Dietary Fats Circadian Dan’s Plan

Certain Dietary Fats Disrupt the Coordination of Metabolism, Others Don’t

Timing of Fats - Dan's Plan

This is my second article on food and the circadian system. The science of body timing rhythms is complicated. But, like diet and exercise, it’s worth investing some mental effort to understand the fundamental aspects of it because not only is it crucial to health and wellbeing, but also because it is a topic on which you can take action!


Circadian RhythmsCoordination

The circadian rhythm is a complex system that helps our body coordinate physiology and behavior across a 24-hour period of a day. The system is controlled by “clock genes” and the proteins they produce. A master clock resides in the brain and is controlled mostly my light exposure through the eye. Each of our cells, however, has its own clocks. The top-down nature of this system has the
master timekeeper synchronize the clocks in the rest of our cells, and together, they function as one coordinated system.  

We can adjust our body timing without causing health problems (e.g., slow change of the seasons). Issues begin, however, when our timing system becomes uncoordinated – or misaligned. This can happen in several ways. The most well-understood way is due to high variability in light exposure from day to day. For example, one day you go to bed at 10p, then the next day you’re up to 3a (with bright artificial light exposure after dark all the way up to sleep), and then the following day you’re asleep at 10p again, etc.  That example constitutes a 5-hour shift in light exposure from day one to two and then again from day two to three. This causes the equivalent of jet lag, where the coordination of our daily rhythm system becomes temporarily misaligned. But this is not the only way to misalign our rhythms; food type of timing matters too.


Fuel Preference Changes across the Day

In my previous article entitled When Is the Best Time to Eat, we discussed research on how enzymes that determine the rate of energy generation from glucose and fats wax and waned across the day. In normal mice, production of sugar burning enzymes – and rate of sugar metabolism – peaked when the animals sleep, whereas the production of fat burning enzymes – and rate of fat metabolism – peaked at a time when the mice are awake and physically active. In mice with deleted circadian genes, however, the amounts of these enzyme levels, and the rate of utilization of sugars and fats did not change over the day. This info suggests that a cells preference for different fuel types modifies over the day, which depends on the activity of clock proteins.

That study helps us better understand the mechanisms behind something that has already been recognized in previous research: erratic eating patterns – including eating very late in your day – appear to disturb the circadian system, which then disrupts metabolism.  Here, we will look at a new study that shows how fat type and timing of intake can affect the timing system in our body.  


Metabolic Control

To maintain a healthy metabolism, our body must precisely regulate levels of circulating energy substances – like fats and sugars. It must also regulate inflammatory signals from our immune system because they too affect metabolism. Eating certain types of saturated fat can cause low-grade inflammation, and being in this chronically inflamed state over time has associated with obesity, diabetes, and cardiovascular disease. So how do particular types of fats mess up our metabolism, and which types don’t?


Different Fats Have Different Effects

As mentioned above, one function of our circadian rhythm is to help coordinate the timing of fatty acid metabolism (another paper on that subject). This interaction, however, does not Butterstrictly flow in one direction. Both inflammatory signals and fatty acids can provide feedback to affect how the clocks themselves function. That’s why Sam-Moon Kim at Texas A&M University and colleagues looked at clock function under the influence of a two types of fats: a proinflammatory type and an anti-inflammatory type.  The first fat tested was palmitate, which is a proinflammatory, long chain saturated fatty acid commonly found in the US diet from things like beef and dairy. I’ve written about this type of fat previously in this article, Why Dietary Fat Is Fattening and When It’s Not (which, by the way, is the most highly read article I’ve written). The second fat tested was DHA, which is a polyunsaturated fatty acid with known anti-inflammatory properties.


The Dietary Fat Palmitate Is a Problem

Previously, work by this research group showed that a high-fat diet in mice slowed the clock timing for immune cells called macrophages, which mediate inflammation. That study also demonstrated that compromising the accuracy of our body clocks is key in how a high-fat diet (in mice) triggers and exaggerates inflammation in fat tissue, and promotes insulin resistance. Interesting, but do all fats cause this? This is a critical question, and as I stated in my article on what dietary fat is fattening, we can not judge all fats as one monolithic substance. Fats are a chemical class, and different fats do different things to the body. On top of that, there is variability to how individuals respond to different fat types. Some people, for example, will tolerate long-chain saturated fats better than others due to their genotype.

In their new study, different fats were administered to collagen-producing cells (fibroblasts) at various points across 24 hours. Then, the researchers observed the inflammatory effect that occurred in response to each fat and at each time point, and finally, how the different inflammatory responses coincided with clock functioning.


Key Findings and Possible Ways to Benefit

Here is what they found and what it could mean for you. First, the saturated fatty acid palmitate produces inflammatory signals, and that effect was maximal at what would be equivalent to you eating that fat around dinner. But again, this is in culture so it’s hard to know how this translate to humans until tested directly. Next, it is these inflammatory signals, stimulated by palmitate, that shift the timing of the clocks in the collagen-producing cells. The more clock timingSalmon shifted, the more exaggerated the inflammatory response was to palmitate. This suggests that the consumption of food sources containing palmitate – like beef, dairy, and eggs – is better handled by the body during breakfast and lunch and that avoiding this type of fat during dinner, or during snacks consumed close to bedtime, might be a wise choice. 

