While all three studies in this research update have been published last year, they are by no means “yesterday’s news” – not even for those of you who “know” the studies which investigated (A) the effects of vitamin D supplementation on the suboptimal testosterone levels of 100 hypogonadal men, (B) the initially very similar but eventually fundamentally different effects of green- and black-tea supplements on the obesogenic effects of high-energy diets, and (C) the beneficial effects of the co-ingestion of plant protein on healthy people’s postprandial glucose levels.
What’s new? Well, study A doesn’t really tell you that vitamin D doesn’t help, study B shows that black tea does not work by simply ruining your appetite, and study C is one of those where context matters.
Vitamin D supplements won’t (re-)start your balls, boys… scientists find “no significant treatment effect on serum TT [total testosterone] or on the remaining secondary outcome variables” (Lerchbaum 2018) in a cohort of Austrian hypogonodal (=low testosterone, i.e. serum TT levels < 10.4 nmol/l) men with suboptimal (< 75 nmol/l) 25-hydroxyvitamin D [25(OH)D] levels.
Subjects were randomized to receive 20,000 IU of vitamin D3/week (n = 50) or placebo (n = 50) for 12 weeks. The primary outcome was the subjects’ total testosterone level (TT), which were measured using mass spectrometry. In addition, the researchers also checked free testosterone, the free androgen index (Ratio of TT to SHBG), sex hormone-binding globulin (SHBG), estradiol, follicle-stimulating hormone (controls sperm production), luteinizing hormone (controls hormone production), metabolic characteristics, and body composition.
Boring? Not really, look…
If you think the study is boring ’cause Lerchbaum et al. (2018) didn’t find the beneficial effect on testosterone you have been hoping for? In that case, you don’t understand the purpose of science and (probably) haven’t looked at the actual data, either. There’s more to it than the putative null-result (“Vitamin D doesn’t help w/ low T”): the D-supplementation didn’t even work for ‘D’ – at least, there were no inter-group differences in the pre- vs. post-supplementation change in vitamin D levels.
Figure 1: The actual message of the study at hand is that ~2,850 IU/d of vitamin D3 do not counter the putatively common (e.g. chronic inflammation) cause of both, low 25OHD and low testosterone levels.
Hence, the #1 take-home message is that 20,000 IU of D3 per week, i.e. ~2,850 IU/d won’t bring low(ish) D-levels up. Against that background, it’s hardly surprising that the effects on testosterone, let alone secondary outcomes such as glucose and lipid metabolism or body composition are non-existent; and – more importantly – the study doesn’t tell us anything about whether actually repleting the levels (w/ higher amounts of different forms of vitamin D) wouldn’t indeed have the desired effect on the testosterone levels of the subjects.
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Study shows that black tea, in particular, protects from diet-induced obesity… While we are talking about rodent data, it is imho worth mentioning that the scientists from the Center for Human Nutrition at the University of California, Los Angeles, USA (Henning 2018) observed quite an intriguing difference between co-feeding green vs. black tea on top of a high-fat (=hyperenergetic, not “low carb keto”) diet.
Figure 2: Body fat percentage (subcutaneous) relative to body weight, left; average energy intake (kcal/d, right | Henning 2018); labeled means of dietary interventions without a common letter differ by diet; P < 0.05.
As you can see in Figure 2, the black tea group was not only the one with significant improvements in what most dieters are really looking for, i.e. reductions in visible body fat (Figure 2, left | if prioritizing these “cosmetic changes” is smart is a whole different question, though), the rodents also shed that body fat in the absence of a reduction in their energy intakes (Figure 2, right).
That’s the effect you’re actually looking for in an anti-obesity agent, considering that most hedonic eating is among the #1 problems in human (vs. rodent) obesity.
As of now, it is yet not clear, what exactly is going on, here. The scientists’ analyses of the rodents’ poop do, however, suggest that it may be a downstream effect of an increase in short-chain fatty acids (SCFA | generally considered a trigger of various of the health benefits from increased consumption of fiber and improvements in your microbiome) in response to black-tea-specific increases in the relative proportion of Pseudobutyrivibriobacteria – in other words: the modulatory effects of black tea on the rodents’ microbiome. Which raises the important question: How much black tea did it take?
