Published December 6, 2024; typo corrected on December 7, 2024
Various factors can cause insulin resistance and glucose intolerance. Those of you who have read my prior blog post about the top causes of insulin resistance will know that insulin resistance is often caused by excess visceral and ectopic fat, but can also be caused by low muscle mass, lack of physical activity, sleep deprivation, stress, chronic inflammatory conditions, certain medications, and several other factors. In that blog post, I made the case that if we are insulin resistant, it is critical to identify and address our specific triggers of insulin resistance.
In this blog post, we will see that lack of exposure to sunlight, or too much exposure to the wrong kind of light at the wrong time of day, can be one such contributor to insulin resistance, leading to glucose intolerance and an increased risk of prediabetes and type 2 diabetes.
There are at least three different mechanisms through which light can affect insulin sensitivity and glucose tolerance, triggered by the ultraviolet, visible, and near-infrared portions of light. In this blog post, I’ll address each of these separately, completing the figure below. I will also share specific guidance on how to use this science to prevent – or reverse – insulin resistance and glucose intolerance.
This blog post will focus entirely on insulin resistance and type 2 diabetes, and not autoimmune forms of diabetes such as type 1 or LADA. Sunlight probably also plays a role in these conditions, but in a different way, and I will therefore cover these conditions in a separate blog post.
Sunlight and Glucose Tolerance: The Role of Vitamin D
A common cause of insulin resistance is a deficiency in certain micronutrients, and one such micronutrient deficiency associated with insulin resistance is vitamin D deficiency.
Now, vitamin D is not really a vitamin, because our body can produce it endogenously. So it should be seen as a hormone, or – more precisely – a hormone precursor. In our skin, under the influence of ultraviolet B, or UV-B, light, the skin converts cholesterol to vitamin D (see figure below). This vitamin D is then stored in this form in the fat tissue, or undergoes a series of biochemical modifications. First, the liver attaches one OH-group, also called hydroxy group, to the molecule, resulting in 25-hydroxy-vitamin D. This is the main circulating form of vitamin D that is usually measured in a clinical lab to assess the vitamin D status of a patient. Both vitamin D and 25-hydroxy-vitamin D are inactive forms. The kidneys and some other cells in the body can then add another hydroxy group, resulting in 1,25-dihydroxy-vitamin D. This is the active form of vitamin D that has numerous functions, mostly through binding to the vitamin D receptor that helps regulate which genes are switched on and off in most cells of the body. It’s been estimated that vitamin D regulates the expression of at least 1,000 and up to 6,000 different genes in the human body. What this means is that whether a cell produces a certain protein may partly depend on whether it receives enough vitamin D.
This is relevant because vitamin D deficiency is associated with insulin resistance, beta-cell dysfunction, glucose intolerance, and an increased risk of type 2 diabetes. The mechanisms through which vitamin D deficiency may trigger insulin resistance are not entirely clear, but they may include direct effects of the active form of vitamin D on the expression of the insulin receptor and anti-inflammatory effects:
- Vitamin D probably is involved in regulating the expression of the insulin receptor in various insulin target tissues, such as muscle, liver, and fat tissue. This is based on data that the human insulin receptor gene promotor in the DNA carries a Vitamin D response element, and that treatment with 1,25-dihydroxy-vitamin D increases the expression of the insulin receptor and insulin-mediated glucose uptake in vitro. This would suggest that vitamin D deficient individuals may have fewer insulin receptors on their muscle, liver, and/or fat cells, which would be expected to directly make these tissues more insulin resistant. However, we do not have conclusive data on the relevancy of this effect in vivo in humans, so the degree to which the association between vitamin D deficiency and insulin resistance is explained by this mechanism has remained unclear.
- In immune cells, vitamin D is critical to enable an appropriate immune response to pathogens, but also plays a role in inhibiting overactive inflammatory responses. Indeed, vitamin D deficiency is consistently associated with a state of low-grade chronic inflammation. And because inflammation is a key trigger of insulin resistance, this vitamin D-deficiency-associated upregulation of inflammation pathways could be one mechanism explaining the insulin resistance commonly seen in vitamin D-deficient individuals.
