Bright Light Exposure Improves Your Workouts Sign. (~8%)

Would be interesting to compare sunlight and artificial light in future studies.

You will remember the circadian rhythm series in which I have previously discussed the relevance of light exposure as a means to set, reset and entrain your internal clock in order to reap all sorts of health and performance benefits.

Bright (>4000 lux), preferable blue (at least having a blue component) light has repeatedly been shown to increase athletic performance. Studies like Kantermann et al. (2012) show, however, that the efficacy of bright light exposure significantly depends on the chronotype of an athlete.

Learn more about the health effects of correct / messed up circadian rhythms

Sunlight, Bluelight, Backlight and Your Clock

Sunlight a La Carte: "Hack" Your Rhythm

Breaking the Fast to Synchronize the Clock

Fasting (Re-)Sets the Peripheral Clock

Vitamin A & Caffeine Set the Clock

Pre-Workout Supps Could Ruin Your Sleep

In said study, the athletes were exposed to 4420 lux for 120 min before and right before a 40-min time trial. Significant performance increases were observed only for those subjects, though, who were performing ∼14.8 h after their midpoint of sleep on free days (MSFsc). Subjects who trained "earlier" on their internal clock (in this case ∼11.8 h after the MSFsc), on the other hand, did not record any benefits.

Back in the day, Kantermann et al. speculated that a short(er) exposure or mudaltion of light intensity and/or timing could likewise have affected their results. Thus, the hypothesis Knaier et al. used in their 2015 contribution to the "light for performance" research was to that different bright light (BL) exposure regimes prior to and during a time-trial applied during the “sensitive” phase of the circadian rhythm result in a dose dependent increase of time-trial power output - meaning: longer exposure and brighter light = maximal performance benefits.

To test this hypothesis the scientists assigned young (25.1 ± 3.1 years) men to three groups with two different light intensities (A = BL, 4420 lx vs. B = ML, 230 lx) for all three randomly chosen exposure times (2h pre + exercise time, 2HEX | 1h pre + exercise time 1HEX | 1h pre 1H).

Figure 1: Study protocol for 2HEX, 1HEX, and 1H. Time-trial: 40 min in duration; bright light/moderate light (BL/ML): continuous randomized exposure (slightly rearranged version of a figurr from Knaier. 2015).

As Figure 1 illustrates we are thus dealing with a total of three trials and their moderate light counter parts which are not illustrated in Figure 1. Thanks to the use of a cross-over design this means that all subjects were exposed to either bright light (BL, 4420 lux) or moderate light (ML, 230 lx).

Figure 2: Total work (in kJ) during the 40-minute time-trial to exhaustion (Knaier. 2015).

The scientists' analyses of the studies results and the normalization of the results according to the subjects' individual chronotype (estimated based on the Munich Chronotype Questionnaire) yielded the following two primary study outcomes:

• Total work performed during the time-trial in kJ in the 2HEX group was significantly higher in the BL setting (527 kJ) than in ML (512 kJ) (P = 0.002), but not in 1HEX (BL: 485 kJ; ML: 498 kJ) or 1H (BL: 519 kJ; ML: 514 kJ) (P = 0.770; P = 0.485). 
• There was a significant (P = 0.006) positive dose–response relationship between the duration of light exposure and the work performed over the three doses of light exposure. 

Overall, the study does therefore confirm that "[a] long duration light exposure is an effective tool to increase total work in a medium length timetrial" - what's new (compared to the previously referenced Kantermann study is the observation that this advantage holds, even if the results are normalized for the subjects' individual chronotype.

Whether and to which extent the "more light equals more performance" equation will hold with (a) even longer or (b) even more intense light, however, is something that will have to be investigated in future dose-response studies. Studies like O'Brien et al. (2000) which has already proven that shortening the exposure time (in this case to 20 minutes only during exercise) will reduce the effects of bright light exposure on cycling performance to zero.

Bottom line: While one hour of bright or 2h of medium intensity light appears to allow for too little 'light accumulation' to have physiologically relevant affects, long duration of exposure to bright light is, as Knaier et al. point out "an effective tool to increase total work at least for the initial phase of a medium length time-trial" (Knaier. 2015); and what's important, the performance increase of ~8% which was observed not just in the Knaier study, but also in a differently designed trial by Thomson, et al. (2015 | cf. Figure 3), is large enough to be relevant for any competing athlete.

