mL) (69.9 nmol/L). Differences at the other time points were for 10 hours, 30.5 ng/mL (95% CI 14.4 to 46.7 ng/mL) (79.3 nmol/L) and for 14 hours, 21.3 ng/mL (95% CI 4.6 to 37.9 ng/mL) (55.4 nmol/L).

• Vitamin D-3 levels at 12 hours after the dose were 116.0 3 ng/mL (301.5 nmol/L) in the low MUFA:PUFA group and 104.2 ng/mL (270.8 nmol/L) in the high MUFA: PUFA group.
  
  Potential covariates, body mass index, total body fat mass, and screening plasma 25(OH)D level were not associated with vitamin D absorption and neither modified the effect of fat on vitamin D absorption.

As the researchers point out, "[t]here were no serious adverse events during the study" and "[c]ompliance with the vitamin D supplement was 100%" (Dawson-Hughes. 2014). So, non of these obvious, but undesirable confounding factors could explain the observed differences between (a) the non-fat vs. fat-meals and (b) the influence of the PUFA:MUFA ratio.
References:

• Dawson-Hughes, Bess, et al. "Dietary Fat Increases Vitamin D-3 Absorption." Journal of the Academy of Nutrition and Dietetics (2014).
• Niramitmahapanya, Sathit, Susan S. Harris, and Bess Dawson-Hughes. "Type of dietary fat is associated with the 25-hydroxyvitamin D3 increment in response to vitamin D supplementation." The Journal of Clinical Endocrinology & Metabolism 96.10 (2011): 3170-3174. 
• Wortsman, Jacobo, et al. "Decreased bioavailability of vitamin D in obesity." The American journal of clinical nutrition 72.3 (2000): 690-693.