5 points to clear brain fog

Fog Head :)Better focus using acupressure points

Brain fog, fuzzy mind, tired in the head – all of these symptoms can be relieved with acupressure. Chinese medicine offers us many acupoints that “clear the mind.”

5 Acupoints to Clear the Mind

1. Du (Governing Vessel) 20
2. Four Extra points Si Chen Cong

These five acupressure points are easy to use and offer immediate relief from brain fog. First, I will show you how to locate them, and then I will explain how to use Meridian Massage to get the best results.

How to locate Du 20

Du 20 is on the center line of the head, even with the tips of the ears. Refer to the images below:

Reference lines to locate Du 20

Step 1 – feel these reference lines on the head.

Now that you have the reference lines figured out, locate Du 20:
Du 20

Si Shen Cong

Si Shen Cong is actually a set of four points surrounding Du 20. (Extra points are not located on meridians.) Si Shen Cong means “Four-Alert Spirit.” (A Manual of Acupuncture, Deadman et. al.)

Each point is 1 cun (an inch) from the sides, front and back of Du 20. Refer to the image below:

Si-Shen-CongMassage to clear brain fog

Apply gentle, yet firm pressure, to each of these points. I like to add tiny circular movements by keeping my contact steady while making little “micro circles.” Explore each point, breathe, explore and allow the energy (Qi) to flow.

If you are massaging these points on another person, add in a little foot massage at the end to balance the flow of Qi from head to foot.

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5+x Sleep Supplements that Work: Valerian, Beer, Cherries, Tryptophan, Theanine | Plus: Effects of Fats, Carbs and GI

While milk with honey is better than milk with glucose (Jalilolghadr 2011), it won’t improve – if anything mess – with your sleep quality when it’s consumed ≤ 1h before bedtime – noteworthy: the same goes for most foods, though.

While I have chosen it as the title image for today’s SuppVersity “Sleep Supplement Special”, there’s actually surprisingly little (not to say “no”) evidence that the notorious hot milk with honey will actually improve your sleep significantly.

That’s in contrast to a number of supplements that are discussed in a recent review by scientists from the Northwestern University; a review that highlights both, the short-comings of the existing research on dietary supplements for insomnia and encourage health practitioners “to explore existing resources and partner with patients to understand their goals and advise on safe and effective use of dietary supplements” (Ring 2017).

Studies related to sleep and sleep supplements at the SuppVersity:

Sleep Like an Athlete!

Phenibut Addic- tive or Harmless?
All About GABA at SHR

Melatonin = Easy Fat Loss?

Letrozole? Use Melatonin Instead

Bone & Tooth? Melatonin Helps

Now, the question obviously is: What’s safe and effective? By expanding on and elaborating their list of supplements, this article may help you – health practitioner or not – to distinguish promises from factual evidence.

  • Valerian – The probably most prominent and certainly one of the best-researched natural sleep aid is the root of Valeriana officinalis – a sleep aid that works… for some.

    Since “[v]alerian and its constituent valerenic acid have demonstrated adenosine (A1 receptor) interactions, GABAA receptor (β3 subunit) agonism, and 5-HT5a partial agonism” (Ring 2017) it may be surprising that only 6/9 studies in a recent review by Bent et al showed no effect on subjective sleep quality. 

    Figure 1: Likelihood that valerian improved sleep quality calculated based on Meta-analysis of 6 studies reporting dichotomous outcomes for sleep quality (adapted from Bent et al. 2006).

    In addition, Bent et al (2006) highlight that “[m]ost studies had significant methodologic problems, and the valerian doses, preparations, and length of treatment varied considerably”. More recently, a meta-analysis by concluded:

    “The qualitative dichotomous results suggest that valerian would be effective for a subjective improvement of insomnia, although its effectiveness has not been demonstrated with quantitative or objective measurements. Nevertheless, its use can be considered for some patients given its safety” (Fernández-San-Martín 2010).

    Objective evidence for the efficacy of valerian is thus still missing… possibly due to the use of low-dose / low-concentration supplements. Speaking of which… here are the dosage suggestions Ring et al. provide in their previously cited review.

    Dosage: It seems as if it took at least 300–900 mg of a standardized extract of 0.8% valerenic acid – the dosage Ring et al. recommend as an alternative for valerian tea (1.5–3 g of root steeped for 5–10 min in 150 mL of boiling water) – to be taken 30–120 min before bedtime. Effects seem to accumulate over time and may not be noticed with the first administration.

High saturated fat intakes linked to less recuperative slow-wave sleep: In their 2016 study, a randomized crossover inpatient study with 2 phases of 5 nights, St Onge et al. observed differential effects of high fiber and high saturated fat intakes on slow-wave sleep While greater fiber intakes predicted less stage 1 (P = 0.0198) and more SWS (P = 0.0286), the percent of energy from saturated fat predicted less SWS (P = 0.0422). 
  • Hops – In beer, it seems to work wonders for some of us… but wait a minute: is that actually the small quantity of 2-methyl-3-buten-2-ol, xanthohumol, and myrcenol from Humulus lupulus and its effect on GABA that’s responsible for these effects of beer?

    The fact that non-alcoholic beer works, as well, would suggest that it’s at least not the alcohol that’s responsible for the improvements in subjective sleep quality (assessed by questionnaires), decrease in sleep latency (=time it takes you to fall asleep), and improvement of overall global score of sleep quality improved (Franco 2012 & 2014).

    Figure 2: We better stay skeptical about the role of hops in the beneficial effects of non-alcoholic beers as it has been observed by Franco et al. in stressed Hungarian students in 2014. It’s well possible that it’s just the carb content of the beer that triggered the improvements in sleep latency and quality in Franco et al. (2014).

    On the other hand, the fact that hops extracts didn’t yield comparably convincing results would suggest that there’s more to beer than hops and/or the brewing process gives rise to metabolites that are driving an efficacy that cannot be achieved with commercial hops extracts – extracts that have, in contrast to the non-alcoholic beer, been tested in people with chronic insomnia. It is thus not clear if it’s the preparation or the subject group (or both) that’s responsible for the mixed results of hops only preparations (evidence in favor of valerian + hops combinations is more promising – even in insomniacs).

    Dosage: Unlike valerian and most of the other agents discussed in this overview, hops is not without side effects. When administered in high(er) dosages (HED ~64mg/kg) to mice in conjunction with ketamine, the mice resulted in a deep narcosis. For me, that’s another reason to rather drink 300ml of a (non-alcoholic) beer with dinner (check out other health benefits of beer) than to take 120–400 mg of hop extract (ideally combined with 374–500 mg of valerian root extract) to up your sleep quality. Immediate effects can be expected.

Blindfolds and earplugs can improve your sleep quality significantly and help resynchronize a messed up circadian rhythm, which is important for both average Joes and athletes | learn more about “Sleeping like an athlete” in my article from June 2017!

Understanding the different sleep phases and their importance – focus on athletes: As Damian Davenne explains in a 2009 review, “[s]leep can be divided into two main electrical states which serve different basic functions. Slow wave sleep (SWS) is a state during which the brain reduces its activities and neuronal activity becomes synchronized. […] This type of sleep is important for athletes because, without its presence at the beginning of the night, growth hormone cannot be released from the pituitary gland” (Davenne 2009). During rapid eye movement sleep (REM), on the other hand, the brain is very active – proposedly consolidating memories, including movement patterns.

It is thus not really surprising that studies have shown that, after REM sleep loss, procedural memory and motor skills can be affected (Stickgold and Walker 2007). Another relevant physiological phenomenon for athletes is the blockade of cortico-spinal pathways at the brain stem and subsequent suppression of motor activity, which induces a state of total muscle relaxation “that allows effective myofibril restoration” (Davenne 2009).

  • Cherries (esp. tart cherries) – Cherries are well-known for their l-tryptophan content, if you fast forward to the corresponding section of this article it is thus not surprising that cherries/cherry-juice seems to be a highly promising sleep quality modulator.

    Next to the serotonin- and melatonin-precursor l-tryptophan, cherries contain a plethora of anti-oxidants, as well as pre-formed melatonin – a cocktail that may well explain why a randomized, double-blind, crossover study on the effect of tart cherries on older adults (age ≥ 65 years) with insomnia found that the consumption of an 8-oz serving of tart cherry juice twice daily for 2 weeks found a statistically significant reductions in insomnia severity (measured as minutes awake after sleep onset).

    Figure 3: Plot of the relative changes in selected markers of sleep quality; p-values for time x group effects indicate statistical significance for insomnia index and wake after sleep onset (Pigeon 2017).

    Moreover, another study in 20 healthy men and women (aged 18 to 40), which detected significant elevations in urinary melatonin, confirms that the benefits are not restricted to the elderly population in whom the natural production of melatonin is known to decrease. After all, the increase in melatonin Pigeon et al. detected in the urine of the subjects, who complained of insomnia but were otherwise healthy, came with significant increases in time in bed, total sleep time, and sleep efficiency (Pigeon 2010).

    Dosage: While pills are available, all promising research has been done using (tart) cherry juice (8 oz consumed 2x per day, chronically). Compared to whole fruits, the juices also have the advantage of being easier to stomach than the significant number of cherries you’d have to consume to get remotely close to the concentration of active ingredients in the currently available proprietary tart cherry drinks. Immediate effects cannot be expected.

Very low-carb and ketogenic diets shift the ratio of SWS to REM sleep in favor of the former: Whether it is a good or bad thing that Afaghi et al. (2008) observed a significant reduction in REM and a corresponding increase in slow-wave sleep (SWS) is still in the open. What is certain, though, is that (a) low-fat high-carb diets have previously been shown to have the opposite effect (Phillips 1975) and that (b) the pro-SWS effects of ketogenic diets can be used in the treatment of abnormal refractory continuous spikes and waves during slow sleep (Nikanorova 2009).
  • L-tryptophan – The serotonin and melatonin precursor may actually help you fall asleep and stay asleep, but the # of studies is limited.