Figure 3: A study by Thompson, et al. (2015) suggests that pre-bed exposition to bright light (30 min) can increase the time-trial performance of athletes on the subsequent morning. Since this will also suppress the melatonin levels of practitioners this is yet a strategy that should not be employed regular (competition only).

The results of Knaier are thus in contrast to a similarly recent study by Nelson et al. (2015) who found that acute short-term dim light exposure can actually lower muscle strength endurance (-18%, albeit with high inter-individual variability). Against that background it should be obvious that, even though, bright light exposure is indeed "likely to increase alertness and reduce sleepiness and help athletes to compensate for disadvantages in competitions at unfavorable times and improve performance" (Knaier. 2015). And don't forget - the scientists from the University of Basel are right: "The ideal duration of expo sure to increase performance and simultaneously interfere as little as possible with athletes’ routine still needs to be found" (Knaier. 2015). In fact, even timing and strategies like the pre-evening light exposure that increased the time trial performance in Thomson et al. (2015 | see Figure 3) must be tested as alternatives | Comment on Facebook!

References:

• Kantermann, Thomas, et al. "The stimulating effect of bright light on physical performance depends on internal time." PloS one 7.7 (2012): e40655.
• Knaier, R., et al. "Dose–response relationship between light exposure and cycling performance." Scandinavian journal of medicine & science in sports (2015).
• Nelson, Arnold G., Joke Kokkonen, and Megan Mickenberg. "Acute short-term dim light exposure can lower muscle strength endurance." Journal of Sport and Health Science 4.3 (2015): 270-274.
• O'Brien, Patrick M., and Patrick J. O'Conner. "Effect of bright light on cycling performance." Medicine & Science in Sports & Exercise (2000).
• Thompson, A., et al. "The effects of evening bright light exposure on subsequent morning exercise performance." International journal of sports medicine 36.02 (2015): 101-106.

Lack of Sun Exposure & Type II Diabetes - Contemporary Evidence Suggests: There is a Link!

"No sun, no diabesity protection." The evidence is equivocal and the number of studies low, but there is evidence that this statement could be true.

Ok, it's November and not exactly sunny in the Northern hemisphere, but if you look back at the months June-August, how much sun exposure did you actually get, this year? Hardly any? Well, that's bad news, because a recent review of the scant scientific evidence suggests that there is "a role of recreational sun exposure in reducing odds of T2DM incidence" (Shore-Lorenti. 2014).

In view of the fact that the contemporarily available evidence is not exactly comprehensive, you should yet consider the following overview of the potential effects and mechanism as a "work in progress".

The effects on circadian rhythm could be behind the Sun's anti-cancer effects

Sunlight, Bluelight, Backlight and Your Clock

Sunlight a La Carte: "Hack" Your Rhythm

Breaking the Fast to Synchronize the Clock

Fasting (Re-)Sets the Peripheral Clock

Vitamin A & Caffeine Set the Clock

Pre-Workout Supps Could Ruin Your Sleep

As Shore-Lorenti et al. point out, the recent International Diabetes Federation (IDF) Diabetes Atlas (6th edition) describes a snapshot of the global diabetes burden in 2013 and projects this forward to the year 2035.1 Cur rently, an estimated 382 million global citizens have diabetes, costing around $1437 USD in 2013 for each person affected by the condition. Projections based on current trends predict that 592 million people will be living with diabetes by 2035; one in ten people will be affected, with an inordinate amount of fund ing required globally to treat diabetes and manage diabetic com plications ($627 billion USD in 2035).

And while scientists are feverishly searching for a solution for the diabesity epidemic, the ongoing research into the effectiveness of vitamin D supplementation in diabetes have yielded inconsistent results (Mitri. 2011). Against that background it appears almost negligent that only few scientists have yet taken a closer look at the factors that trigger vitamin D sufficiency or rather the global low vitamin D epidemia.

Lack of sun"low vitamin D" - that's not all!

Figure 1: Australians who use sunscreen chronically have 50% reduced vitamin D levels (Matsuoka. 1988)

A lack of sufficient (unprotected) sun exposure - previous studies have shown that chronic sunscreen use decreases circulating concentrations of 25-hydroxyvitamin (Figure 1 | Matsuoka. 1988) - is one of the factors of which researchers speculate that it contributes to the development of vitamin D deficiency even in those of us who live in areas with a high annual sun-exposure.

