Can Mobile Phone and Computer Screens Cause Obesity? (2)
If you haven't read the previous post on this topic, here it is:
Can Mobile Phone and Computer Screens Cause Obesity?
What Is the Difference Between Blue Light and a High-Fat Diet?
I have to return once again to the issue of modern light sources and the filtering of daylight by windows and glasses. It seems that inadequate research before the widespread adoption of new LED light sources may be responsible for a number of health problems. We could already observe changes when fluorescent computer screens were introduced, when it became apparent that their light could cause vision problems.
Our ancestors were fairly lucky when fluorescent tubes were introduced into schools and workplaces. Fluorescent lights were developed in such a way that they are still used today as control sources of white light in animal studies. That does not mean they have no effect; it only means that the effect was sufficiently small that it went unnoticed. LED light sources are different.
I really like this figure from an approximately 10-year-old study. It compares the spectral properties of daylight and artificial light sources. Note that the morning and midday daylight spectra do not differ very much, whereas at sunset the light is redder and the blue-violet component is strongly suppressed. I don't know why morning light resembles midday light. Personally, I think that actual early-morning light will be similar to twilight, but probably nobody gets up that early these days. This fits well with the fact that the blue-violet component of light activates OPN5 and wakes us up for daytime activity. At the same time, it counteracts the effects of blue light by suppressing lipolysis and thermogenesis.
Modern light sources stand out for their narrow-band spectra. Apart from the light from incandescent bulbs, which are thermal sources, we see nothing but sharp fluorescent peaks. I would especially point out that fluorescent lamps have a small violet peak in addition to the blue peak. We can also look at it directly in an image from the OSRAM catalog.
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| OSRAM NATURA T8 L 36 W/76 |
I have highlighted in green the violet-light region around 400 nm and 360 nm. This is light that activates the biological photoreceptor OPN5, which has its greatest sensitivity around 380 nm, but behind the eye's lens its peak sensitivity is at approximately 425 nm. LED-based light sources, however, completely ignore this region.
The effect of light on biological mechanisms is a severely underestimated area of science. Do animal studies ever specify the type of lighting, the bulbs or fluorescent lamps used, and their exact models? I haven't noticed that. When authors describe the lighting conditions, we usually know only that the animals were kept on a 12-hour light/12-hour dark cycle. But we are not told what light sources were used or whether daylight was also present. That is a shame, because older research was certainly conducted under different lighting conditions than newer research. I think newer studies use LED lighting more often than fluorescent lamps. Everyone wants to save energy. The results of older research will not be reproducible in the new environment. That is quite a fundamental problem.
Scientists should know that light has an effect. For example, the above-mentioned study on C. elegans already showed how different the effects of different light sources on the results can be. It is not a simple relationship in which the shorter the wavelength and the bluer the light, the worse the effect. That is not the case at all. It is probably not even the direct effect of the higher quantum energy of photons that damages the tissues of organisms illuminated with monochromatic blue light. Organs are located deep inside the body, where no direct blue radiation can reach them, yet they are still damaged by blue light. How is that possible? Could it be caused by fats released through lipolysis induced by blue light?
But rather than making the obvious assumption that lipolysis induced by blue LED light counteracts obesity, the opposite is probably true.
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| WAT - white adipose tissue, BAT - brown adipose tissue, UCP1 - marker of thermogenesis in BAT, no change in activity |
What Is My Hypothesis?
I think that stored fat, combined with exposure to blue light, mimics a very high-fat diet during fasting. The stored fat is simply released too quickly and floods the body, much as it does on a high-fat diet. How much damage this causes to the organism then depends on the composition of unsaturated and polyunsaturated fatty acids in triglycerides, specifically how easily they undergo peroxidation under oxidative stress and how many aldehydes are produced in the presence of hydrogen peroxide.
There are many studies on mice and other animals fed high-fat diets. Typically, during the first few days of a study, oxidative stress damages the liver mitochondria, causing the animals to overeat. The dietary fats then have to be stored in adipose tissue, where they also damage mitochondria and trigger cellular senescence.
We do not know exactly what is damaged first in the mitochondria, but we can assume it is mitochondrial cardiolipin, because oxidative stress "liberates" linoleic acid from cardiolipin and produces the aldehyde HNE, a toxin that suppresses the activity of numerous enzymes, slows metabolism and the breakdown of HNE itself, and also triggers the polyol pathway and chronic inflammation. By choosing the right fat composition, we can prevent these processes and avoid mitochondrial damage even on a high-fat diet.
Can Blue Light Cause the Same Problem?
Let's look at the time course of one such experiment involving blue light exposure in mice fed a standard low-fat mouse diet. Mice exposed to blue LED light gain weight easily, but what is interesting is that this is not because they consume more food. On the contrary, they eat less and still gain weight.