    Intriguingly, much of the existing evidence of tryptophan’s efficacy is >35 years old, with a review by Ernest Hartmann (1982) highlighting three things

    • “the weight of evidence indicates that L-tryptophan in doses of 1 g or more produces an increase in rated subjective sleepiness and a decrease in sleep latency (time to sleep)”,
    • “there are less firm data suggesting that L-tryptophan may have additional effects such as decrease in total wakefulness and/or increase in sleep time”, and
    • “negative results occur in entirely normal subjects—who are not appropriate subjects since there is ‘no room for improvement'”

    Mixed results are also reported in severe insomniacs and in patients with serious medical or psychiatric illness (details are beyond the scope of this SuppVersity article).

    Figure 4: Graphical illustration of the number (N=y) of studies showing significant, benefits, trends or no change according to a 1982 review in the Journal of Psychiatric Research by Ernest Hartmann (1982)

    As my plot of the number of studies showing significant benefits, trends and no effects highlights, a reduced sleep latency is what appears to be the most certain benefit you can get from 1g+ of l-tryptophan taken ~30 minutes before bed. Potential benefits may be seen from the same regimen (for the # of occasions you wake up and/or toss and turn, as well as the total sleep time.

    Dosage: No clear benefits have been observed for higher dosages (even though studies tested boluses of up to 15g), but it seems advisable especially for lower dosages to consume them “on empty”, i.e. at least without other protein foods. Effects – at least the sleepiness – may be expected with the first administration.

High GI-carbs significantly speed up (-49%) how long it will take you to fall asleep: While high GI carbs (GI = 109) still have a bad rep, studies indicate that consumed 4h before bed will speed up the sleep latency of healthy individuals by a whopping 49% (9.0 ± 6.2 min vs. 17.5 ± 6.2 min for otherwise identical low-GI meals (GI =50) | Afaghi 2007)… to consume the meal 4h before bed is important, by the way. In the same study, Afaghi et al. observed that the same meal given 1 h before bedtime increased the sleep latency back to 14.6 ± 9.9 minutes. Other studies even suggest detrimental effects with high GI ingestion too close to bedtime (so stick to the 4h) – including milk + glucose (higher GI) vs. the notorious milk + honey mix (lower GI) when consumed ~60 minutes before bed.

General beneficial effects of carbs have been observed, among others, by Porter and Horne (1981) who provided six male subjects with a high-carbohydrate meal (130 g), a low-carbohydrate meal (47 g), or a meal containing no carbohydrate, 45 min before bedtime. The high-carbohydrate meal resulted in increased REM sleep, decreased light sleep, and wakefulness. As Halson et al. (2014) point out in their review, “the caloric content of the meals was [yet] not matched in the study”.

  • l-theanine – Usually supplements that are so heavily advertised as Just Chill™ and NeuroSleep™ don’t work, but for these l-theanine things could be different.

    As the authors of the previously cited review in Current Sleep Medicine Reports point out in their review, “[s]everal studies have shown that intake of L-theanine significantly increases α-wave activity in different areas of the cerebral cortex, leading to a relaxed state without drowsiness” (Ring 2017).

    Figure 5: 200mg/day l-theanine reduce the cortisol release in response to stress (Kimura 2007).

    In conjunction with its ability to increase dopamine and serotonin, and reduce stress-related norepinephrine and cortisol levels, salivary IgA, and heart rate in response to an acute stressor. Plus: L-theanine has been shown in animal studies to partially reverse caffeine-induced reductions in slow wave sleep (Jang 2012) – effects that can occur even with your average morning Joe (i.e. not just with caffeine consumption late in the day | Landolt 1995).

    The reason why I still used “could” in the headline of this paragraph is that there is, more or less, only one convincing study to demonstrate beneficial effects on sleep quality in human beings: a 2011 study by Lyon et al. that investigated the effects of Suntheanine® (a branded l-theanine product) on objective sleep quality in boys with attention deficit hyperactivity disorder (ADHD) and showed objective (actigraph) improvements in sleep percentage and sleep efficiency after 6 weeks.

    Figure 5: . (a) Sleep length, (b) sleep efficiency, and (c) intermittent awakening WASO data interpreted from actigraph measurements in 10 male subjects. The values represent mean § standard error. Statistical significance was measured using Student’s paired t-test (Rao 2015).

    Similar objective improvements in sleep efficiency and intermittent awakening (WAS) are also reported by Rao et al. (2015) for healthy subjects (see Figure 6).

    Dosage: While you will see recommendations ranging from 50 to 400 mg of L theanine taken 30–60 min before bedtime, the “proven” dosage is 200mg. That’s more than 4 cups of high l-theanine green tea and thus not really achievable by consuming freshly brewed green tea before bed. As Ring et al. point out, you have to be careful, though, because “[l-t]heanine can have an antihypertensive effect, so it should be used with caution when combined with antihypertensive medications” (Ring 2017).

  • Melatonin – Your body’s own sleep aid is rather a circadian re-aligner than a true sleeping pill – that’s why it works mostly for problems with falling asleep.
    The decrease in sleep onset latency can but doesn’t necessarily result in increases in total sleep time. That’s why many users who expected benzo-esque results are disappointed.

    On the other hand, melatonin has none of the nasty side effects of your average BZD-Z drugs: memory and cognition impairment, psychomotor retardation, or next-day hangover effects (if dosed correctly | Wilson 2010). Likewise, an often-heard of physical dependence has never been observed (Zhdanova 1996).

    Dosage: Dosing melatonin is difficult because the optimal dosage differs between individuals. Accordingly, Ring et al. (2017) suggest a dosage plan starting with 0.3mg and increasing to 3mg (max. 6mg) if the desired effects don’t occur.

Two Hours of Extra-Sleep Before Sleep Deprivation Minimize the Performance Decrements Due to 24h Sleep Deprivation | more

So, what works? Here’s a list: (1) standardized valerian extracts (300-900mg) 60 min before bed, (2) non-alcoholic beer (0.3 L) with dinner, (3) tart cherry juice at a dosage of 8 oz consumed twice per day for days or weeks, (4) ca. 1g of l-tryptophan w/out amino acids competing for uptake (e.g. BCAAs) 30 minutes before bed, (5) l-theanine dosed at 100-400mg/d 30-60 minutes before bed, taking it thrice a day may boost the effect (w/out causing drowsiness) all work, are safe, and worth trying out.

Experimentation may be necessary to find out what works for you – one-size-fits-it-all advice is unwarranted!

The above is especially true for melatonin, which didn’t make the A-list, because it’s more of a circadian re-aligner than a sleep aid. This doesn’t make it less useful, though – on the contrary: if used correctly (1-2h before bed at 0.3-6.0 mg depending on your tolerance) it can have far-reaching beneficial effects on both, your sleep latency, quality, and duration as well as your overall health.

What neither melatonin nor any other sleep aid can make up for, though, is sleep hygiene.

One supplement that has evidence to support its effect, which I still won’t recommend, though, is (*) Kava Kava (Piper methysticum), which messes w/ the cytochrome enzyme cascade (CYP450), will affect the metabolism of both meds and other dietary supplements, and has been linked to liver failure (albeit outside of RCTs lasting up to 6 months | Clouatre 2004), as well as the following concoctions that are often recommended but don’t have convincing scientific backup: (i) chamomile, despite proven interactions of apigenin in chamomille w/ the GABA receptor, (ii) passion flower, (iii) California poppy, (iv) skullcap, (v) lemon balm, (vi) St. John’s wort, (vii) lavender, and (viii) magnolia bark | Comment on Facebook!