Vitamin D deficiency also seems to be directly affecting beta-cell function. The pancreatic beta-cells are among the few cell types other than the kidneys that can convert the inactive circulating form 25-hydroxy-vitamin D to the active hormone, 1,25-dihydroxy-vitamin D, and vitamin D signaling in pancreatic beta-cells seems to play a direct role in regulating the expression of insulin. Consistent with these molecular effects, vitamin D-deficiency is associated with reduced insulin secretion from pancreatic beta-cells.
There is A LOT more to say about this, because we can obviously get vitamin D from food and supplements as well, and you may wonder about who should consider supplementing, at which dose, etc. I will cover all of this in a later blog post, simply because covering all of that here is well beyond the scope of this blog post, which is focused on light.
What I wanted to cover here is that if you are vitamin D deficient, it could make you insulin resistant and impair your insulin secretion, both of which would lower your glucose tolerance and increase your risk of type 2 diabetes. And if you are vitamin D deficient, it also means that you may benefit from more direct sunlight on your skin. So I have two suggestions: first, if you haven’t recently had this done, get your vitamin D level measured, and take action if you are found to be vitamin D decent; second, seek out the sun more often, in a way that is safe and minimizes the negative consequences of UV radiation: keep your exposure to midday sun brief, and wear sunscreen and sunglasses as needed. Wearing sunscreen does reduce vitamin D synthesis in the skin; however, a good strategy may be to wear sunscreen on the face only, and limit exposure to direct midday sunlight so that you don’t get sunburn in those parts of your body that are not covered by sunscreen.
Well, but how long would you need to be in the sun to produce enough vitamin D to meet your daily requirement? The answer to that question depends, of course, on the amount of UV-radiation your location gets at that time, and also on variables such as your skin color and how much clothing you wear. You can experiment with the different variables affecting vitamin D synthesis yourself using this online calculator: you can enter the month and day, the latitude and longitude of your location, your skin type, and which time of day you are outside, whether there are clouds in the sky, and a few other variables, and the system will tell you how long you would need to be outside to make 1,000 IU of vitamin D, assuming that about 25% of your skin is exposed to the sun. 25% of your skin is equivalent to your face, neck, arms and hands.
To give you an idea, someone with white skin living in Boston, MA, would need to expose 25% of their skin to the midday sun in August for around 12 minutes to make about 1,000 IU. In January, that same person would not be able to make any vitamin D in Boston, no matter how long they are outside and even if the day is pretty cloudless. By contrast, the same person living in Miami, Florida, would need about 10 minutes of midday sun at any time of the year. That is simply because Miami is closer to the equator, and UV irradiation is much less seasonal there than in the northern parts of North America. If someone has darker skin, or wears more clothing, or if it’s a little cloudy, then more time in the sun would be needed to make these 1,000 IU of vitamin D.
That is also why, depending on a large number of factors such as where you live, your age, the color of your skin, the amount of clothes you wear, you may still require supplemental vitamin D. And I certainly feel that using a vitamin D supplement is preferable to risking getting a sunburn. Again, this will be covered in detail in a separate blog post. However, it’s also important to understand that increased vitamin D synthesis is not the only beneficial effect of sunlight exposure on blood sugar regulation. This means that even if it helps you avoid vitamin D deficiency, taking vitamin D supplement is not the same as being in the sun regularly. And that has to two with the other two reasons that sunlight exposure can be beneficial for glucose tolerance.
Sunlight and Glucose Tolerance: Avoidance of Circadian Disruption
Another very important role of light is that it helps us regulate our circadian rhythms. What does circadian rhythm even mean?
Well, all biological processes are, to some degree, regulated in a circadian fashion, meaning that they change in a roughly 24-hour cycle. An obvious one is that we get tired and need to sleep at some point during a 24-hour period. But our circadian rhythm is about a lot more than sleeping and being awake. Basically every process in every cell is to some degree regulated by our circadian rhythm. And that circadian rhythm is mostly established by two primary inputs: our exposure to light, and when we eat.
Let me give you an example that is directly relevant to our metabolic health.