After four weeks of a regimen involving 5 hours of blue light exposure per day, we see changes only in the form of elevated fasting glucose levels and a greater decrease in glucose levels in response to insulin stimulation. My personal explanation is that blue LED light increased lipolysis and released free fatty acids (FFAs) from fat stores, especially during the resting period. Free fatty acid levels increase the liver's processing of fats and regulate gluconeogenesis.
The fact that we observe increased gluconeogenesis as elevated fasting glucose is a sign of insufficient gluconeogenesis in the liver and increased gluconeogenesis in the kidneys. This is why fasting glucose is higher, but the export of fats from the liver back to adipose tissue is also increased. Increased fat turnover would be beneficial only if fat burning could also be increased, for example in brown adipose tissue. However, that did not happen. More sunlight's full-spectrum white light may be needed for that.
So far, the effects are quite similar to those of a high-fat diet. But when mice are switched rapidly to a high-fat diet, they overeat; here, they do not. The processes are probably slower in this case.
Free fatty acids released from adipose tissue through increased lipolysis stimulate increased gluconeogenesis to facilitate fat storage, thereby raising insulin levels. Acetyl-CoA produced from FFAs stimulates both fat storage and gluconeogenesis. If fats can be stored easily, they will be stored without increased gluconeogenesis. Problems with fat storage cause obesity and alter metabolism.
The adipose tissue must already be damaged during the first few weeks of the experiment. In addition to lipolysis, blue light probably has other effects that damage adipose tissue. Overloaded adipose tissue responds defensively, leading to increased gluconeogenesis to increase fat export from the liver. However, this export is not possible, so food intake decreases.
This continues into week eight: FFAs and gluconeogenesis are elevated, as is fat storage, but glucose intolerance has worsened further, and insulin levels are no longer sufficient to compensate for gluconeogenesis. Glucose levels rise after meals, triggering the hepatic polyol pathway and fructose production, suppressing antioxidant defenses, and subsequently leading to HNE production from linoleic acid and the onset of chronic inflammation. By week 20, we therefore see a further decline in insulin's effects.
Interestingly, by week 40, the groups had converged again. At week 32, insulin sensitivity was at its lowest, but then something happened. It was as if insulin production had been suppressed, insulin sensitivity had increased, and glucose levels had also decreased. What could have happened? Could the activation of lipolysis by blue light have switched off after a longer period of the experiment? Or had the linoleic acid in the adipose tissue been depleted?
Lipolysis preferentially releases polyunsaturated fats (PUFAs), and this may be the most problematic aspect of blue light. It creates conditions in which fat is burned very rapidly, but this produces oxidative stress and aldehydes. It places heavy demands on antioxidant defenses and on the enzymes that remove aldehydes, especially ALDH2.
The improvement by week 40 could therefore also have been caused by depletion of excess linoleic acid and the associated change in FFA composition. The mice were on a low-fat diet, so they must have had excess linoleic acid stored in their fat reserves. It is very interesting that, from a state of the greatest insulin resistance, the mice were able to restore their metabolism within just a few weeks to a level comparable to that of the control group.
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| Damage to the reproductive organs caused by blue LED light |
But even this did not protect them from permanent changes to organs located deep inside the body, in places blue light never reaches. Well, this is probably no longer such a mystery to us. The damage was likely caused by excess free fatty acids released by blue LED light, much as happens with an improperly composed high-fat diet.
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| Changes in sperm head shape following exposure of mice to blue LED light |
You might now be thinking that you must avoid blue light from LED bulbs at all costs. But that may not be necessary at all. The blue light in sunlight is not actually dangerous and probably serves an indispensable function as well. If we supplement narrow-band blue LED light with violet-indigo LED light, the results for the group exposed to the complete LED spectrum might be comparable to those of the control group. Violet light probably suppresses lipolysis through the OPN5 receptors in the eye, thereby counteracting the effects of purely blue light. White light should simply have a complete spectrum, not just a few peaks across the color spectrum.
Perhaps all we need to do is fill the gaps in the spectrum with additional LEDs so that we can turn problematic light sources into healthy, energy-efficient bulbs. We just need to devote more research to this.
Next
References:
Spectral properties of smart LED lamps
Violet-light suppression of thermogenesis by opsin 5 hypothalamic neurons
Metabolic responses of light and taste receptors – unexpected actions of GPCRs in adipocytes
Cell-autonomous light sensitivity via Opsin3 regulates fuel utilization in brown adipocytes
A Retinal Ganglion Cell That Can Signal Irradiance Continuously for 10 Hours
The Hidden Cost of Blue Light: Multiorgan Pathology Induced by LED Exposure in Mice
The Hidden Harms of Modern Lighting and the Fight to Bring Back Incandescent Bulbs
Kinetics of the depletion of linoleic acid in mice
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