  • Afaghi, A., O’connor, H., & Chow, C. M. (2007). High-glycemic-index carbohydrate meals shorten sleep onset. The American journal of clinical nutrition, 85(2), 426-430.
  • Afaghi, A., O’Connor, H., & Chow, C. M. (2008). Acute effects of the very low carbohydrate diet on sleep indices. Nutritional neuroscience, 11(4), 146-154.
  • Bent, S., Padula, A., Moore, D., Patterson, M., & Mehling, W. (2006). Valerian for sleep: a systematic review and meta-analysis. The American journal of medicine, 119(12), 1005-1012.
  • Clouatre, D. L. (2004). Kava kava: examining new reports of toxicity. Toxicology letters, 150(1), 85-96.
  • Davenne, Damien. (2009) “Sleep of athletes–problems and possible solutions.” Biological Rhythm Research 40.1: 45-52.
  • Dement, W C. (2005). “Sleep extension: getting as much extra sleep as possible.” Clinics in Sports Med, 24: 251–268.
  • Fernández-San-Martín, M. I., Masa-Font, R., Palacios-Soler, L., Sancho-Gómez, P., Calbó-Caldentey, C., & Flores-Mateo, G. (2010). Effectiveness of Valerian on insomnia: a meta-analysis of randomized placebo-controlled trials. Sleep medicine, 11(6), 505-511.
  • Franco, L., Sánchez, C., Bravo, R., Rodríguez, A. B., Barriga, C., Romero, E., & Cubero, J. (2012). The sedative effect of non-alcoholic beer in healthy female nurses. PloS one, 7(7), e37290.
  • Franco, L., Bravo, R., Galán, C., Rodríguez, A. B., Barriga, C., & Cubero, J. (2014). Effect of non-alcoholic beer on Subjective Sleep Quality in a university stressed population. Acta Physiologica Hungarica, 101(3), 353-361.
  • Halson, S. L. (2014). Sleep in elite athletes and nutritional interventions to enhance sleep. Sports Medicine, 44(1), 13-23.
  • Hartmann, Ernest. “Effects of L-tryptophan on sleepiness and on sleep.” Journal of psychiatric research 17.2 (1982): 107-113.
  • Jalilolghadr, S., Afaghi, A., O’Connor, H., & Chow, C. M. (2011). Effect of low and high glycaemic index drink on sleep pattern in children. JPMA-Journal of the Pakistan Medical Association, 61(6), 533.
  • Jang, H. S., Jung, J. Y., Jang, I. S., Jang, K. H., Kim, S. H., Ha, J. H., … & Lee, M. G. (2012). L-theanine partially counteracts caffeine-induced sleep disturbances in rats. Pharmacology Biochemistry and Behavior, 101(2), 217-221.
  • Kimura, K., Ozeki, M., Juneja, L. R., & Ohira, H. (2007). L-Theanine reduces psychological and physiological stress responses. Biological psychology, 74(1), 39-45.9
  • Landolt, H. P., Werth, E., Borbély, A. A., & Dijk, D. J. (1995). Caffeine intake (200 mg) in the morning affects human sleep and EEG power spectra at night. Brain research, 675(1), 67-74.
  • Lyon, M. R., Kapoor, M. P., & Juneja, L. R. (2011). The effects of L-theanine (Suntheanine®) on objective sleep quality in boys with attention deficit hyperactivity disorder (ADHD): a randomized, double-blind, placebo-controlled clinical trial. Alternative medicine review, 16(4), 348.
  • Ozeki, Makoto, Lekh Raj Juneja, And Shuichiro Shirakawa. “The Effects Of L-Theanine On Sleep Using The Actigaph.” Japanese Journal Of Physiological Anthropology 9.4 (2004): 143-150.
  • Nikanorova, M., Miranda, M. J., Atkins, M., & Sahlholdt, L. (2009). Ketogenic diet in the treatment of refractory continuous spikes and waves during slow sleep. Epilepsia, 50(5), 1127-1131.
  • Phillips, F., Crisp, A. H., McGuinness, B., Kalucy, E. C., Chen, C. N., Koval, J., … & Lacey, J. H. (1975). Isocaloric diet changes and electroencephalographic sleep. The Lancet, 306(7938), 723-725.
  • Pigeon, W. R., Carr, M., Gorman, C., & Perlis, M. L. (2010). Effects of a tart cherry juice beverage on the sleep of older adults with insomnia: a pilot study. Journal of medicinal food, 13(3), 579-583.
  • Porter, J. M., & Horne, J. A. (1981). Bed-time food supplements and sleep: effects of different carbohydrate levels. Electroencephalography and clinical neurophysiology, 51(4), 426-433.
  • St-Onge, M. P., Roberts, A., Shechter, A., & Choudhury, A. R. (2016). Fiber and saturated fat are associated with sleep arousals and slow wave sleep. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine, 12(1), 19.
  • Stickgold, R and Walker, M P. (2007). “Sleep-dependent memory consolidation and reconsolidation.” Sleep Med, 8: 331–343.
  • Wilson, S. J., Nutt, D. J., Alford, C., Argyropoulos, S. V., Baldwin, D. S., Bateson, A. N., … & Gringras, P. (2010). British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. Journal of Psychopharmacology, 24(11), 1577-1601.
  • Zhdanova, I. V., Wurtman, R. J., Morabito, C., Piotrovska, V. R., & Lynch, H. J. (1996). Effects of low oral doses of melatonin, given 2–4 hours before habitual bedtime, on sleep in normal young humans. Sleep, 19(5), 423-431.

5+x Sleep Supplements that Work: Valerian, Beer, Cherries, Tryptophan, Theanine | Plus: Effects of Fats, Carbs and GI syndicated from http://suppversity.blogspot.com

Nine Recent Studies on Vitamins, Fruits+Veggies, Ketogenic Dieting for Endurance Athletes, Blood Pressure, Cognitive Function, Depression & Gene-Diet-Interactions from 10/17

Looking for the very latest on nutrition science? Look no further: most of the results presented in this installment of the short news have not yet been officially published after their presentation on a conference of the Nutrition Society.

I hope you don’t mind that I decided to pool the most interesting of the latest studies from the Proceedings of the Nutrition Society in a single article. With the articles on vitamin D, B-vitamins, ketogenic diets in endurance athletes, and so on and so forth all being addressed individually, you can still skip studies you may not be interested in and get the gist (read the title and the last paragraph of each bullet point) within seconds.

As it is usually the case for short-news that are based on presentations at a conference, it will take time for the full papers to be written, reviewed and published. Accordingly, I cannot tell you how many eggs the subjects in the keto-diet study ate and whether they consumed their stakes rare or well-done… so please don’t ask 😉

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!?
  • 6 months vitamin D supplementation effectively improved 25OHD levels, but without boosting cognitive function in healthy community-dwelling older adults, randomised double-blind placebo-controlled pilot trial shows (Aspell 2017).

    A recent study from the Trinity Centre for Health Sciences at the St. James’s Hospital (Aspell 2017) shows that 2,000IU of D3 supplemented daily does increase the 25OHD levels by almost 50%, but the battery of tests the scientists ran to determine if this would have downstream beneficial effects on the cognitive health of the 68.5y-old (mean) subjects, 18.3% of whom were D-ficient at baseline, did not show effects on global cognitive function.

    No clear benefit of ‘D’ on cognition.

    Yes, conducting a study that lasts for more than 6 months may yield these benefits, but, in general, the study at hand seems to confirm that the vitamin D ain’t the messiah as which it was celebrated in the past decade.

  • Milk significantly decreases LDL in 78 healthy, pre-menopausal women with habitually low intakes of milk (<250ml) who more than doubled their intake (Yeates 2017).

    After decades of being everybody’s darling, milk has recently gotten a pretty bad reputation… you as a SuppVersity reader know that milk is not rat poison as some mainstream media claimed in the past (re-read my “Mill Kills [NOT]“). Accordingly, you will not be surprised that an extra 430ml/d of full-fat milk had (a) no effect on body composition, glucose management, total cholesterol, and triglycerides, but did (b) significantly reduce the levels of LDL in the 18-45-year-old women.

    Sign reductions in LDL w/ milk

    If we assume that you are lactose tolerant and like it, go for your milk people. A 1mmol/L reduction in LDL is associated w/ a 22% reduced risk of major cardiovascular events (Baigent 2010) – even in people with LDL levels as low as 2 mmol/L! Personally, I don’t like the taste of pure milk, but dairy products like quark, yogurt, and cheese (likewise a falsely vilified health food) are a staple in my diet.

  • Overrated? Increasing fruit and veggie intake, alone, doesn’t improve blood pressure according to six randomized controlled fruit and vegetable intervention trials that were pooled analysis by British researchers (Elsahoryi 2017).

    People expect wonders from fruits and veggies, wonders of which a recent study from the Queen’s University Belfast have now shown that they won’t occur even if the participants of RCTs actually managed to increase their fruit and veggie (FV) intake, significantly.

    When pooling the slopes and standard deviations from the six largest trials, there simply isn’t a significant decrease in either systolic or diastolic blood pressure per portion change in fruit and vegetable intake.

    No effect of adding F/V to (bad) diet

    Let’s be clear here, this doesn’t mean that fruit and veggies don’t have to play an important role in healthy diets. It does, however, tell you that – in the absence of other dietary changes, weight loss, and increased physical activity – simply adding a couple of servings on top of your mad Western diet ain’t going to save your heart, kidney, and other organs from the damaging effects of increased blood pressure.

  • Personalized nutrition: Riboflavin attenuates increase in blood pressure in pregnant women w/ MTHFR 677C→T gene polymorphism (O’Sullivan 2017)

    Having increased blood pressure during pregnancy is not just a temporary problem. In fact, studies show that it will also increase the risk of blood pressure disturbances later in life. Accordingly, the results of the latest study from the Ulster University, the University College Dublin, and the University College Cork are of great importance…

    … at least for those women who harbor an MTHFR 677C→T gene polymorphism and have been shown to be at greatest risk of abnormal blood pressure levels during pregnancy (McNulty 2017), this increased risk can be mitigated by a high Riboflavin status.

    No, this doesn’t mean that riboflavin supplementation will help!

    It will take RCTs to confirm or refute the hypothesis that supplemental riboflavin is going to help women with MTHFR 677C→T gene polymorphism control their blood pressure during pregnancy, and rejoice: the study is already underway.

  • New study doesn’t support link between high folate + low B12 and various measures of cognitive function in adults over 50 (O’Connor 2017).

    While folate has long been considered a super-vitamin, recent studies showing a high prevalence of elevated folate and low B12 levels in older people w/ cognitive problems suggested that, at least, unbalanced high folate levels could be a serious problem for granny and grandpa.

    A recent re-analysis of data from The Irish Longitudinal Study on Aging didn’t find either the Mini-Mental State Examination (MMSE) scores, or the Montreal Cognitive Assessment (MoCA), or the verbal fluency to be superior in subjects w/ normal B12:folate ratios  (see Figure) compared to peers with an abnormal cobalamine to folate ratio below 258pmol/L:45.3nmol/L.

    This doesn’t mean that high folate and, even more so, low B12 ain’t no problem! And still evidence that simply popping pills ain’t just missing: it looks as if it didn’t help.

    It is important to note that the lack of associations between a low-B12-high-folate profile in a single cohort does (a) not negate the existence of such a relationship. Furthermore, there’s (b) plenty of evidence that having adequate levels of both, folate and vitamin B12 and (thus) low levels of homocysteine are of essential importance to cognitive function as we age (Wolters 2004). The bad news, however, is that meta-analyses show that simply popping pills is not the solution: “Randomized trials show no effect of folic acid, with or without other B vitamins, on cognitive function within 3 years of the start of treatment.” (Wald 2010).

  • Without fortified foods and B-supplements, it’s hard to cover get enough B to ward off depression, scientists from the University of Ulster write (Moore 2017).

    The scientists base this statement on a re-analysis of data from the Trinity Ulster Department of Agriculture Ageing Cohort with more than 5000 subjects that found significantly higher levels of all relevant B-vitamins with increasing fortified food intakes.

    Table 1: B-vitamin levels in subjects relying on natural food sources, only, consumers of different amounts of fortified foods and supplement users (Moore 2017).