Let’s look at a liver cell, a hepatocyte. Let’s assume it’s the middle of the day, and we have just had lunch. Because we usually eat at this time of day, the liver cell has upregulated many proteins that prepare it to deal with that meal. Glucose that was just absorbed into the blood passes the liver, and some of it is taken up into the liver cells and converted to glycogen, the storage form of glucose in the body. Fructose and alcohol that were just consumed are almost completely removed from the blood by the liver cells, and both are partly converted to fat, which then accumulates in the liver cell. Micronutrients from the foods we just ate need to be dealt with. For example, the liver will take up and store vitamins such as vitamin A or minerals such as iron and copper. Similarly, our food may also contain toxins, and the liver is the primary organ responsible for removing these from the blood and detoxifying them. All of these processes require specific proteins in the liver cells. For example, the liver needs to make specific proteins to transport copper into the cell, and store it safely. Similarly the hepatocyte needs specific enzymes to convert glucose into glycogen, or fructose and alcohol into fat. And it needs a whole machinery of proteins to detoxify toxins we may be consuming. So, all of these processes are operational in the fed state.
Now, let’s look at the same hepatocyte at 2 AM at night. We have not eaten anything for 7 hours, so we are in a fasting state, and hopefully deeply asleep. Now, it would not make sense for the liver to keep making all of the proteins it needs to take up and store glucose or vitamin A or copper, right? Because there is no glucose, vitamin A, or copper coming in from the GI tract, because we haven’t eaten any food in 7 hours. It also makes no sense to keep all of the proteins available that the cell needs to detoxify stuff, or to convert fructose or alcohol to fat. The liver therefore reduces the amount of these proteins it makes, potentially to zero. And instead, it now makes an entirely different set of proteins from its DNA. For example, the liver cell may make enzymes that can break down stored glycogen or synthesize new glucose from scratch, for example from amino acids, so that it can secrete a trickle of glucose into the blood to keep blood glucose levels stable all night. The liver cell will also take some of the fat that may have accumulated inside the cell throughout the day and either burn it for energy, ATP, or convert it to ketones, which can then also be secreted into the bloodstream, to be used by other tissues as an energy source. Now is also the time for liver cells to upregulate repair processes, because there are fewer other demands on the liver cell. So now the cell can increase proteins involved in, say, DNA repair or autophagy, where the cell breaks down any protein, organelle, or other cellular component that isn’t working properly or that is no longer needed. For the cell to remain healthy and maintain optimal function, all of these processes are critical.
Now, I said earlier that the two primary factors that determine this circadian rhythm are light and food intake. Food intake makes sense, because the liver can directly sense the incoming nutrients and respond to them, right? But what about light, how can the liver see whether it’s day or night? Well, as we may see later, liver cells may actually be able to sense light, but let’s ignore that for now. For now, let’s focus on the fascinating fact that each liver cell also has a clock. No kidding here. There are a number of proteins, the concentration of which ebbs and flows roughly in a 24-hour cycle, and through the concentrations of these proteins, the cell can tell what time of day it is. Well, but how is that clock set to the light-dark rhythm outside? It is set by being connected to the Master clock in a part of the brain called the SCN, and that Master clock is kept in alignment with the outside light by receiving information about ambient light directly from the eyes.
Let’s talk briefly about how this works. The figure above is a cross-sectional view through a human head and brain. In the brain, we have two areas that are most relevant for our circadian rhythm. The SCN and the pineal gland. That’s the gland that secretes melatonin, the hormone that helps us sleep. When our eyes sense bright light, and particularly light in the blue part of the spectrum, with a wavelength of around 445 to 480 nm, this stimulates the production of a protein called melanopsin. Melanopsin has two major functions. First, it coneys to the SCN that it is day, which is of key importance in maintaining our normal circadian rhythm. And second, melanopsin suppresses the production of melatonin in the pineal gland. As a result, the concentration of melatonin in the brain remains low as long as we are exposed to bright and particularly blue light. And at night, when ideally no light hits our eyes, no melanopsin is formed and this allows melatonin to be produced in the pineal gland, which then in turn helps us sleep through the night.
So when our eyes sense bright light, the eyes convey to the Master clock in the SCN that it’s day, and that information is then conveyed to all of the cellular clocks in each cell of the body. So that provides the cells with clues as to what’s coming next. Already before the meal, for example, the liver cell may start to make bile acids, to help with the digestion of fat.
Now you can probably start to see where this is going. Under ideal conditions, think caveman and cavewoman prior to the invention of fire, food intake occurred only when there was daylight. That was very predictable. Nutrients such as glucose, fructose and all of the micronutrients were coming in during the day, at the same time that the eyes and the Master clock conveyed to the liver cells that it was daytime. All of the processes needed to deal with incoming nutrients were switched on. And vice versa, when it was dark, there was reliably no food coming into the body, and the liver could switch on all of these fasting programs, including all of the repair processes.