Figure 3: Phenolic composition of the tea extracts that were used in the study by Henning et al. (2018).
Well, the scientists “calculated that mice fed the GTP diet in average consumed 240 mg of GTP and 320 mg of BTP per kg body weight” – for a human being that’s ~19-26mg/kg and hence an initially hefty-looking dose of >1.5g/day. When you come to think about it, you’d just have to consume one cap with every meal, which does no longer seem so impossible, does it?
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Plant proteins may help you manage your post-prandial glucose levels… now the question is: do they do this to a greater extent than dairy proteins? While the former is something you’ll probably have read elsewhere, already, the important follow-up question to the latest research by Sze-Yen Tan and colleagues from Singapore Institute for Clinical Sciences (SICS) is the reason why you (hopefully) read every SuppVersity article – context + extra-info.
How’s that? Well, the Asian scientists did not include a dairy protein group when they “examine[d] the effects of protein supplementation from three plant sources to a sugar-sweetened beverage on postprandial glycemic responses in healthy adults” (Tan 2018). To be specific, the scientists conducted a randomized, crossover acute feeding study consisting of four treatments: (1) chocolate beverage alone (50 g carbohydrate), or (2) added with 24 g (a) oat, (b) pea or (c) rice proteins. It is also worth mentioning that the scientists’ subjects were twenty Chinese males (mean ± SD age 26 ± 5 years; body mass index 21.5 ± 1.7 kg/m²) who ingested the test drink after an overnight fast – hence, the results may differ for people from another gene pool and/or for your second, third, or fourth meal of the day.
Figure 4: Insulin (yellow, left), glucose (green, middle), and GLP1 (blue, right) iAUC (measured over 180 minutes) among Asian males following the control, oat, pea, and rice protein test beverages (Tan 2018).
As you can see in Figure 5, all three proteins (which contained ~2g of leucine, each, by the way) did indeed modify the glucose response to the test-meal, however they also have in common that they failed to produce a statistically significant reduction in postprandial glycemia and one may argue that the increase in insulin you can see in Figure 4 could be regarded as a detrimental effect, however – specifically for pea protein, where it the increase in insulin is complemented by a lower increase in the “satiety hormone GLP1”, of which you may know that analogs are meanwhile used as anti-diabetes drugs (#ligratude).
Figure 6: Changes in participants’ perception on hunger (a), fullness (b), desire-to-eat (c), preoccupation with foods (d), and amount of foods could be eaten (e) following the control, oat, pea, and rice protein in 20 Asian males (Tan 2018)
In fact, it is possible that the disconnect between insulin and GLP1 does at least partly explain why pea protein had the smallest (p > 0.05, though) effect on the “amount of foods could be eaten” (assessed by asking subjects, not with buffet | see Figure 6)
Reason enough to take another look at a comparable study using whey protein… well, not so easy to find one in healthyindividuals, but there is one: “Glycemia and insulinemia in healthy subjects after lactose-equivalent meals of milk and other food proteins: the role of plasma amino acids and incretins” (Nilsson 2004).
Figure 5: The risk for cardiovascular death increases threefold as 2-hour post-challenge glucose levels increase from 54 to 199 mg/dl, although these readings are all in the nondiabetic range – in other words: highly relevant also for those of you whose HbA1c says that don’t have blood glucose problems (O’Keefe 2007).
Why exactly are postprandial glucose (and triglyceride) excursions relevant for you? The answer is simple: They’re hallmark features of metabolic disease that have been clearly linked to cardiovascular disease – a link of which O’Keefe et al. (2007) write that the “cardiovascular toxicity of postprandial dysmetabolism is mediated by oxidant stress, which is directly proportional to the increase in glucose after a meal” – with the latter triggering a “transient increase in free radicals acutely triggers inflammation, endothelial dysfunction, hypercoagulability, sympathetic hyperactivity, and a cascade of other atherogenic changes” (ibid).
The Danish study evaluated the effect of common dietary sources of animal or vegetable proteins on concentrations of postprandial blood glucose, insulin, amino acids, and incretin hormones [glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1] in healthy twelve healthy volunteers who were served test meals consisting of reconstituted milk, cheese, whey, cod, and wheat gluten (28g protein) with equivalent amounts of lactose. A standardized load of white-wheat bread w/ equal amounts of total carbs was used as a reference meal.