    Since low levels of folate, vitamin B6, and riboflavin all being associated with a 47-48% increased risk of depression in the same cohort, that’s bad news for people who avoid both: fortified foods and supplements.

    If you want to stay mentally healthy as you age, watch your B-vitamin intake!

    When we hear about B-vitamins and aging, we usually think about cognitive decline. That the ever-increasing rates of depression in older individuals may also be driven by a lack of B-vitamins, on the other hand, is commonly overlooked. Unfortunately, the same goes for the general lack of folate, vitamin B6, and riboflavin in the diet of older individuals – a lack that can be compensated by both: fortification and supplementation, as the data from the study at hand suggests.

  • 9 grams of milk hydrolysate are enough to significantly ameliorate the glucose response to a standardized breakfast in healthy young men (Keane 2017).

    It’s not news that whey protein, in general, and its fastest absorbing incarnation, i.e. hydrolyzed whey protein, can significantly improve the glucose-response to standardized meals. What scientists and functional food designers alike didn’t know, yet, is whether the effects that have been previously observed with 20g and more will also occur with significantly lower intakes of a form of milk protein that … let’s be honest, here… simply tastes like crap.

    Now, a brief glance at the glucose curves Keane and Gibney recorded in their recent RCT with 13 young, healthy, male participants, indicates that even 9 grams of hydrolyzed milk protein are enough to elicit significant improvements in post-prandial glucose levels.

    Insulin haters rejoice: The low dosage doesn’t even significantly elevate insulin

    In that, the study at hand didn’t just demonstrate that even low(er) amounts of the bitter milk hydrolyzate can significantly reduce glycemic excursions in response to a standardized breakfast. It did also show that 9 grams of hydrolyzed milk protein can do so without exorbitant increases in insulin (as you can see insulin will still increase, but according to Keane and Gibney only non-significantly, while 12g still produced a significant increase), of which I’ve previously told you that they are one out of three interrelated factors that are responsible for the reduced glycemic response (the other ones are the associated increases in GLP-1 and GIP).

  • Ketogenic diet reduces iron status in endurance athletes to an extent that may compromise their performance, US researchers demonstrate (McSwiney 2017).

    After 12 weeks on a ketogenic diet (<50g/d carbohydrates >75% energy from fat), the trained endurance athletes in a recent study from the Waterford Institute of Technology showed significantly reduced markers of iron status.

    Table 2: Differential effect on “iron” levels of endurance athletes on high-CHO vs. ketogenic diet.

    While the control diet, which delivered 65% of the energy as carbohydrates and only 20% as fat (protein intakes were identical between groups), conserved the total and corpuscular levels of the oxygen-carrying hemoglobin, the subjects who had been randomly assigned to the ketogenic diet exhibited significant reductions in all three: Hb, MCH, and MCHC.

    The significant reduction in oxygen-carrying hemoglobin could be a problem for keto-athletes, but that was not tested in the study at hand

    The study didn’t include performance testing, but unlike the decrease in hematocrit (many will even think that’s a health benefit as high levels are associated W/ increased mortality and heart disease | Gagnon 1994 – keep in mind, though, endurance athletes usually hover at the lower end of the Hct range where similar problems may occur) in the high-carb group, the significant reduction in total (-9.3%; p < 0.05) and corpuscular hemoglobin could significantly impair the oxygenation of skeletal muscle and thus negatively affect the exercise performance of endurance athletes. 

Non-Adherence and Design Problems: Two Reasons Why Recent Diet Study May Fail to Show Benefits of High(er) Protein + Dairy Intakes in Overfat (>37%) Women | learn more

Bottom line: In as much as I want to make it easier for you to get the gist out of today’s research update, I am not going to summarize the already summarized bottom lines to the individual studies again. That simply doesn’t make sense. So, if you want the gist and implications, read the headlines and the last paragraph of each of the mini-write-ups.

What I can and will do for you, though, is to warn you of “luxury yogurts” of which a recent study from the Food Safety Authority of Ireland (Kemp 2017) says that they are generally no healthy food choices. With levels of sugar and/or saturated fats way beyond what the health claims on the labels mislead the average consumer to believe | Comment!

  • Aspell, N., Healy, M., Mc Partlin, J., Lawlor, B., & O’Sullivan, M. (2017). Effects of vitamin D supplementation on cognitive function in healthy, community dwelling older adults: Results from a randomised double-blind placebo-controlled pilot trial. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S002966511700132X.
  • Baigent, C., Blackwell, L., Emberson, J., Holland, L. E., Reith, C., Bhala, N., … & Collins, R. (2010). Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials.
  • Elsahoryi, N., Patterson, C., McKinley, M., Neville, C., Baldrick, F., Mulligan, C., . . . Woodside, J. (2017). The effect of increased fruit and vegetable consumption on systolic and diastolic blood pressure in six randomized controlled fruit and vegetable intervention trials: A pooled analysis. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S002966511700129X.
  • Gagnon, D. R., Zhang, T. J., Brand, F. N., & Kannel, W. B. (1994). Hematocrit and the risk of cardiovascular disease—the Framingham study: a 34-year follow-up. American heart journal, 127(3), 674-682.
  • Keane, L., & Gibney, E. (2017). The effect of various doses of a milk protein hydrolysate on the post-prandial glycaemic response in a healthy male cohort. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S002966511700146X.
  • Kemp, B., White-Flynn, T., Lyons, O., Cronin, B., O’Donovan, C., Donovan, C., & Flynn, M. (2017). Is it yoghurt or is it a dessert? Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001422.
  • McNulty, Helene, et al. “Riboflavin, MTHFR genotype and blood pressure: a personalized approach to prevention and treatment of hypertension.” Molecular aspects of medicine 53 (2017): 2-9.
  • McSwiney, F., Wardrop, B., Volek, J., & Doyle, L. (2017). Effect of a 12 week low carbohydrate ketogenic diet versus a high carbohydrate diet on blood count indicators of iron status in male endurance athletes. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001458
  • Moore, K., Hughes, C., Hoey, L., Ward, M., Porter, K., Strain, J., . . . McNulty, H. (2017). Role of fortification and supplementation in achieving optimal biomarker status of B-vitamins for better mental health in older adults. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001215
  • O’Connor, D., Laird, E., O’Halloran, A., Molloy, A., & Kenny, R. (2017). Variations in vitamin B12 and folate balance: Implications for cognitive function? Findings from The Irish Longitudinal Study on Ageing (TILDA). Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001227
  • O’Sullivan, E., Pentieva, K., Ward, M., McAuley, A., Strain, J., McNulty, B., . . . McNulty, H. (2017). Riboflavin, MTHFR 677C→T and blood pressure in pregnant and non-pregnant women. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001240.
  • Wolters, M., Ströhle, A., & Hahn, A. (2004). Cobalamin: a critical vitamin in the elderly. Preventive medicine, 39(6), 1256-1266.
  • Yeates, A., Gilmartin, N., O’Kane, S., Pourshahidi, L., Mulhern, M., & Strain, J. (2017). The effect of cow’s milk consumption on cardiometabolic health in women of childbearing age. Proceedings of the Nutrition Society, 76(OCE3). doi:10.1017/S0029665117001318.

Nine Recent Studies on Vitamins, Fruits+Veggies, Ketogenic Dieting for Endurance Athletes, Blood Pressure, Cognitive Function, Depression & Gene-Diet-Interactions from 10/17 syndicated from http://suppversity.blogspot.com

Vitamin D — Replacing D3 W/ Calcifediol in Fortified Foods May Cut D-ficiency Epidemic | Plus: High/Low Vit-D Jobs

Many of these foods contain significant amounts of calcifediol (25OHD). It’s thus not as if we would be exposing us to an unknown research chemical, bros.

With vitamin D it is as with all the hype-research subjects: Now that everybody and his mama have published a paper discussing how awesome and important vitamin D is (mostly in the absence of experimental evidence from controlled human trials that would clearly support this “awesomeness”, by the way), the number of studies on vitamin D starts to decline, while their quality (at least in parts) increases.

In this Vitamin D Research Update, I will address two of these post-hype studies. Both with practical relevance in terms of the prevention and resolution of vitamin D deficiencies:

Learn more about vitamin D at the SuppVersity

How Much Vitamin D Shall You Take?

Leucine, Insulin, Vitamin D and Your Gainz

Vitamin D Speeds Up Exercise Recovery

One Svg of Fish or Eggs Satisfy Your Needs?

Vitamin D an Essential Supp For Athletes?

New Dosing Suggestions for Mr./Mrs. Average
  • More evidence in favor of the superiority of calcifediol vs. cholecalciferol (vitamin D3) as a supplement to replete low vitamin D levels (Guo 2017) may even suggest that its time to revisit vitamin D3 as the goto form for fortified/functional foods.
    What do you need for a high 25OHD picnic at the beach? Eggs! And you know what? Eggs and other foods may kick your D3 supplements’ ass.

    You will remember that I’ve previously addressed the existence and potential usefulness of calcifediol, a prohormone to calcitriol that is produced in the liver by hydroxylation of vitamin D3 (cholecalciferol) – a process that takes approximately 7 days under normal conditions and may be impaired in those who need to normalize their vitamin D levels the most: the obese and metabolically deranged.

    The results of the study at hand are yet by no means relevant only for sick people. Even healthy paleo folks will love them. After all, we “evolved to consume” 25OHD in our diets… you don’t believe it? Well, it’s readily available from fish and other dietary sources, I wrote about before.

    Moreover, previous studies, while being somewhat inconsistent, have already suggested: calcifediol from foods or supplements is more potent than its more common counterpart, cholecalciferol aka vitamin D3.