OK, now, let’s look at modern people. Many days, we are not going outside during the day and our eyes barely ever see bright sunlight, so our Master clock never receives a clear signal when a new day starts. In contrast, we are exposed to indoor lights, and often we are watching TV or playing video games late into the night. And maybe you can already see how the lack of exposure to sunlight and rich exposure to artificial light can lead to confusion in our circadian rhythm systems as to when a day starts and when it ends. Now add to this that food intake often also occurs at random times. Maybe we have breakfast when we get up at 7 AM, eat and snack all day, and wrap up the day with some potato chips at 11:30 PM before going to bed. What this lifestyle leads to is what we call circadian disruption, because now all of our cells do not get clear signals about what to do at any given moment. Let’s go back to our liver cell. It’s 11:30 AM, and we last ate at 7 PM, that is, four and a half hours ago. The liver cell runs the entire fasting program discussed earlier, including burning of fats, DNA repair, and increased autophagy. Suddenly, the owner of that liver cell eats a few handfuls of potato chips, and the liver cell is flooded with nutrients, at a time of day when it’s not expecting this at all. First of all, the liver cell is less able to deal with the incoming nutrients, and so, for example, our blood sugar response may be much higher than if we had eaten the same potato chips for lunch. Probably worse, though, is that, within just a few minutes, the liver cell switches its entire program to deal with the incoming nutrients. Burning fat is stopped. DNA repair processes stop. Autophagy is downregulated. And even if we only eat a few bites, these processes will be stopped for 1-2 or even 3 hours while the liver cell deals with the incoming nutrients. The next morning, when we wake up for breakfast at 7 AM, our liver hasn’t had a full night to recover, burn accumulated fats, and clean up, it had maybe half a night’s worth of recovery. If that happens just once, that’s probably not a big deal. But if it’s a regular occurrence, it will lead to a total disruption of a finely tuned circadian system. And remember, I only used liver cells as an example here. This process is very similar for every cell type in our body, and I think it’s fair to say that maintaining a normal circadian rhythm is one of the most important things we can do to prevent most – if not all – chronic diseases.
And what does maintaining a normal circadian rhythm entail? I’d say it means, ideally, three things:
First, eating in a fairly narrow window during the day, while fasting for an extended period over night.
Second, being exposed to bright sunlight during the day, and no light and particularly no blue light at night.
And third, getting at least seven hours of good quality sleep at night (or whatever number of hours you need to feel well rested).
Now, how is the maintenance of a normal circadian rhythm linked to glucose tolerance?
Regarding the first point, we have good evidence that following time-restricted eating, or TRE, and particularly early TRE where all of our food intake occurs in the early part of the day, is associated with better glucose tolerance. This is likely because TRE makes it more difficult to overeat, and in fact often leads to lower energy intake and weight loss, but also because early TRE in particular ensures that our food intake is better aligned with the natural light-dark cycle and our internal circadian rhythm. I discussed these points in more detail in two prior blog posts about TRE.
I have also mentioned before, in the blog post about the primary causes of insulin resistance, that sleep deprivation is a risk factor for insulin resistance. This has to do with the lack of sleep itself, but possibly also with associated factors, such as getting up and being exposed to light or even food at night, all of which could lead to a disruption of our normal circadian rhythm.
OK, that brings us to light itself. What do we know about how our light exposure affects our glucose tolerance? Well, we do have evidence from observational studies that a lack of exposure to bright sunlight during the day is associated with insulin resistance and glucose intolerance, and an increased risk of type 2 diabetes. We also have of evidence that exposure to light at night increases the risk of type 2 diabetes.
That impact of light at night could partly be related to disruptions in the normal circadian pattern, and also due to suppression of melatonin production in the pineal gland in the brain, which could cause sleep issues. As illustrated in the figure above, it is likely that a lack of bright light during the day and too much artificial light at night affect glucose tolerance through an increased risk of vitamin D deficiency, a higher risk of sleep deprivation, and a higher likelihood of food intake at night; however, it is also possible that circadian disruption itself has additional negative effects on our body’s ability to maintain normal glucose homeostasis
Sunlight and Glucose Tolerance: Improved Mitochondrial Function
And this brings us to the third mechanism through which light affects glucose tolerance, and that has to do with near-infrared light.