Now, if restoring the 25-OHD (vitamin D) levels to normal does not work the anti-diabetic magic it is supposed to do and our D-levels are low due to insufficient sun-exposure, it appears only logical to assume that a lack sun-exposure and not a lack of vitamin D is one of the factors that contributes to the ever-increasing rates of diabesity - in conjunction with the usual subjects, obviously: The consumption of a junk-food diet and a lack of exercise, which is without doubt the #1 reason people in the Western Obesity Belt develop obesity, diabetes and the other characteristics of the metabolic syndrome.

Against that background it's all the more surprising that evidence for an association between sun exposure and fasting serum glucose level is scarce.

"Typically, the lowest glucose levels occur during summer and levels peak in winter or early spring. One of these analyses [Shore-Lorenti et al. reviewed] went beyond simply observing trends in fasting glucose throughout the year: fasting plasma glucose was positively correlated with a measure of available sun and inversely correlated with temperature." (Shore-Lorenti. 2014)

The study, the researchers from the University of Melbourne have in mind was conducted by Suarez, L. & Barrett-Connor, E. in 1988, already.
If you look at the data Suaraez & Barret-Connor generated, you can see - even without their statistical sophisticated analysis - that there is a significant correlation between possible sun exposure (Figure 1, left) and the fasting plasma glucose levels (Figure 1, right).

But sunlight gives you skin cancer, right? If you are the typical white-skinned tourist who grills in the sun for 8h a day in his 2-week beach holiday (=intermittent high exposure), yes! A chronic exposure to a moderate doses of sunlight, on the other hand, has been associated with a significant 27% reduced risk of melanoma (Nelemans. 1995).

Since physical activity may follow a similar circannual rhythm, it's yet difficult to exclude that the effects Suarez & Barret-Connor observed were not corroborated (or corrupted?) by an increase in physical activity. However, Shore-Lorenti et al. believe that ...

"[...c]onsidering that the unadjusted analyses and three of four of the studies included in the best evidence synthesis (including the study adjusting for physical activity) are in agreement, it is possible that future research may confirm that sun exposure reduces fasting glucose" (Shore-Lorenti. 2014).

Shore-Lorenti et al. also point out that the highest level of evidence (moderate) for an association between sun exposure and T2DM outcomes in adults originates from the study by Lindqvist et al. (2010). In their paper, the researchers from the Karolinska University Hospital report a reduction in odds of developing T2DM given increased recreational (rather than occupational) sun exposure. 

Figure 2: Leisure time sun exposure is associated with a significantly reduced risk (up to 50%!)
of developing T2DM in Swedish adults (Lindqvist. 2010)

In subjects with a low BMI the beneficial effect of using the tanning bed and sunbathing is even more pronounced (-60% risk). In the obese, however, it is significantly reduced (-10%) compared to the average reductions you see in Figure 2.

The fact that only leisure time, but not occupational sun exposure was linked to a significant reduced risk of developing type II diabetes may, as Shore-Lorenti et al. point out be due ...

"[...] to the frequency of sun exposure (perhaps leading to tolerance), duration, intensity and site of exposure (sun protective clothing and behaviour differences between the two settings), or perhaps selection biases for such work (for example, fair-skinned people may avoid occupational sun exposure or a less healthy lifestyle may be associated with manual labour)."

Incidentally, a similar disparity between recreational and occupational sun exposure is well described for risk of developing melanoma (Chang. 2009).

A review by Chen et al. (2008) provides low-level evidence for an association between sun exposure and fasting insulin levels; fasting serum insulin was higher in summer than in winter. Overall, the results are yet inconclusive. A fact, Shore-Lorenti et al. ascribe to "the lack of adjustments made by the included study – particularly for BMI" (Shore-Lorenti. 2014)

Overall, we are thus left with the above overview (Table 1) as a conclusion of which the mere number of "unkown"s and "inconsistent"s tell you that we are not yet at the point to draw a water-proof conclusion.

Circadian Rhythmicity - Sunlight a La Carte: How to "Hack" Your Circadian Rhythm With 30min of Light Therapy Per Day | more

Bottom line: All in all, it appears to be likely that a lack of direct and regular moderate sun exposure is among the many lifestyle factors that increase your risk of developing type II diabetes.

The ameliorative effects of obesity, researchers like Lindqvist et al. (compare Figure 2) have observed, on the other hand, should remind you that you won't get away with "just" getting enough sun exposure. Regular physical activity and a whole foods diet for obesity prevention are at least as important as the hours you spend in the sun | Comment on Facebook!

Speaking of hours in the sun, the overall beneficial effects are more likely to be related to the beneficial effects of sun exposure on circadian rhythmicity than on its effect on other chemical processes, such as the formation of vitamin D.