    • Jetter et al. (2014) have studied both the pharmacokinetics of a single dose and chronic supplementation for 15 wk with vitamin D3 and 25(OH)D. Their data showed that longer-term 25(OH)D3 supplementation was superior to vitamin D3 for increasing vitamin D status.
    • Figure 1: A 2012 study by Bischoff-Ferrari et al. suggested that calcifediol may be the better vitamin D supplement (compared to vitamin D3) because it (left) increases 25OHD (std serum marker of vitamin D status) and (right) triggers consistent (vs transient in vitamin D3) decreases in systolic blood pressure in healthy postmenopausal women w/ low baseline 25OHD.
    • Bischoff-Ferrari et al. (Bischoff-Ferrari 2012) showed that 20 mg 25(OH)D3/d over 4 mo had significant benefits for lowering systolic blood pressure (SBP) compared with vitamin D3 in 20 healthy postmenopausal women.

    The latest paper by Jing Guo which “investigated whether consumption of dairy drinks fortified with either 25-hydroxycholecalciferol [25(OH)D3] or cholecalciferol (vitamin D3) had differential effects on 24-h circulating plasma 25(OH)D3 concentration (a marker of vitamin D status) and cardiometabolic risk markers” (Guo 2017), is thus in good company:

    Fortification w/ calcifediol produces significantly higher increases in serum “vitamin D” levels than the current “gold standard” vitamin D3 – at least if added to dairy

    The above is in essence the message of the corresponding randomized, controlled, 3-way crossover, double-blind, postprandial study, Guo et al. conducted in in 17 men with suboptimal vitamin D status [mean +/- SEM age: 49 +7- 3 y; body mass index (in kg/m²): 26.4 +/- 0.6; and plasma 25(OH)D3 concentration: 31.7 6 3.4 nmol/L].

    The subjects were randomly assigned to consume 3 different test meals (4.54 MJ, 51 g fat, 125 g carbohydrate, and 23 g protein), which contained either

    • a nonfortified dairy drink (control), 
    • a 20 µg (800IU) 25(OH)D3-fortified (+HyD3) dairy drink, or 
    • a 20 µg (800IU) vitamin D3–fortified (+D3) dairy drink.

    All were served with toasted bread and jam on different occasions, separated by a 2-wk washout period. A double-blinded protocol was maintained throughout the study until all of the statistical analysis was completed. Throughout the study, participants were asked to maintain their normal diet and lifestyle, to avoid taking any dietary supplements, and to minimize sun exposure.

    Fellow armchair scientists, please note, neither the “low dosage” nor the fact that it is an acute-response study are “design flaws”. 

    In fact, the 800IU are all that regulatory bodies all around the world will allow being present in one serving of fortified food as it still represents the official RDA for vitamin D. In a similar vein, the acute-response design is in line with the research interest and practically relevant if we assume that a dairy drink like that would be consumed on a daily basis.

    Do not forget: We have data from previous longitudinal studies showing that supplementing (vs. fortification) with calcifediol is more effective than vitamin D3 (re-read my previous article about fish for additional points of reference), too. Another reason not to fret about the scientists’ choice not to conduct a long-term study (I am sure that will follow, btw).

    Furthermore, Heaney et al. have shown that cholecalciferol (D3) is rapidly, i.e. within hours converted to 25OHD, converted – especially if supplied in small(er) quantities to subjects with initially low(ish) levels, subjects like the 17 men in the study at hand. The study at hand is thus an addition to the existing evidence and its results …

    “Plasma 25(OH)D3 concentrations (the primary outcome) were significantly higher after the +HyD3 dairy drink was consumed compared with +D3 and control (P = 0.019), which was reflected in the 1.5-fold and 1.8-fold greater incremental area under the curve for the 0–8 h response, respectively. The change in plasma 25(OH)D3 concentrations from baseline to 24 h for the +HyD3 dairy drink was also 0.9-fold higher than the +D3 dairy drink and 4.4-fold higher than the control (P < 0.0001), which were not significantly different from each other” (Gao 2017).

    …well worth considering. Based on the results of the study at hand, previous evidence and the previously voiced assumption that fortified foods are consumed on a daily (or almost daily) basis, this result would, after all, suggest that people may maintain more stable and sufficient vitamin D levels at much lower levels of fortification.

    Figure 2: Maximal and absolute changes in 25OHD during the follow-up and at the end of the 24-h follow-up; all expressed in nmol/L over baseline and highly significant (Gao 2017).

    Furthermore, replacing vitamin D3 (cholecalciferol) with ready-made 25OHD (calcifediol) in all fortified foods may solve a problem that has, in my humble opinion, hitherto been largely overlooked: the fact that people with certain metabolic diseases will have reduced levels of vitamin D 25-hydroxylase aka CYP2R1, the liver enzyme that converts D3 to calcifediol.

In case you’re asking yourselves: Yes calcifediol is the same stuff your doctor, or rather, the lab of his choice will measure to judge your vitamin D status. Why haven’t we been supplementing with that all along…? Well, Holick identified this D2/D3 metabolite as a marker of vitamin D status in the 70s, but it took decades before scientists got interested in its potential use as a supplement or drug – a drug that will work irrespective of potential limitations/defects of 25-hydroxylation in the liver and an impaired/inhibited conversion of dietary/supplemental vitamin D3.
  • In the case of a patient with NAFLD, for example, the +172% higher increase maximal and 93% higher post-24h increases in 25OHD with calcifediol are pitted against a 20% reduced presence of the enzyme in his liver cells (vs. healthy control | Barchetta 2012) – a reduction that will then be of significantly reduced relevance, because the RDA of 25OHD would come in ready-made form from fortified foods. That’s particularly true in view of the fact that early studies with vitamin D3 suggest that high doses may suppress the activity of 25-hydroxylase to an extent that the level of 25OHD will actually decline (because the conversion of D3 stalls | this was observed by Mawer et al. as early as in 1976).

    Before making a switch from D2/D3 to straight 25OHD (calcifediol), it will yet have to be investigated if overexposure to calcifediol is as safe as overexposure to vitamin D3, which will – when a certain 25OHD level is reached – stop being converted at high rates (Heaney 2017).

  • Whether you need “extra D” in your diets may well depend on your job, a one of a kind systematic review suggests (Sowah 2017).

    In their latest systematic review, Canadian researchers evaluated vitamin D levels in different occupations and identified groups vulnerable to vitamin D deficiency. At the surface level, their results are not exactly surprising:

    • Compared to outdoor workers, indoor workers had lower 25OHD levels (40.6 ± 13.3 vs. 66.7 ± 16.7 nmol/L; p < 0.0001), with 78% vs. 48% of the indoor vs outdoor workers being deficient (25OHD<50 mmol/L).
    • The mean 25OHD levels were even lower in shift-workers. With 80% of them being deficient, they are also the #1 risk group for having D-levels way below 50 nmol/L.
    • Interestingly enough, lead/smelter workers and coalminers had comparatively high levels of 77.8 ± 5.4 and 56.6 ± 28.4, respectively. 

    Likewise noteworthy are the differences among healthcare professionals, medical residents and healthcare students of whom the latter two groups had the lowest levels of mean 25-(OH) D, 44.0 ± 8.3 nmol/L and 45.2 ± 5.5 nmol/L, respectively – a mean value below the deficiency cut-off. Practicing physicians, on the other hand, just made the cut with a mean 25OHD level of 55.0 ± 5.8 nmol/L, which was significantly different from both, medical residents (p < 0.0001) and healthcare students (p < 0.0001).

    Figure 3: Occupational groups, % deficiency (<50 nmol/L), and relative risk (Sowah 2017).

    The physicians’ 25OHD levels are in turn dwarfed by nurses and other healthcare employees who had above average 25OHD levels of 63.4 ± 4.2 nmol/L and 63.0 ± 11.0 nmol/L, respectively. Taken together, medical students, with an overall prevalence of vitamin D deficiency of 72%, were the worst, nurses, with “only” 43%, the best-nourished subjects with a medical background.

    Jobs <> vitamin D — We know a lot, but we don’t know all the details

    Unfortunately, potential confounders such as gender and body composition were not consistently reported in the primary studies and were therefore not analyzed. Since the suspect that the descriptions of occupational characteristics may be incomplete, too, the significance of the data from this review remains limited… and still, with respect to the previously discussed study, it clearly suggests that adding calcifediol to cereals, orange juice and milk, instead of the currently used vitamin D3 may have a significant impact on the prevalence of cereal munching non-health-conscious medical students, patients who are served milk and orange juice in the hospital and shift worker who may be eating all of these and other foods that are either already fortified or will be in the future.

Until now, your body fat determined your D3 requirements (learn more); with obesity or rather the metabolic syndrome, in general, and NAFLD, in particular inhibiting the conversion of D3, using straight 25OHD may yet offer a non-fat dependent alternative.

Bottom line: In the absence of sufficient long-term safety data on calcifediol, it is unlikely that the FDA, European, Canadian, or Australian authorities will soon change their fortification rules/recommendations for foods such as milk, calcium-fortified orange juice, breakfast cereals, American cheese, margarines, and yogurt (FDA; Calvo 2004).

The existing studies, including those that were conducted in the offspring in our metabolically next relatives, piglets, do yet show that even intakes that are “5 or 10 times the recommended level had no adverse effects on any of the biological parameters measured” (Rosenberg 2016), while the tissue concentrations in muscle+liver increased signif.

Drugs with calcifediol as their main ingredient are yet already sold worldwide (including the US) under more than 10 brand/drug names. It is generally prescribed for hyperparathyroidism secondary to renal impairment, hypocalcemia, and renal osteodystrophy. In these populations long(er)-term studies (>3 months) like Barros et al. (2016) clearly indicate that “[v]itamin D reposition with oral calcifediol, in a bi-weekly [10,000 IU] or monthly regimen, is safe and effective in improving 25(OH)D blood levels and in decreasing PTH”. With the already small amount of vitamin D in fortified foods, there’s, accordingly, no real reason to assume that a 1:1 replacement and thus an increase in the expected effects on people’s serum vitamin D levels of 50 to 80%, compared to vitamin D3, would be harmful – irrespective of milder forms of kidney disease, by the way.