Now this is a really exciting area of research. We just discussed that spending more time in natural daylight is associated with better insulin sensitivity, better glucose tolerance, and a lower risk of type 2 diabetes. And, again, this could be due to the fact that sunlight exposure helps us make vitamin D, or because daylight exposure helps us maintain our natural circadian rhythm and sleep better. However, it is also possible that natural sunlight improves glucose tolerance because of a direct impact of light, and specifically the red and near-infrared portion of natural light, on the function of our mitochondria. Let me explain.
Near-infrared light, which, like ultraviolet light, is not visible to us, accounts for 52-55% of all light photons coming from the sun that hit our bodies if we are outside (see figure below). Some people even argue that near-infrared light makes up around 70% of the sunlight energy we are exposed to, because sunlight consists of mostly near-infrared in the mornings and evenings. So, if our bodies evolved to work best with some exposure to UV light, and to regulate our natural circadian rhythm through our exposure to light in the visible spectrum, should we maybe also ask ourselves whether this huge part of sunlight that is in the near-infrared spectrum may also have effects on our body? The near-infrared light is a huge amount of light energy, and in my opinion, it would make a lot of sense that our bodies evolved to use this somehow.
And yes, there is indeed some really intriguing research that strongly suggests that the red light of the visible light spectrum as well as the near-infrared light play an important role in maintaining optimal mitochondrial function.
Well, the first and obvious question is: how can this be? Most of the cells in the human body never see light, right? Well, that is not correct. Ultraviolet light does not penetrate the body, and is instead entirely absorbed in the very top layer of the skin. In a layer that is maybe one one-tenths of a mm thick, about the thickness of hair. That’s why UV light is potentially so damaging, because all of its energy needs to be dealt with by a very thin layer of cells. Similar for the blue and green and yellow portions of visible light, which also does not penetrate deep into the skin. Red light goes a little deeper. The photo below shows what happens if you shine a flashlight at your hand, you can see some light shining through, and the light that shines through is all red. That is because only the red portion of visible light can pass through the tissue deep enough to come out on the other side. Now, near-infrared light can pass even deeper into the body, based on some data 8-10 cm deep, that’s 3-4 inches. That means that 100% of all cells in children will receive near-infrared light if they are in the sun, and still about 70% of cells in adults. A substantially smaller portion in adults who carry extra body fat, by the way.
Near-infrared light can even penetrate the skull and reach the brain. Bones are not much of an obstacle for near-infrared light.
So, yes, if we are exposed to red and near-infrared light, such as from the sun, the light will reach many or even most of the cells in our body. And what does that now have to do with mitochondria and glucose tolerance?
Well, remember that mitochondria are the power plants of each cell. Fuel such as glucose or fatty acids can be burned here, just like coal is burned in a coal power plant. Under the influence of oxygen, O2 here, the mitochondria make ATP and carbon dioxide, CO2. ATP is a chemical form of energy that the cell uses for many different processes. So this isn’t just to power your muscle contractions and movements. ATP is a very big deal for most biological processes inside of our cells.
Now, the interesting part: mitochondria that are exposed to red or near-infrared light work more efficiently than those that are not exposed to red or near-infrared light. That means that per unit of time, they burn more glucose or fatty acids and produce more ATP. This is a fairly new area of science, and we need a lot more research to really know what’s going on here, but we have some data already about potential mechanisms through which red and near-infrared light may affect the efficiency of ATP production by the mitochondria.
The first potential mechanism is that red and near-infrared light acts directly on one of the key enzymes in the mitochondria that convert fuel to ATP. This enzyme is called cytochrome C oxidase, and its responsiveness to light is in its name. Cytochromes are what we call chromophores; they absorb light of a specific wavelength. In the case of cytochrome C oxidase, near-infrared light increases the activity of the enzyme.
The second potential mechanism is that red and near-infrared light may reduce the viscosity of the water within mitochondria. Water with reduced viscosity is smoother, providing less resistance, so this would allow all of the molecules to move around more easily. Again, this is expected to speed up the process of making ATP and make it more efficient.