References:

• Chang, Yu-mei, et al. "Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls." International journal of epidemiology (2009): dyp166. 
• Chen, Shui-Hu, et al. "Community-based study on summer-winter difference in insulin resistance in Kin-Chen, Kinmen, Taiwan." Journal of the Chinese Medical Association 71.12 (2008): 619-627.
• Lindqvist, Pelle G., Håkan Olsson, and Mona Landin-Olsson. "Are active sun exposure habits related to lowering risk of type 2 diabetes mellitus in women, a prospective cohort study?." Diabetes research and clinical practice 90.1 (2010): 109-114.
• Mitri, J., M. D. Muraru, and A. G. Pittas. "Vitamin D and type 2 diabetes: a systematic review." European Journal of Clinical Nutrition 65.9 (2011): 1005-1015.
• Nelemans, P. J., et al. "An addition to the controversy on sunlight exposure and melanoma risk: a meta-analytical approach." Journal of clinical epidemiology 48.11 (1995): 1331-1342.
• Shore‐Lorenti, Catherine, et al. "Shining the Light on Sunshine: a systematic review of the influence of sun exposure on type 2 diabetes mellitus‐related outcomes." Clinical endocrinology (2014).
• Suarez, L., and E. Barrett-Connor. "Seasonal variation in fasting plasma glucose levels in man." Diabetologia 22.4 (1982): 250-253. 

Hack Your Biological Clock: Light-Induced Circadian Phase Shifts Work So Well That You Better Watch Out to Avoid Accidental Phase Shifting When You Check Your Mails

If you do it on purpose, "hacking" your biological clock can be highly beneficial. If you're doing it out of pure ignorance, though, you're in trouble.

In view of the impeding return to standard time, it's probably a good thing, in view of the iPhones, iPads and Facebooks of this world it could turn out to be a serious health problem, though: the ease with which you can "hack" your biological clock - on purpose, but also incidentally.

How easy it really is to turn the biological clock of life forward and backward has in fact only recently  been confirmed by Seong Jae  Kim and colleagues from the Northwestern University Feinberg School of Medicine and the Technology Evaluation Center of BlueCross BlueShield Association (Kim. 2013)

Fast forward / backward, please!

All the scientists had to do to make sure that the 29 healthy young (25.1 ± 4.1 years, M:F=8:21) and 16 healthy older subjects (66.5 ± 6.0 years, M:F=5:11) who participated in the said study experienced a 2h shift in the onset of their natural melatonin release was to expose them in a randomized order to 2h light pulses of 2 different intensities: 2,000  and  8,000lux)

Figure 1: Graphical summary of the implications you of the data from Kim et al. (2013)

As you can see in the graphical illustration of the implications in Figure 1 the scientists used the core body temperature minimum (CBT_min) of their subjects as a reference.

Suggested Read: "90 Min Sleep Restriction - How Bad is It Really? Changes in Insulin Resistance Last For One Week" | more

"Subjects were admitted for four nights and three days under dim light during daytime hours with eight hours of sleep in dark at their habitual time (dark bars). Blood samples were taken throughout the baseline and post -treatment nights to assess lightinduced [sic!] changes in the circadian melatonin rhythm.

On the third night, subjects were exposed to light at one of 3 time points ( -8h, -3h, or 3h) relative to the core body temperature minimum (CBTmin) measured on the baseline night. They were exposed to a 2-hour light pulse (including a 15 min ramp up and ramp down) of 2,000 lux on one laboratory stay and 8,000 lux on a different laboratory stay, in a randomized order, separated by at least 3 weeks." (Kim. 2013)

I guess it may come as a surprise that the scientists were able to show that the effect size / efficiency of the procedure was significantly influenced by the time of pulse, but not by its intensity, the age of the subjects or interactions between age and intensity, or time of pulse and intensity.

What did make a difference, though was the lag (=length of the time shift that was achieved), though.  Administered -8h before core body temperature minimum (CBT) the average phase delays  were -0.72h for  2,000lux and -0.50h for  8,000lux. When it was administered +3h after the CBT the researchers observed only a minimal phase advance of +0.05h for  2,000lux, while the 8,000 lux light produced a phase shift of + 0.18 h. In both cases the standard deviations were however so large that a significant difference could not be found.