In that, it remains speculative (see previous elaborations wrt Guo’s study) if these benefits would indeed be more pronounced in those individuals who – due to metabolic disease and a subsequent lack or deficiency of 25-hydroxylation capacity in the liver – require significantly higher amounts of regular vitamin D3 to achieve normal serum levels | Comment!


  • Barchetta, Ilaria, et al. “Liver vitamin D receptor, CYP2R1, and CYP27A1 expression: relationship with liver histology and vitamin D3 levels in patients with nonalcoholic steatohepatitis or hepatitis C virus.” Hepatology 56.6 (2012): 2180-2187.
  • Barros, Xoana, et al. “Comparison of two different vitamin D supplementation regimens with oral calcifediol in kidney transplant patients.” Journal of nephrology 29.5 (2016): 703-709.
  • Bischoff‐Ferrari, Heike Annette, et al. “Oral supplementation with 25 (OH) D3 versus vitamin D3: effects on 25 (OH) D levels, lower extremity function, blood pressure, and markers of innate immunity.” Journal of Bone and Mineral Research 27.1 (2012): 160-169.
  • Calvo, Mona S., Susan J. Whiting, and Curtis N. Barton. “Vitamin D fortification in the United States and Canada: current status and data needs.” The American journal of clinical nutrition 80.6 (2004): 1710S-1716S.
  • Guo, et al. “A 25-Hydroxycholecalciferol–Fortified Dairy Drink Is More Effective at Raising a Marker of Postprandial Vitamin D Status than Cholecalciferol in Men with Suboptimal Vitamin D Status.” The Journal of Nutrition. First published (2017): ahead of print September 20, 2017 < doi: 10.3945/jn.117.254789 >
  • Heaney, Robert P., et al. “25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions.” The American journal of clinical nutrition 87.6 (2008): 1738-1742.
  • Jetter, Alexander, et al. “Pharmacokinetics of oral vitamin D 3 and calcifediol.” Bone 59 (2014): 14-19.
  • Mawer, E. B., and A. Reeve. “The use of an isolated perfused liver to study the control of cholecalciferol-25-hydroxylase activity in the rat.” Calcified Tissue International 22 (1976): 24-28.
  • Rosenberg, S. J., et al. “Tolerance evaluation of overdosed dietary levels of 25‐hydroxyvitamin D3 in growing piglets.” Journal of animal physiology and animal nutrition 100.2 (2016): 371-380.
  • Sowah, et al. “Vitamin D levels and deficiency with different occupations: a systematic review.” BMC Public Health  (2017) 17:519 < DOI 10.1186/s12889-017-4436-z >

Vitamin D — Replacing D3 W/ Calcifediol in Fortified Foods May Cut D-ficiency Epidemic | Plus: High/Low Vit-D Jobs syndicated from http://suppversity.blogspot.com

α-GPC and Low Thyroid? Fat Loss+Muscle Gains, Possible? More Protein in Shift-Work Diet, 7kg Lower Fat Mass & TC?

In today’s installment: Alpha-GCP and reduces thyroid function; accurate body fat measurement in contest prep confirms recomp effect; more protein keeps shift workers lean and healthy.

Since I didn’t want to bore those of you who are (for whatever reason) not interested in significantly annotated summaries of the studies presented at the last ISSN conference, I’ve deliberately taken a break before publishing the next installment of the #ISSN17 series; with this one answering important questions such as: Can alpha-GPC supplements give me hypothyroidism? Can lean individuals still do a “recomp”, i.e. lose significant amounts of fat while gaining muscle in short periods of time – What does a gold-standard measurement w/ the 4-C method say? And, last but not least, is a higher protein intake the landmark feature of those night shift workers who don’t get obese and sick and how does it work? Interested? Alright, here we go…

Fasting and alpha-GPC have sth in common: Nootropic, pro-GH (initially), anti-thyroid effects

Breakfast and Circadian Rhythm

“Lean Gains” Fast Works

Habits Determine Effects of Fasting

Fasting Works for Obese, Too!?

IF + Resistance Training = WIN

ADF Beats Ca-lorie Restriction
  • Alpha-GCP, nootropic and alleged GH booster, impairs thyroid function? To answer this question in the affirmative, the data Bellar et al. presented at #ISSN17 is clearly not sufficient. It is, however, interesting to note that Bellar’s experiment in forty-eight healthy clearly confirmed the authors’ hypothesis that “increasing CNS acetylcholine can affect dopamine levels, which can, in turn, affect other hormones such as Thyroid stimulating hormone (TSH)” (Bellar 2017).

    To test this hypothesis, the researchers from the University of Louisiana at Lafayette, the Louisiana State University, and Ball State University fed the aforementioned young men 500 mg A-GPC, 250 mg A-GPC, or Placebo. Within 1-2 h after the ingestion of the supplement, the authors found that…

    • serum free choline was significantly elevated in the two A-GPC groups as compared to placebo (132% and 59% respectively)
    • serum TSH was significantly depressed in the 500 mg A-GPC group compared to other treatments (p < 0.04).

    At least acutely and (probably) transiently, the answer from the subheading does, therefore, have to be answered affirmatively.

    What’s the verdict on alpha-GPC and your thyroid?
    It’s as simple as “big effect = big side effect”. You cannot have the soothing effect of increased CNS acetylcholine without its “downsides”. Without knowing how long/if the effects on TSH and thus downstream effects on the production of thyroid hormones persist, there’s no reason to panic, though.

    Figure 1: The reduction in TSH could be a response to the increase in GH many supplement users are actually aiming to achieve when they consume alpha-GPC supplements. If that’s the case, the decreased TSH can be expected to be as transient as the increase in growth hormone (which is btw. irrelevant for your gainz, bro).

    Moreover, if alpha-GPC does what it’s advertised for, the TSH suppression could also be a result of a growth hormone surge (Kawamura 2012). GH depresses the secretion of thyrotropin and thus TSH, but by increasing the peripheral conversion of thyroxine to triiodothyronine, the occasional transient GH spike from alpha-GPC will not have your metabolism tank… let alone trigger hypothyroidism. What would happen in response to chronic administration of alpha-GPC is still up in the open, though.

  • You cannot shed body fat and gain muscle at the same time? Yes, you can! One of the reasons people tend to blow up to crazy body fat levels when bulking is the still prevalent believe that you’d have to be in a significant caloric surplus to pack on muscle. In fact, I overheard a trainer at the gym tell a skinny fat rookie only recently: “You got to eat… you need a big energy to gain muscle.”

    Many active and retired practitioners, on the other hand, often talk about “recomp” and thus refer to losing fat and adding muscle to their frames simultaneously. One of the poster presentations at #ISSN17 seems to suggest that – at least in the early phase of a drug-free contest prep – this is exactly what’s happening.

    Figure 2: The case study shows: When you combine exercise and diet in the right way(s) you can gain lean mass (+4%) and lose body fat (-35%) – data measured using the 4-C model (Tinsley 2017).

    Using a former NCAA Division II athlete who had previously competed in 4 physique competitions, Grant M. Tinsley tried to elucidate more information about the way(s) the human body changes when it is exposed to a carefully timed and balanced combination of diet and exercise intended to maximize fat and minimize muscle loss.  At the commencement of the study, the subject was beginning an 18-week preparation phase prior to competing in a National Physique Committee (NPC) competition in the Figure division. Tinsley further explains:

    “Throughout the preparation phase, the athlete was closely advised by her coach, a competitive bodybuilder with 20+ years of coaching experience. The athlete meticulously tracked dietary intake, supplement use and exercise sessions. Additionally, the athlete was assessed monthly in the university research laboratories” (Tinsley 2017).

    These assessments included dual-energy x-ray absorptiometry (DXA) and multi-frequency bioelectrical impedance analysis (MF-BIA). Body volume and total body protein were calculated using DXA output (Wilson 2013, body composition was assessed using the 4-compartment model as described by Lohman & Going (Lohmann 1993).

Figure 3: The use of a 4-compartment model to assess body composition is a strength of this case study at hand because it isn’t as easily fooled as the DXA alone as it was used in Wilson’s recent keto paper I wrote about recently (illustration from Ellis 2000)

For all dieters out there: Don’t trust ‘your’ DXA blindly: A neat side-finding of the study at hand was that there were “substantial differences in body fat percentage between DXA and 4C”. In fact, throughout the first 3 months of the preparation period, DXA overestimated body fat percentage by 4.5% on average compared to the 4-compartment model. Accordingly, Tinsley advises: “When possible, more advanced methods of body composition assessment, such as the 4-compartment model, should be utilized in physique athletes to allow for more accurate evaluation” (Tinsley 2017) especially when accurate data can make the difference between victory and defeat.

More from another ISSN#17 paper: If you’re not working with athletes, but overweight/obese clients, your best choice, next to the 4c model, is air displacement plethysmograph (ADP | BodPod). Of the latterTrexler et al. (2017) reported at #ISSN17 that it “provided more valid estimates for cross-sectional and longitudinal changes in body composition in comparison to DXA and US” (Trexler 2017) – with DXA performing better than ultrasound.

    Based on 4-compartment calculations, Tinsley reports that “the athlete’s body fat decreased from 18.3% to 12.3% over the first 3 months of preparation” (Tinsley 2017). This alone wouldn’t be surprising. The fact that, Tinsley observed concomitant decreases in fat mass (12.0 kg to 7.8 kg) and increases in fat-free mass (53.3 kg to 55.2 kg), on the other hand, is noteworthy.

    What’s the verdict on ‘recomp’?

    In view of the existence of several RCTs that showed concomitant increases in muscle mass and decreases in fat mass in obese individuals who were subjected to combined diet and (resistance) training, the ‘news’ here is that this works with lean(er, more) athletic people as well. With that being said, Trexel et al. reported very similar results from a mixed cohort of fifteen physique athletes – 7 male, 8 female drugfree (according to interviews) athletes competing in bikini (n=7), figure (n=1), physique (n=5), or bodybuilding (n=2) classes. In case you missed this one, you can read up on it here!