Third and lastly, near-infrared light may stimulate the expression of melatonin within the mitochondria. Now, this is confusing. We mentioned earlier that blue light hitting the eyes leads to a suppression of melatonin production in the pineal gland in the brain, and that blue light, therefore, keeps us awake. Now, what I am saying here is that elsewhere in the body, within the mitochondria of each cell, another part of light, namely near-infrared light, INCREASES the production of melatonin? Yes, that at least is the hypothesis. As Tan and colleagues summarize, while we don’t have direct evidence that the concentration of melatonin in mitochondria increases with exposure to red or near-infrared light, several pieces of evidence show near-identical molecular effects on mitochondria that have been treated with melatonin vs. near-infrared light. Now, why is this important here?
Well, it’s highly relevant because the production of ATP by the mitochondria is a tricky process because oxygen is involved. Every once in a while, something goes wrong in the process of burning fuel in the mitochondria, and some of the oxygen molecules form what we call reactive oxygen species, or ROS. ROS are highly reactive molecules that can damage the entire machinery of the mitochondria. To stick with the power plant analogy, imagine an accident in the power plant, a major fire breaking out, and some or all of the machines and instruments being damaged. So, how do we prevent this? A power plant may have some firefighters, and mitochondria have antioxidants to deal with reactive oxygen species. And melatonin is one of the most powerful antioxidants known to us.
OK, to summarize, mitochondria are more effective at converting fuel, such as glucose and fatty acids, to chemical energy, ATP, if they are exposed to red or near-infrared light. The mechanisms seem to involve a direct effect on one of the enzymes involved in the energy production process, cytochrome C oxidase, by lowering the viscosity of water in the mitochondria, and potentially by increasing the production of a key antioxidant, melatonin.
OK, so how is all of this relevant for glucose tolerance?
Well, one prediction would be that if red or near-infrared light really makes the burning of glucose and fat to ATP more efficient, then this should (a) increase ATP synthesis; (b) increase the take-up of glucose from the blood into these cells; and (c) increase the amount of CO2 that is exhaled.
One team tested this hypothesis. In a randomized controlled study, they shone red light on the backs of people before they had an oral glucose tolerance test, or OGTT, done. And on another day, they repeated the process, but unbeknownst to the participants, did not shine the red light onto their backs. This was a placebo control. And take a look at what they found: the increase in blood glucose levels in response to drinking the 75g glucose beverage was a lot smaller in participants after they had been exposed to the red light. In other words, their glucose tolerance was substantially improved. The increase in blood glucose above the baseline was a whopping 28% lower after exposure to the red light. And not only that, they also exhaled measurably more CO2, as the model would predict.
Now, it’s important that we don’t get carried away too much here. This is one study, and even though it confirmed a hypothesis that was based on prior research, it’s just one study. This needs to be confirmed, and in general, there is a lot more to learn about this. It is, for example, unclear whether this effect can be triggered only by a high dose of red light of a very specific wavelength, as in this study, or whether this would translate to exposure to normal sunlight. However, I’d say that there is reason to be cautiously optimistic that this line of work could give us a better understanding of the factors involved in the development of glucose intolerance and type 2 diabetes, and certainly holds some promise for interventions to improve the condition. These data are certainly also consistent with the data showing better glucose tolerance and a lower risk of type 2 diabetes in people who spend more time in natural sunlight. So, in addition to the fact that more sunlight improves our vitamin D status and our regulation of a natural circadian rhythm, this could be an alternative mechanism explaining the association between sunlight exposure and a lower risk of type 2 diabetes.
Now, one particular area of research that I would like to see in the future is how regular exposure to near-infrared light, or a lack of exposure to near-infrared light, may affect the two key factors that determine glucose tolerance: insulin sensitivity and beta-cell function. I am saying this because, for years, there have been numerous publications that have described that in pancreatic beta-cells that become dysfunctional, a key cellular observation has been … mitochondrial dysfunction. And similarly, in liver and muscle cells, a common observation associated with insulin resistance has been … mitochondrial dysfunction. I am not suggesting that a lack of near-infrared light is the only cause of mitochondrial dysfunction. However, it could be one contributing factor.
How may this be relevant for you? It is relevant because most of us are now living in an environment that is devoid of near-infrared light.
Take a look at the spectrum of sunlight. As mentioned earlier, about 52-55%, and maybe more, of the energy coming from the sun is near-infrared light. This varies a bit from morning to mid-day and evening, but in all cases, much of the light that hits us when we are outside is near-infrared light.
