ONLINE DRIVERS MEDIA

"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, its 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, thats 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".
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" - thats 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 its 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).
Since physical activity may follow a similar circannual rhythm, its 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.
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. 

Cortisol is not your enemy. In fact, cortisol is one of the few hormones you really need to survive.

Cortisol is a problem. However, just as it is the case with insulin, its not the fact that your body produces it thats problematic. Its the fact that it tends to so in copious amounts and chronically, simply at the wrong time or - believe it or not - not at all / enough. All that, i.e. changes / problems with the natural rhythm, the up and down, the spikes and troughs that get lost, when you are chronically stressed and/or inflamed - thats the actual problem and not the fact that your body produces a hormone without which you cant survive. Against that background, it may go against everything the supplement industry is trying to tell you, but still cannot be really surprising to hear that E. Allansson Kjölhede and colleagues from the Linköping and Ume a Universities present in their latest paper in Acta Pædiatrica results that show that obese children have low, not high cortisol levels (Kjölhede. 2014).

Using three salivary samples from 342 children aged 6–12 years the scientists had tried to reconcile previous, inconsistent findings and found that the

"average cortisol levels in early morning, late morning and evening were significantly lower in overweight and obese children than in their normal weight counterparts."

Whats particularly interesting is that the early morning spike, we have identified as critical component of a healthy biorhythm, previously (see "All About Cortisol"), was reduced by -33% (see Figure 1):

Figure 1: Morning (8:30 am), late morning (10:30 am) and evening (9:00pm or pre-bed, if earlier) salivary cortisol in 342 normal-weight, overweight and obese children (Kjölhede. 2014).

As Kjölheide et al. point out, these results should be followed up by more comprehensive studies that would allow us to better classify and understand the "relationship between stress and obesity in
children" - and I would like to add: Which of these comes first - being obese or having low morning cortisol and thus not being able to benefit from the "wake-up and get going" effects of cortisol.
Thats also interesting, because previous studies by Toledo-Corral et al. have shown that a dampened cortisol awakening response is not just associated with obesity, it is also a predictive factor of higher carotid artery intima-media thickness (CIMT) in overweight African American and Latino youth (Toledo-Corral. 2013), which in turn is a risk factor for myocardial infarction and stroke.

And Ursache et al. (just because its funny: "Ursache" means "cause" in German ;-) report that  dolescents with insulin resistance exhibited

• a blunted cortisol awakening response (CAR),
• smaller hippocampal volumes, and 
• greater frontal lobe atrophy 

compared to controls. Closer scrutiny of the data also revealed that "a smaller CAR was associated with higher BMI which was in turn associated with fasting insulin levels" (Ursache. 2012).

Despite the fact that it is virtually impossible to tell what exactly the "ursache" for the irrefutable correlation between low morning cortisol levels and high body fatness, artery intima-media thickness, myocardial infarction and stroke is, the cumulative evidence clearly speaks against the use of cortisol-reducing drugs and supplements - at least if their effects are not extremely short-lived and will thus not mess with the natural up-and-down thats lost not just in obese, but also in chronically fatigued patients.

Reference: 

• Champaneri, Shivam, et al. "Diurnal salivary cortisol is associated with body mass index and waist circumference: the Multiethnic Study of Atherosclerosis." Obesity 21.1 (2013): E56-E63.
• Toledo-Corral, Claudia M., et al. "Blunted nocturnal cortisol rise is associated with higher carotid artery intima-media thickness (CIMT) in overweight African American and Latino youth." Psychoneuroendocrinology 38.9 (2013): 1658-1667.
• Tominaga, Yuji, et al. "Licorice Flavonoid Oil Effects Body Weight Loss by Reduction of Body Fat Mass in Overweight." Journal of health science 52.6 (2006): 672-683.
• Tominaga, Yuji, et al. "Licorice flavonoid oil reduces total body fat and visceral fat in overweight subjects: A randomized, double-blind, placebo-controlled study." Obesity research & clinical practice 3.3 (2009): 169-178.
• Ursache, Alexandra, et al. "Preliminary evidence for obesity and elevations in fasting insulin mediating associations between cortisol awakening response and hippocampal volumes and frontal atrophy." Psychoneuroendocrinology 37.8 (2012): 1270-1276.
• Zenk, John L., et al. "The effect of 7-Keto Naturalean™ on weight loss: A randomized, double-blind, placebo-controlled trial." Current therapeutic research 63.4 (2002): 263-272.