But this study had other interesting findings, too. Most notably, the polyunsaturated fatty acid, DHA, found in foods like salmon, inhibited the inflammation caused by palmitate. And because DHA suppressed the signals that are possibly the cause of shifting cellular timekeeping, it also prevented the cell clocks from being reset to the wrong time. This could mean that having DHA with your hamburger at night could halt the clock shifting effect from the palmitate in the burger. It also implies that eating fish, instead of a burger, might be a good idea for dinner.



Of key importance to this research is not only the idea that different fat types have different effects on our cell clocks but also that not all tissues respond in kind.  In fact, Julie Pendergast at the University of Kentucky and colleagues showed that seven days of a high-fat diet advance cellular clock timing in the liver, but simultaneously delay clock timing in the spleen. So, eating the wrong type of fat at night is similar, physiologically, to effects from exposing yourself to wild fluctuations in the timing of light exposure day to day, which is another lifestyle pattern that causes clock misalignment, metabolic imbalance, and ultimately, disease. The findings from Kim discussed above lend further support to growing and consistent body of work.

The coordination of body rhythms is fundamental to long-term health. Obviously, more clinical work is needed on this specific subject, but so far, most of the research – from cell culture all the way to real-world human physiology – seems to align nicely. If you’re already managing your light exposure day, evening, and night, then managing the timing of different types of dietary fat ingestion may just be another way to optimize the system.

  • “In their new study, different fats were administered
    to collagen-producing cells (fibroblasts) at various points across 24

    It is incredibly difficult to translate the results from applying specific types of fatty acids directly to isolated cells in a petri dish into any meaningful dietary advice. If one were to do this, however, it seems that the fact that high sugar diets result in the liver converting the sugar to palmitic acid and stuffing them into triglycerides would be the best hypothesis as to one mechanism by which high sugar diets cause an increase in systemic inflammation.

    I doubt the amount of palmitic acid found in naturally-occurring fats, even from fatty cuts of animals (which are mostly stearic acid, especially if from pastured animals and not CAFO animals), is meaningful in terms of pro-inflammatory effects.

    Other types of saturated fats have been shown to reduce inflammation in the liver and reverse both alcoholic and nonalcoholic fatty liver disease. Having said all this, I would still caution leaping from a petri dish to your dinner plate. 🙂

    • danpardi

      Hi @aaronblaisdell:disqus, thanks for the note, Professor. I absolutely agree that it’s can hard to make research like like this prescriptive. But yes, let’s discuss. I definitely was cautious not to implicate fats in general, or even saturated fats, in my assessment. Palmitate was tested and so I did not generalize the findings beyond it. We do see that a diet high in saturated fat (but maybe not all types, but it’s rarely distinguished clearly) can cause inflammation in humans, and so can excessive sugars. And so perhaps this specific fatty acid, consumed directly or produce by the liver in the metabolism of sugars, is a causative commonality in chronic low grade inflammation.

      However, here are a few other thoughts about my method (of my madness):

      1). I like to take all information from science and first do a direct translation to humans. Doing this helps me internalize and understand the information better, and ultimately, it’s hypothesis forming. From there, I better understand how we can build off of the info to move one step closer to actual human interventions to test it’s merits.

      2). As I wrote, “Obviously, more clinical work is needed on this specific subject, but so far, most of the research – from cell culture all the way to real-world human physiology – seems to align nicely.” Part of the way I write is to try to make it simpler for a reader to grasp the main points from complex information without being unfaithful to the truth of the idea. But with all simplification efforts, this happens to some degree. And what’s really important here is that this research was not interpreted in a vacuum, nor is it the first of its kind. Actually, its building on a now substantial base of research, which I wrote, is showing regular consistencies. So while this research was a well controlled study in a culture, the findings line up with what we are seeing in whole animals. Also, the fact that it’s taking place in a culture doesn’t mean it’s NOT reflecting what’s going on in a whole animal, and not saying you do this, but sometimes people forget that. Let me point to another example of this. At Washinton State University, James Kruger hypothesized twenty years ago that sleep is controlled by local sleep networks responding to extracellular signals that reflect energy usage over the day. Recently, he cultured neurons into neural networks, splashed them with TNF-alpha, and they performed seemingly identically to how local sleep is controlled in living humans. Sometimes stuff from cultures, yeast, worms, and non-human animals is more applicable to humans than what seems possible.

      3). Risk of n=1 testing? In the last sentence, I wrote “If you’re already managing your light exposure day, evening, and night, then managing the timing of different types of dietary fat ingestion appears to be another way to optimize the system.” How dangerous is it for a person to eat less palmitic acid at night, especially given that there is no conflicting information that eating it at night is especially health promoting, and two also given that palmitic acid appears to be problematic in more ways that described here? Personally, I feel there is low risk here and potentially a chance to optimize to I’m going to give it a shot. Thoughts?

  • Alex McMahon

    Interesting food for thought! do you think when starches are higher at a meal fats should be kept lower and vice versa ?

    • danpardi

      Hi Alex, well this line of work didn’t really address that subject. It was looking at fat type and it’s influence on the timekeeping of clocks in various cell lines (immune cells and then fibroblasts, or collagen-producing cells). Carbs could also influence circadian timing but there is less information on this. What we do know is that diets high in sugar intake associate with more arousals and less slow wave sleep, which could result from sugar impacting circadian functions, but right now, there is more info on how certain fats do this. See this blog for more info:

      • Alex McMahon

        Hey Dan, didn’t mean to go off topic for this post but had the thought and thought I’d ask your opinion. Thanks for passing along the link to the other article.