Contrast this to today: if we are indoors and use energy-efficient lighting such as LEDs, these emit only light in the visible spectrum. In contrast, the old, energy-inefficient incandescent light bulbs produced a lot of near-infrared and infrared light, which is also why they became hot to the touch and were so “inefficient”. Then, add to this that infrared light from the sun used to penetrate simple single-pane windows. With energy-efficient glass in modern buildings, that is no longer the case. This modern glass is designed to keep warmth, which is essentially infrared radiation, inside, and the side effect of that is that near-infrared and infrared radiation of the sun are kept out. As a result, you may not be exposed to any near-infrared light in your home, your office, your factory floor, your gym, or any other modern indoor environment. And if this is indeed an essential ‘nutrient’, that would almost certainly not be ideal.
Now, I am not suggesting we abandon energy-efficient lighting or switch back to single-pane glass windows. However, I do anticipate that the research I have shared here will lead to technological advances that help us create energy-efficient buildings that also provide healthier light for the people living in them. Some LEDs are already available that emit near-infrared light, and that can be dimmed or programmed to limit blue light at night, but these are quite expensive still and hard to find.
Summary, Conclusions, and Suggestions
To summarize, our exposure to light can affect glucose tolerance and its key determinants, insulin sensitivity and beta-cell function. Potential mechanisms through which light affects glucose tolerance include that …
… first, UV-light triggers vitamin D synthesis in the skin, which helps us avoid vitamin D deficiency;
…. second, exposure to bright sunlight during the day, and a lack of bright and particularly blue light at night improve our circadian rhythm and – linked to this – our sleep;
… and third, exposure to red and near-infrared light improves mitochondrial function.
Now, one very important thing to understand here is that I am not suggesting that exposure to light is a cure-all kind of thing. What I am suggesting is that our lack of exposure to sunlight or exposure to blue light at night could be one of the potential causes or contributors to your glucose intolerance. And if that is the case, then improving your relationship to light may well be one step that can help you normalize your glucose tolerance.
So what does the science suggest that we can do about this specifically? I can see four actionable items:
First, make sure you are not vitamin D deficient. Have your plasma 25-hydroxy-vitamin D level measured, and make sure it’s above 20 ng/mL (50 nmol/L) at all times. In my opinion, ideally, you’d aim for the higher end of the normal range, somewhere between 30-50 ng/mL (75-125 nmol/L). If you are vitamin D deficient, make sure you get some direct sunlight every day, and/or take a supplement. Again, exactly who should consider supplementing, and how much, will be covered in a separate blog post.
Second, make sure to go outside every day during daylight hours. Keep exposure to strong mid-day sun to a few minutes and wear sunscreen and sunglasses as needed during that time. But other than that, I’d encourage you to reconsider your relationship with the sun. Try to find ways to be outdoors more, ideally several times a day, and even if it’s just for a short walk, an errand you run on a bike, or a half an hour in the park or your garden. Spending time in shady green spaces, such as parks, forests, or your backyard, is also a great idea. Near-infrared light reflects off many surfaces, particularly green surfaces, and so you’ll be exposed to near-infrared light to some degree even under the canopy of a tree, or sitting in the shade in your backyard. And even a cloudy day is usually brighter than the light we get indoors, and it’s certainly a much wider-spectrum light than what our indoor lighting usually provides. Clouds filter out some of the near-infrared light, but I would argue that particularly when near-infrared light is hard to get is it probably important to spend some time outdoors.
Third, sleep in an entirely dark room. Use blackout shades in your bedroom, and remove or cover any light source, including nightlights or the display of an alarm clock. If you need to visit the bathroom, use as little light as possible.
And fourth, keep your exposure to artificial light, particularly blue light, limited after the sun has set. Use software that filters out blue light on your electronic screens such as your smartphone, tablet, computer, or TV, and use mostly dim lighting after the sun has set. There are also specific lightbulbs that do not emit blue light that you could use in the evening.
One objective here is to help you avoid circadian disruption. My strong suggestion is to combine these suggestions with a form of time-restricted eating, ideally early time-restricted eating, and your chances are good that your body will return to its natural circadian rhythm.
Thank you, and take care!
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References
- Voltan et al.; Vitamin D: an overview of gene regulation, ranging from metabolism to genomic effects. Genes 2023; 14: 1691.
- Maestro et al.; Identification of a vitamin D response element in the human insulin receptor gene promoter. Journal of Steroid Biochemistry and Molecular Biology 2003; 84: 223-30.