8h is where the sweet spot it + phase advances are difficult to achieve

The "wake-up protocol" (Figure 1, 2nd row on night 3), in the course of which the subjects were woken up 3h before the CBT and thus while they were already sleeping had paradoxical and unpredictable effects:

"Light exposure targeted 3h before CBT min was distributed in both phase delay and advance regions  (-3.2h to +2.5h) relative to the melatonin midpoint." (Kim. 2013)

Needless to say that this is not a suggested protocol, but a good example of the mess that happens, when your sleep gets interrupted by light exposure.In other words, the procedure is identical irrespective of your age and the "power" of the lamp you use - the one thing that counts is the timing of the pulses.

How intense is the light around me? In order to give you a better idea of how intense 2,000 and 8,000lux are, I've compiled a couple of reference values:

• Dim interior lighting < 100 lux
• Residential indoor lighting < 500 lux
• Bright indoor lighting (e.g. task lighting, kitchens, offices, stores) < 1,500 lux
• Sunlight + cloudy sky + shadow < 5,000 lux
• Sunlight + in shadow < 10,000 lux
• Full, but not direct daylight daylight < 25,000 lux
• Outdoor direct sunlight < 120,000 lux

Don't forget that the frequency (=color) of the light is about as important as its intensity; only blue / green light and light with blue and/or green components (e.g. the light of an LED display) will get the job done.

In the discussion of their results, the researchers point out that their findings are in line with previous studies by Duffy et al. (Duffy. 2007), ...

"[...]who found that there was no difference between young and older adults in the magnitude of  phase delays of the melatonin rhythm following 6.5 hour light exposure of more than 1,000 lux." (Kim. 2013)

They also reference a study by Sletten et al. (2009) that compared the effectiveness of blue and green light in young and older adults. In the said study, the researchers determined that the phase advances in response to blue light were  slightly larger than advances in response to green light in both young and older adults. The perceived effects on subjective alertness and sleepiness, on the other hand, were significantly more pronounced in the younger participants in the blue light condition.

As Kim et al. point out, their own previous analysis seem to indicate that blue light is much more effective, when it comes to the induction of phase advances than green light - in fact, in one of their studies, the exposure the use of green and red light did not yield satisfying results at all (Green. 2004).

So does this mean you have to use one of the fancy blue-light lamps?

Despite the fact that there is little doubt that "blue" (~430nm) light is more effective than green light and that red light does not work at all, you may be shocked to hear that running Facebook on your laptop screen is probably enough to get the job done.

The reasons are simple: Firstly, what you see there is "blue" or at least "blueish", anyway. More importantly, however, the fancy LCD and LED displays in modern notebooks, tablet PCs and smartphones have an outstanding luminosity (=they are bright enough) and, as you can easily see in the graphs below, "blue enough".

WLED

GB-LED

How bad is it? It really depends on the "how blue" your screen is going to be. Many cheaper LED monitors use the "blueish" WLED technology - the "true color" GB-LED displays are mostly used, where true color actually matters - in print and design.

The spectral data does also tell you that you will never "lack" blue light to convince your body that it's time to rise and shine, not time to sleep, even if you have one of the modern "true color" displays. Much contrary to the clock in the lower right of your screen, your biological clock will thus basically freeze in "daylight mode" the very moment you sit down in front of your screen.

Yes, things can become worse - you don't even have to sit there for hours

I know what you're thinking, you, a SuppVersity Veteran from hour one, obviously new all that and the only thing you do after 8PM, to make sure you can be in bed ad 10PM and get your 8h of sleep before you have to shower at 6AM on the next morning is to check the occasional text massage on your phone, right? Well, bad news:

"According to published data, a phase shift is often not completed immediately after a light pulse (Pittendrigh et al., 1958; Watanabe et al., 2001)." (Kim. 2013)

Actually the saturation effect, i.e. the presence of identical phase shifts for 2,000 and 10,000 lux, confirms it: It does not take hours to biohack yourself!

It goes without saying that this is a good thing, if you actually plan to advance / delay the onset of melatonin release, it is however a serious problem if you "just head back to check your emails" right before you are heading to bed.

So how do you "biohack" your rhythm, then? If you want to try the no guesswork approach, the first thing you would have to do is to try and find your core body temperature minimum. Unfortunately, this is - despite the existent correlation with oral, rectal and gut temperature - not an exactly easy undertaking, as it will occur right when you are supposed to sleep, not to fumble around with a thermometer.

Use fasting another means to sync your internal (light control) and peripheral biological clock. Learn more in the last installment of the Circadian Rhtythmicity Series: "Intermittent Fasting (Re-)Sets the Peripheral Clock" | read more

So we just assume that his would be at ~4am (where it should be if you lived by the natural clock, i.e. sunrise and -set), which would mean that you would be able to master ...