    What? You’re asking yourself why the Tinsley study still made the cut, if Trexel’s study had more subjects, featured both, men and women, and was already discussed at length? Well, Tinsley used the “gold-standard 4-compartment model”, Trexel et al. “only” amplitude-mode ultrasonography and skinfold measurements. Just like classic DXA scans of which Tinsley observed that “it substantially overestimated body fat percentage in the observed athlete” these methods have a comparatively (vs. 4-C) high margin of error (see info box). To point you to a study using the 4-C model was thus (IMHO) useful.

  • Health care workers’ protein intake may determine their body composition and health. More protein = leaner and healthier? Likewise right from #ISSN17 is the insight that “surpassing general PRO recommendations (0.8 g/kg) may advantageously influence body composition and blood lipid profile” (Pihoker 2017) – highly advantageous in terms of body weight, BMI, body fat, and blood lipids (see Figure 4).

    Before you rejoice, however, please note: This insight was phrased based on observational data from thirty-three female healthcare shift-workers (Mean ± SD: age = 30.6 ± 9.2 yrs, height = 164.7 ± 6.8 cm, weight = 66.5 ± 10.2 kg, body mass index (BMI) = 24.5 ± 3.7 kg/m2) who were tested following a minimum eight-hour fast. That’s not ‘bad’, but it’s not the result of a randomized controlled study, which leaves room for a lot of uncontrollable confoundable variables such as ‘people who eat more protein are generally more health-conscious, work out more regularly and/or consume overall healthier diets’.

    At least one of these potential confounders could be excluded by the scientists, though. Next to being scanned with DXA to assess fat mass (FM), lean mass (LM), bone mineral content (BMC), and body fat percentage (%fat), the subjects also filled three-day dietary logs (2 workdays, 1 off-day) based on which the scientists estimated the average kilocalorie (kcal), carbohydrate (CHO), PRO, and fat intake. For the final analysis, participants were initially stratified into two groups using protein intake of ≥ 1.2 g/kg bodyweight (‘adequate’, n=15) or <1.2 g/kg BW (‘deficient’, n=18). Between-group differences were evaluated using a series of independent t-tests. Relationships between dietary intake estimations (kcal, PRO, CHO, and fat) and body composition and blood variables were analyzed using Pearson’s bivariate correlations.

    The results of this battery of tests revealed that the subjects in the “adequate protein” group (the scientists words), i.e. those who consumed more than 150% of the RDA per day had -10.81±2.89 kg (p=0.001) lower body weights, significantly less body fat (∆=6.73±2.34 kg, p=0.008), lower levels of pro-atherogenic non-HDL cholesterol (∆=17.09 ± 7.83, p=0.037), and a comparatively low ratio of total to HDL cholesterol (TC:HDL ∆=0.54±0.25, p=0.039) that’s indicative of a significantly reduced risk of heart disease.

    Figure 4: Body composition of shift workers w/ protein intakes >1.2g/kg vs. intakes <1.2g/kg (RDA = 0.8g/kg).

    In that, it is interesting to note that no other dietary variable correlated significantly with these measures – neither the total energy intake, nor the “macros”, i.e. the distribution of energy on proteins, fats and carbs [note: this does also mean, that there was no further benefit of even more protein].

    What’s the verdict on high(er) protein intakes for health workers?
    Again, we’re just talking about observational data, but the lack of significant relationships between other/all measured dietary variables, body composition, and blood measurements does indeed, as the scientists write, “suggests that protein plays a special role in terms of the body composition and blood lipids in shift-working personnel. And let’s be honest: Why shouldn’t a protein intake beyond the demarcation line of 0.8g per kg/d do just that!?

    The evidence in favor of the beneficial effects of high(er than RDA) protein diets on appetite is quite conclusive. If we take into consideration that high protein foods often replace/reduce the consumption of classic low protein snacks, any deliberate or unconscious increase in protein intake will – at least hypothetically – address two of the main nutritional problems of health-care shift-workers (Lowden 2010).

    Moreover, data from Ishizuka et al. 1983 even suggests that high protein meals consumed at night may have an indirect and for shift-workers very welcome effect on the circadian rhythm as they, but not regular or high fat/high carb meals trigger a profound release of cortisol independent of the time of the day. In contrast to low protein meals, shift workers’ circadian clock will thus get the same cortisol-related feedback (Åkerstedt 1978) in response to a meal at night as they’d get during the day – certainly no disadvantage in view of the fact that the latest research indicates that the weight and metabolic problems of shift workers are at least aggravated if not triggered by circadian desynchronization (Broussard 2016), which can, in turn, be triggered and (partially) reversed by food timing (Vetter 2017).

High Protein Breakfast Lowers Weight (8%), Waistline (4%) + HbA1c (12%) in T2DM – Especially if the Protein is Whey | read the full article

What’s the verdict, then? Let’s go study by study, here. On Alpha-GPC: I’ve already summarized “the verdict” for alpha-GPC towards the end of the first segment (see headline). In short: In view of the fact that the only convincing evidence of interference with thyroid hormone metabolism comes from a short time study and considering the fact that these short-term detrimental effects could be a side-effect of the GH boosting effect (many) people pay for when they buy alpha-GPC there’s no reason to freak out because of the results of Bellar’s study.

If you insist on freaking out, do so if this is the first time you realize that any side effect of dietary supplements is, when all is said and done, just a regular effect you didn’t pay for and (often) didn’t expect to see. In that, the rule of thumb is: potent intended effect = potential for potent side-effect.

On ‘recomping’: While Tinsley’s case study did observe a significant body-recomposition effect, it is important to note that even the 4-C model the scientist used isn’t 100% accurate and that a 1.9kg change of lean mass measured in a single subject ain’t enough to “prove” the claim that you can build muscle and lose fat concomitantly. Nevertheless, in conjunction with the increase in total body protein content (from 10.4 kg to 10.9 kg), the case-study at hand still adds to the evidence that this kind of ‘recomp’ isn’t impossible to achieve – and that not just for the obese (there are several studies showing that diet + exercise can trigger fat loss + muscle gain in the obese), but also for normal-weight/even lean individuals.

The observational data on high-protein diets for shift-workers may, when assessed in isolation, not be very convincing. In view of what you’ve learned about the general effect of high(er) protein intake on food intake, body composition, and health, it does yet confirm an evidence-based hypothesis many of you probably already had. Plus: the potentially corrective circadian effects of high(er) protein meals at night I discussed in the corresponding subsection of this article would only add to the general metabolic benefits of increased protein intakes | Comment on Facebook!

  • Åkerstedt. “Circadian rhythms in the secretion of cortisol, adrenaline and noradrenaline.” European journal of clinical investigation 8.2 (1978): 57-58.
  • Bellar, et al. “Evaluation of the effects of two doses of alpha glycerylphosphorylcholine on thyroid stimulating hormone levels.” Proceedings of the Fourteenth International Society of Sports Nutrition (ISSN) Conference and Expo (2017).
  • Broussard, Josiane L., and Eve Van Cauter. “Disturbances of sleep and circadian rhythms: novel risk factors for obesity.” Current Opinion in Endocrinology, Diabetes and Obesity 23.5 (2016): 353-359.
  • Ellis, Kenneth J. “Human body composition: in vivo methods.” Physiological reviews 80.2 (2000): 649-680.
  • Ishizuka, B., M. E. Quigley, and S. S. C. Yen. “Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain.” The Journal of Clinical Endocrinology & Metabolism 57.6 (1983): 1111-1116.
  • Kawamura, Takashi, et al. “Glycerophosphocholine enhances growth hormone secretion and fat oxidation in young adults.” Nutrition 28.11 (2012): 1122-1126.
  • Lohman, Timothy G., and Scott B. Going. “Multicomponent models in body composition research: opportunities and pitfalls.” Human body composition. Springer US, 1993. 53-58.
  • Lowden, Arne, et al. “Eating and shift work—effects on habits, metabolism, and performance.” Scandinavian journal of work, environment & health (2010): 150-162.
  • Pihoker, et al. “Characterization of body composition, blood lipids, and nutrition profile in female healthcare shift-workers when stratified by protein intake.” Proceedings of the Fourteenth International Society of Sports Nutrition (ISSN) Conference and Expo (2017).
  • Tinsley, Grant M. “Substantial body recomposition during contest preparation in an experienced female figure competitor: results of 4-compartment model and total body protein calculations.” Proceedings of the Fourteenth International Society of Sports Nutrition (ISSN) Conference and Expo (2017).
  • Trexel, et al. “Estimating body composition at baseline and tracking changes during weight loss: Validity of common methods in comparison to a criterion four-compartment model.” Proceedings of the Fourteenth International Society of Sports Nutrition (ISSN) Conference and Expo (2017).
  • Vetter, Celine, and Frank AJL Scheer. “Circadian Biology: Uncoupling Human Body Clocks by Food Timing.” Current Biology 27.13 (2017): R656-R658.
  • Wilson, Joseph P., et al. “Improved 4-compartment body-composition model for a clinically accessible measure of total body protein.” The American journal of clinical nutrition 97.3 (2013): 497-504.

α-GPC and Low Thyroid? Fat Loss+Muscle Gains, Possible? More Protein in Shift-Work Diet, 7kg Lower Fat Mass & TC? syndicated from http://suppversity.blogspot.com

Syntha 6 Isolate Review

syntha-6 Isolate

BSN Syntha 6 is well-known for its fantastic taste, and has become one of the world’s top selling protein powders. However, some purists have argued that it is not fast absorbing enough for post training, and contains too much carbohydrate. As a result, BSN have hit back and released it, a stronger, leaner, faster version of the regular Syntha 6.


The ingredients are far simpler than the regular Syntha 6. It contains a blend of two different protein isolates, whey (WPI) and milk protein. This is an industry first, in which a company has released an isolates only protein blend. The other ingredients present are just for flavouring and mixability. In each 38 g serve of Isolate, you get around 150 calories, 25 g protein, 7 g carbohydrates, and 2 g fat.