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9 Responses
Very interesting and I appreciate your blogs so much. In the summary – I wondered if this wasn’t quite what you meant to say: first, UV-light triggers vitamin D deficiency in the skin, which helps us avoid vitamin D deficiency;
Oh yes, sorry. That’s a typo. Should be “UV-light triggers vitamin D synthesis in the skin”. Thank you.
I’ve been told to keep my vitamin D fairly high because of bone density issues. I’ve also been told to be very careful about getting sunlight exposure because I am very fair and have had some issues with skin cancer. I’ve been taking 2000 IU a day and last tested the result was 44.1 ng/ml. But just reading a consumer lab piece about Vitamin D, they discussed many studies that seemed to indicate that might be too high though generally lower than 50 seems to be okay. I see you are going to discuss Vitamin D in a later blog post and I look forward to that. One reason I follow you is – yes, it can be confusing with so many different opinions.
I recommend levels between 30 and 50 ng/mL, and see no evidence that this is too high. In fact, it’s within what we consider the normal range.
If you have had skin cancer before, it does make sense to take a vitamin D supplement and minimize mid-day sun exposure. However, morning and evening sun may still be fine, as that is much lower in UV light and very rich in near-infrared light.
This information was fascinating to me, and very novel info, which will be very pertinent and applicable for me, since I have Type-2 and RA. I will have to explore ways to make sure and get out during the day more often, even in the cold Colorado winter!
Thank you! So informative and cutting-edge! I am thinking about red light therapy and/or infrared sauna therapy to help with glucose tolerance/insulin sensitivity. Which therapy type would best help achieve these goals, and could you please explain the differences between how these two therapies work?
Hi Elizabeth,
I’d say it’s too early to answer your question. To this point, we only have data from one RCT that used red light. Both red light and near-infrared light have beneficial effects on the mitochondria, but the specific effect seems to depend to some degree on the specific wavelength. For example, I mentioned in the blog post that cytochrome C oxidase, one of the key proteins involved in synthesizing ATP in mitochondria, works more efficiently if hit with near-infrared light. The specific wavelength required for this specific effect is around 830 nm, which is in the near-infrared portion of the spectrum. That means that red light would not be likely to affect cytochrome C oxidase activity; however, it may act through another mechanism, such as increased melatonin production or lower viscosity of mitochondrial water. That is not well understood yet, to my knowledge.
One key difference between red and near-infrared light is that near-infrared light can penetrate deeper into the body, so it’s probably worth combining red and near-infrared light. Also, I like to think about this in terms of the light humans were exposure to throughout evolution, which is a mixture of red and near-infrared light from the sun or fire. Thus, my best guess is again that a combination of red and near-infrared light would be best.
The main issue is that we don’t have enough studies to test which specific wavelengths, at which specific wattage affects blood glucose levels and all of its determinants (glucose tolerance, insulin sensitivity, beta-cell function). I suspect that we will see a lot more data coming out on this soon.
Cheers
Mario
Excellent article. A couple of comments on Vitamin D, (1) one of the foremost researchers in VD, Dr Michael Holick has produced a free app, “dminder”, for smart phones that calculate skin VD production, automatically applying the factors as in your calculator link. It is very simple to use and has been validated. (2) His research has also calculated the amounts of VD produced in different skin types, for differing times of exposure, different latitudes, skin types etc. From memory a type 1 skin exposed for 30 mins in latitudes below 50 deg N in summer can produce between 10K and 20K IU VD, doses significantly higher that national guidance. (3) it is now known that active VD needs to be constantly replaced as once bound to its receptor on immune cells during infection, it activates that cell and is subsequently converted to 24,25 (OH)2 vit D and is excreted. (4) with the increasing use of LC MS/MS, at last count 22 metabolites have been identified, the biological activity of many are unknown. (5)supplementation of VD, toxicity is often cited as an issue, this is overplayed, research indicates that levels up to 300nmol/L does not cause any dysregulation of Ca homeostasis; (6) VD taken with vit K2 MK7 probably increases that threshold, since K2 is required for Ca transport to bone. (7) Prof A Dalgliesh, the UK professor of oncology, who treats stage 4 melanoma patients ensures they have serum levels >100nmol/L, the higher the better. He’s also demonstrated that excessive UV-B does not cause melanoma. Hope this is of interest, David
Hi David,
Thank you for sharing.
Cheers
Mario