The results of the study are in line with what we see in Tan’s more recent plant protein study, the insulin release increased with protein supplementation, however, unlike Tan et al. Nilsson et al. did the necessary tests to link the rise in insulin to the rate of appearance of specific amino acids, with the strongest correlations for leucine, valine, lysine, and isoleucine.
Dairy proteins seem to be more potent, however…
An important contrast to the results of the study at hand, however, was the statistically significant reduction in postprandial glucose the Danish researchers found in response to the two tested dairy proteins, i.e. milk-powder and whey protein where the postprandial glucose AUC was a whopping -62% and -57%, respectively, lower than in the control group.
It cannot be emphasized enough, though, that this happened more or less in response to serious increases in post-prandial insulin, which was almost 2-fold elevated in the dairy protein groups – that’s somewhat less than what we see (albeit in different subjects and with different controls and other study variables) in the study at hand, for pea or oat protein.
Figure 7: Studies in young healthy males (here Nilsson 2004) show that dairy protein can have more powerful effects on glycemia than they were observed in the study by Tan et al. However, these improvements are the result of doubled insulin levels not everyone is going to be happy with.
So what’s the verdict, then? You will remember from previous articles that dairy protein may have the edge when it comes to building muscle. Pea, however, is a pretty fierce competitor, of which you can even find studies that suggest that it could be the superior muscle builder (vs. whey). In the long-run, the exuberant increase in insulin with dairy proteins could give them an edge that has been almost forgotten in the day and age of the insulin-scare: the muscle-remodeling effects of increased IGF1- and metabolite-levels (Alessi 1996; Rommel 2001). How much of a contribution (quantitatively) these increases actually make and whether acne, which is thought to be promoted by the very mTOR+IGF1 effects for which we all love whey so much (Melnik 2011), is the only side effect of increased IGF1 levels in people without pre-existing malignant cells (=already developing cancer), is something that goes beyond the scope of this science update whose take-home message reads as follows: Dairy is still the top dog wrt to improvements in post-prandial glucose management, but whey, milk, and casein protein work their magic via (literally) doubling the insulin production, which is something not everybody will be happy about.
What to expect in 2019? That’s it for today. I hope you enjoy this format because I plan to write more of these research updates in the future. I will also finally take baby steps to transition the SuppVersity to another technical backbone. Currently, my favorite WordPress, but if you have better suggestions or alternatives such as medium.com, let me know. The same goes for the type and format of articles and the question whether I should transplant the “news” from Facebook.com/SuppVersity to the new landing page, where they could/would be properly archived and wouldn’t “disappear” into thin air 😉
Alessi, Dario R., et al. “Mechanism of activation of protein kinase B by insulin and IGF‐1.” The EMBO journal 15.23 (1996): 6541-6551.
Henning, Susanne M., et al. “Decaffeinated green and black tea polyphenols decrease weight gain and alter microbiome populations and function in diet-induced obese mice.” European journal of nutrition 57.8 (2018): 2759-2769.
Lerchbaum, Elisabeth, et al. “Effects of vitamin D supplementation on androgens in men with low testosterone levels: a randomized controlled trial.” European journal of nutrition (2018): 1-12.
Melnik, Bodo C. “Evidence for acne-promoting effects of milk and other insulinotropic dairy products.” Milk and Milk Products in Human Nutrition. Vol. 67. Karger Publishers, 2011. 131-145.
Nilsson, Mikael, et al. “Glycemia and insulinemia in healthy subjects after lactose-equivalent meals of milk and other food proteins: the role of plasma amino acids and incretins.” The American journal of clinical nutrition 80.5 (2004): 1246-1253.
Rommel, Christian, et al. “Mediation of IGF-1-induced skeletal myotube hypertrophy by PI (3) K/Akt/mTOR and PI (3) K/Akt/GSK3 pathways.” Nature cell biology 3.11 (2001): 1009.
Tan, Sze-Yen, et al. “Influence of rice, pea and oat proteins in attenuating glycemic response of sugar-sweetened beverages.” European Journal of Nutrition 57.8 (2018): 2795-2803.