It is an even better product than the regular Syntha6 for meeting your daily protein requirements. With its high whey protein isolate component, it is also excellent for post workout recovery. As with all proteins, you are unlikely to see immediate gains. However, after consistent use and training, muscle and strength gains should be expected.

Taste & Mixabilty

The regular Syntha 6 has a huge following because of its premium taste. I am happy to report that people familiar with it will not be disappointed with the taste of Syntha6. SIt tastes and mixes every bit as well as the regular Syntha 6. The texture is thick like the origina. However it is not as smooth, a characteristic of milk proteins. For those unfamiliar with the original Syntha 6, the taste of it  is amazing, probably one of the best protein powders around. However, unlike the original Syntha 6, there is currently only a limited range of three flavours. Chocolate, vanilla, and strawberry.


Synth 6 Isolate provides both fast (whey protein isolate) and slow release (milk protein isolate) proteins. This makes it an excellent all round protein for use immediately after training, or during the day. The fast proteins will make it into your muscles very quickly, to start rebuilding, while the slow release proteins will protect your muscles from catabolism and sustain muscle development over a longer period. This together with the awesome taste of what you would expect from BSN, makes Synth 6 Isolate a real winner.


Despite being a protein isolate, Synth 6 is still relatively low in protein content. With the industry standard of around 90% protein for a protein isolate, it is well short of this with a mere 66% protein content. So even though Synth 6 Isolate may be sort after by many people, it may not be wanted by those wanting a purer power.


Although it may not be the purist protein isolate available on the market, it is by far one of the best tasting. If you are looking for something that tastes just as good as the original Syntha 6, but with a fraction of the carbs, then be sure to add Syntha 6 Isolate to your next shopping list.

Syntha 6 Isolate Review syndicated from https://ivoamatheis.tumblr.com

Weight Loss Foods

Weight Loss Food for weight loss diet to lose body fat for body shaping, body sculpting, muscle toning, exercise fitness programs.

Weight Loss Eating Weight Loss Food For Fat Loss, Body Shaping, Body Sculpting, Fitness Modeling, Weight Loss Programs

#1 Priority – Vegetable and Fruits Carbohydrates or “Carbs” *


Vegetables – Cellulose Vegetables


Cellulose Carbohydrates | Low Glycemic Carbohydrates (Low Glycemic Carbs)

Cellulose carbohydrates contain cellulose fiber which increases metabolism and helps you feel full after eating; low glycemic carbs give you sustained energy – an endurance energy, increased stamina

Greens, Lettuce, Spinach, Romaine, Red Leaf, GreenLeaf, Kale, Chard, Broccoli, Cauliflower

Greens, lettuce, salads, have been proven over the centuries to be the most effective weight loss food. They are not only extremely nutritious from giving you essential vitamins, minerals, to antioxidants, anti-carcinogenic qualities. In other words, every day, scientists and researchers find positive effects of vegetables. The bottom line is they work. They are the most proven methods to lose body fat, plus increase immunity, enhance your life, memory, energy,  etc.



Berries i.e.  Strawberries, Blueberries, Blackberries, 

Raspberries, Boysenberries, Acai, Melon I.E. Cantaloupe, Honeydew Melon, Honeydew (Sweet Melon), And To A Degree, Watermelon, Apples, then Oranges, Plums, etc

Berries are low glycemic, plus full of antioxidants and anti-carcinogenic properties, plus full of fiber; cantaloupe is one of the best foods you can eat, full of Vitamin A, fiber, etc, Apples contain pectin, which aides in weight loss.


Vegetables – Starchy Vegetables


Yams, Sweet Potatoes, Squash, Corn, etc

Starchy carbs


#2 Priority – protein: low fat protein or lean protein


Whey Protein

Has been proven to be extremely effective for weight loss, fat loss, muscle toning, muscle gaining; has calcium which has been proven to increase fat reduction; naturally has a higher number of branched chain amino acids (BCAA or BCAAs) which promote lean muscle tissue, increase satiety / decrease appetite, therefore, keeps you feeling full. Note: a whey protein shake for breakfast is by far the most effective and successful way to start and maintain your weight loss diet, since you start your day ‘on the right foot’ a solid meal of protein with a full stomach, especially if you use fruit, such as bananas, strawberries / most berries. Plus it’s very fast to make.


Low Fat Fish i.e. Sole, Halibut, Canned Tuna, Pollack, Cod; 

Shellfish i.e. Calamari / Octopus Rings (as long as not the fried kind), Scallops, Mussels

Low fat fish and low fat shellfish are extremely effective in fat loss. Many professional bodybuilders, especially female fitness models focus on sole, canned tuna, halibut, calamari rings, even scallops for their protein before a bodybuilding contest or a fitness model contest or show. Fish is by far an excellent source or protein, especially for weight loss, be aware of the mercury levels, therefore, be consciously aware of the source and location.


Low Fat Cottage Cheese, Fat Free Cottage Cheese

Similar to whey protein in being a highly effective weight loss food, including first of all, a complete protein, high in calcium, which has been proven to help people lose body fat, and in the end, it works. For years, people have been consuming low fat cottage cheese, because it works for weight loss. Again, every in balance. A half cup to a cup is fine. Add some pineapple, apples, peaches, berries, you’ll be even better, especially if you make this as a snack or an in between meal.


Skim milk, non fat milk, low fat milk, 1% milk

Milk contains casein, which helps promote muscle tissue and lasts longer in the stomach for more amino acid delivery to your muscles. Milk is better for body sculpting, body building because of the amino acid profile. Low fat, 1% milk, contains the fat which may help with weight loss. Still, milk in general is very highly ineffective as a health food.


Chicken Breast (White Meat), Chicken (Dark Meat), 

Turkey Breast (White Meat), Turkey (Dark Meat), Pork Loin (Lean Pork)

Even though sole and calamari are extremely effective weight loss proteins, chicken breast is by far the staple of most bodybuilders and fitness models  for losing weight, weight loss, fat loss, body sculpting, body shaping. Turkey has a high amount of the amino acid, Tryptophan (L-Tryptophan), which has sedative like properties, is a sedative like amino acid, which may make you feel sleepy or drowsy. Pork loin is excellent for lean muscle mass. Pork loin as a very high number of branched chain amino acids (BCAA or BCAAs) which promote lean muscle tissue, increase satiety / decrease appetite, therefore, keeps you feeling full and increases muscle definition.

Medium Fat Fish i.e. Salmon, Fresh Tuna, 

Sea Bass To High Fat Fish i.e. Mackerel, Anchovies, Herring, Eel

These fish have excellent fat for weight loss, anti inflammation effects  and anti inflammatory properties, though since extremely high in fat, limit salmon and fresh tuna to 3 ounces once per week, especially since high probability high in mercury and obviously, fat. This includes your sushi and sashimi. Note: most shark fin, shark, sword fish steak / sword fish are extremely high in mercury and you are well advised to very cautious in consuming these products.


Egg Whites

Cheaper source of protein, probably the cheapest source of protein, high in branched chain amino acids (BCAA or BCAAs), incomplete protein so sometimes mixed with another complete protein like sliced turkey, chicken breast, nonfat cheese, low fat chess like low fat Swiss cheese, like in an omelet or scrambled eggs; sometimes mixed with egg yolk if not trying to lose fat.


Red Meat, Lean Red Meat i.e. Sirloin

Sirloin (lean red meat) (limit to once a week), especially lean sirloin or low fat sirloin; most beef fat tends to put on weight, increase in body fat, good for many football players, especially line men, sumo wrestlers, and anyone else trying to quickly gain weight


#3 Priority – Grains – Grain Carbohydrates / Grain Carbs 


Grains – Brown Rice, Wild Rice, Sourdough Bread, Ezekiel Bread, Rye Bread


Brown rice is one of the best foods you can eat, just limit to one to two cups a day if trying to lose weight, wild rice is an excellent source of fiber and very close to same health and weight loss benefits as brown rice. Sourdough bread is low glycemic through it’s sourness. Ezekiel bread is a complete protein and a complex carbohydrate through it’s combination of carbohydrate sources. It is also in the bible. Rye bread is another excellent low glycemic high carbohydrate fuel source. Rye bread is of the best quality carbs you can consume for body sculpting, fitness modeling, weight loss, or a fat loss program.


Starch Carbohydrates, or Starchy Carbohydrates and / or 

High Glycemic Carbohydrates (High Glycemic Carbs)

White rice, white bread, etc. Limit and substitute with the previous as much as possible.

* note: many people think of first which kind of protein should they should eat or put protein as their highest priority primarily due to the fad of Atkins diet. This is a mistake for people who are interested in body sculpting, muscle toning, and especially those interested in weight loss, fat loss, or just losing weight.

Simple Breakdown Of Weight Loss Food

Vegetables – Salads, Broccoli, Asparagus, Eggplant

Fruits – Berries, Cantaloupe, Honey Dew Melon

Vegetables – Yams, Sweet Potatoes, Squash

Protein – Whey Protein, Low Fat Fish, Shellfish, Chicken Breast, Egg Whites, Lean Meat I.E. Sirloin, Pork Loin

Grains – Brown Rice, Wild Rice

Detailed Breakdown Of Weight Loss Food

The Following Are Still Good For You, And You Should Still Eat Them, Yet Not As Effective For Weight Loss As The Previous, so eat mostly the previous plus some of the following:

Vegetables – Corn, Beans

Fruits – Apples, Oranges, Grapes, Peaches, Pears, Nectarines, Plums, Watermelon

Protein – Skim Milk, 1% Milk, 1% Cottage Cheese, Low Fat Yogurt, Medium Fat Fish, Chicken Brown Meat

Grains – Rye Bread, Ezekiel Bread, Whole Wheat Bread

Weight Loss Foods syndicated from https://ivoamatheis.tumblr.com