• the impeding -1h phase shift on Sunday (US 11/03 vs. EU 10/27) at 3:00 (AM) by sitting in front of an appropriately bright light from 6pm to 8pm, and  
• the subsequent +1h phase shift in spring by sitting in front of a bright light on Thursday, Friday and Saturday morning at 7am for 2h

Actually, both does not appear so difficult, right? And I bet that some of you are in fact inducing a decent phase delay on a regular basis when they sit in front of a bright computer or television screen after sundown. Am I right? If so: Is it really any wonder you always wake up unrefreshed when your alarm clock rings?

References:

• Longo DL et al. Harrison's Online. Featuring the complete contents of Harrison's Principles of Internal Medicine, 18e.
• Kim SJ, Benloucif S, Reid KJ, Weintraub S, Kennedy N, Wolfe LF, Zee PC. Phase-shifting Response to Light in Older Adults. J Physiol. 2013 Oct 21. [Epub ahead of print]
• Sletten TL, Revell VL, Middleton B, Lederle KA, Skene DJ. Age-related changes in acute and phase-advancing responses to monochromatic light. J Biol Rhythms. 2009 Feb;24(1):73-84.

Prepare for the Winter: Get your Supply of Vitamin D Supplements

Figure 1: In Great Britain Vitamin D3
supplementation appears indicated
at least in the winter month

A recent study by researchers (Webb. 2010) from the School of Earth Atmospheric and Environmental Sciences at the University of Manchester highlight the importance of maintaining "late-summer 25-OH(D3) levels" throughout the winter month. In their investigation among 125 white Caucasians aged 20-60 years in Greater Manchester they found:

Dietary vitamin D remained low in all seasons (median 3.27 mug/day, range 2.76-4.15) while personal UV exposure levels were high in spring and summer, low in autumn and negligible in winter. Mean 25(OH)D levels were maximal in September (28.4 ng/mL; 28% optimal, zero deficient (< 5 ng/mL)), and minimal in February (18.3 ng/mL; 7% optimal, 5% deficient). A February 25(OH)D level of 20ng/mL was achieved following an average late summer level of 30.4 (25.6 to 35.2) and 34.9 (27.9 to 41.9) ng/mL in women and men, respectively, with 62% variance explained by gender and September levels.

With 50ng/ml 25(OH)D being what is currently considered an optimal vitamin D status by many, additional vitamin D supplementation would thus be warranted even in the summer month. This holds true in view of the results from another recent study (Michaëlsson. 2010) reporting higher all-cause / cancer mortality for very low (<46 nmol/L) or very high (>98 nmol/L) levels of 25(OH)D in a community-based cohort of elderly men (mean age at baseline: 71 y; n = 1194) in Upsala.

Further Evidence: Sunlight Alone is Insufficient to Rise Vitamin D Levels in Non-Western Immigrants

Wicherts et.al. (Wicherts. 2010) published the results of an investigation into the effectiveness of a) sun exposure or b) supplementation with daily 800 IU or 100,000 IU once in three months on serum 25(OH)-D3 levels in 211 otherwise healthy non-western immigrant in the Netherlands.  As you can see in table 1, the initial high dose of 100.000 IU raised 25(OH)D levels significantly faster but to a lower extent than the 800 IU daily dosing:

Table 1: Proportion (%) of participants with serum 25(OH)D<25, 25−50, 50−75, or >75 nmol/l at baseline, 3, 6, and 12 months according to treatment group 800 IU/day, 100,000 IU/3 months or sunshine exposure (Wicherts. 2010. Table 2)

Otherwise, Wickerts' study confirms the results of earlier investigations,

mean serum 25(OH)D increased to 53 nmol/l with 800 IU/day, to 50.5 nmol/l with 100,000 IU/3 months, and to 29.1 nmol/l with advised sunlight exposure.

Though, even according to the "old" reference ranges, a 25(OH)D level <30 nmol/l does not ascertains a sufficient supply with a vitamin the importance of which scientists come to realize only in the last couple of years. Wicherts would thus not only have to conclude that

[...] Vitamin D supplementation is more effective than advised sunlight exposure for treating vitamin D deficiency in non-western immigrants,

but also, that vitamin D supplementation is indicated in non-western (dark skinned) immigrants to the northern hemisphere, where sun exposure is limited and insufficient to provide them with sufficient amounts of vitamin D.