Emotional Plants with Motion (Sunlight Sonata IV)
—Yes, you will probably sunburn easily if you follow a low-fat diet with "healthy" seed oils.
In the last chapter, Sunlight Sonata III, I included this image of prehistoric man looking forward to inventing factory oils :

Today I’d like to share an exploration with Claude AI (◆CAI) on the topic of sunlight and digestion; and, the disruptive effects of a low-fat diet and high consumption of seed oils on the body’s proper utilization of sunlight.
◆CAI: The relationship between sunlight exposure and digestive health represents a fascinating intersection of photobiology, metabolism, and nutrition that extends far beyond the well-known vitamin D pathway. When we examine how dietary fats—particularly the modern shift toward seed oils and low-fat diets—interfere with our body's ability to utilize sunlight effectively, we uncover a complex web of interconnected systems that have evolved together over millions of years.

ME: It’s easy to forget that we’re basically a digestion tube with a more complicated, process of a worm: a mouth, digestion, an anus. But we are not buried in the earth, —humans inherited a world of light.
◆CAI: A. Sunlight and Digestive System Integration. The digestive system operates on multiple circadian rhythms that are directly influenced by light exposure. The master circadian clock in the suprachiasmatic nucleus coordinates with peripheral clocks throughout the gastrointestinal tract, regulating everything from gastric acid production to intestinal permeability patterns. ¹ Morning sunlight exposure helps synchronize these digestive rhythms, optimizing the timing of digestive enzyme release, gut motility, and even the composition of our microbiome. ²
The gut-brain axis becomes particularly relevant here, as sunlight exposure influences both serotonin production in the gut (where 90% of the body's serotonin is produced) and the vagal nerve signaling that coordinates digestive function with our circadian biology. ³ This explains why people often experience improved digestion and reduced gastrointestinal symptoms when they maintain consistent morning light exposure routines.
ME: The spherical bi-layer of cells and organelles depends on many different types of phospholipids, glycolipids and cholesterol. Cellular structures are weakened when all the structural elements found in animal products are not available due to low-fat diets or excessive reliance on factory produced oils.
◆CAI: B. The Membrane Fluidity Connection. Perhaps the most critical aspect of how diet affects sunlight utilization lies in cellular membrane composition. Our cell membranes, including those lining the digestive tract, are composed primarily of phospholipids whose fatty acid composition directly reflects our dietary intake. ⁴ When we consume high amounts of Polyunsaturated Fatty Acids (PUFAs) from seed oils—such as linoleic acid from soybean, corn, and sunflower oils—these fats become incorporated into our cellular membranes.
The problem arises because PUFAs are highly susceptible to lipid peroxidation when exposed to light, particularly UV radiation. ⁵ This creates a paradoxical situation where the very sunlight that should be beneficial becomes potentially harmful due to our membrane composition. Saturated and monounsaturated fats, by contrast, provide much more stable membrane foundations that can better withstand light exposure while maintaining optimal membrane fluidity for cellular function. ⁶
◆CAI:C. Mitochondrial Function and Light Sensitivity. The digestive system is metabolically demanding, with intestinal cells having some of the highest mitochondrial densities in the body. These mitochondria are exquisitely sensitive to both light exposure and membrane composition. ⁷ When cellular membranes are enriched with unstable PUFAs, mitochondrial membranes become more susceptible to oxidative damage from light exposure, potentially impairing the very photobiomodulation effects that should enhance cellular energy production. ⁸
Furthermore, the cytochrome c oxidase complex in mitochondria—a key target of red and near-infrared light therapy—requires optimal membrane environments to function effectively. High PUFA content can disrupt this delicate system, reducing the beneficial effects of sunlight on cellular energy production. ⁹
ME: It’s perhaps best to think of Vitamin D as a hormone since it has so many health implications.
◆CAI: D. Vitamin D Metabolism and Fat-Soluble Vitamin Absorption. The synthesis and utilization of vitamin D3 requires adequate fat intake and proper bile acid production. ¹⁰ Low-fat diets can significantly impair the absorption of vitamin D3 (whether synthesized in the skin or obtained from diet), as this fat-soluble vitamin requires dietary fats to trigger bile release and facilitate absorption in the small intestine. ¹¹
More critically, the conversion of vitamin D3 to its active hormone form (calcitriol) occurs partially in the kidneys but also locally in many tissues, including the intestinal epithelium. This local conversion requires adequate cholesterol availability, as vitamin D3 synthesis begins with 7-dehydrocholesterol in the skin. ¹² Low-fat diets that restrict cholesterol intake can therefore impair both the initial synthesis and subsequent activation of vitamin D.
ME: (Recall the previous discussion on Cod Liver Oil as a great source of Vitamin A & D.)
ME: Gallstones are probably a result of lack of fat in the diet,— bile and cholesterol are part of the liver’s metabolic magic.
◆CAI: E. Bile Acid Synthesis and Circadian Metabolism. Bile acids serve as both digestive aids and signaling molecules that regulate circadian metabolism. The synthesis of bile acids from cholesterol follows circadian patterns that are influenced by light exposure. ¹³ When dietary fat intake is inadequate, bile acid production decreases, which can disrupt these metabolic rhythms and impair the digestion and absorption of fat-soluble vitamins, including vitamin D.
Additionally, bile acids activate farnesoid X receptor (FXR), a nuclear receptor that plays crucial roles in metabolic regulation and has been shown to interact with circadian clock genes. ¹⁴ This represents another pathway through which adequate dietary fat intake supports the body's ability to respond optimally to light exposure.
ME: Nearly half of Americans have some type of gut problem.
◆CAI: F. Inflammatory Cascade and Gut Barrier Function. High consumption of omega-6 PUFAs from seed oils shifts the body's inflammatory balance toward a pro-inflammatory state through increased production of arachidonic acid and its inflammatory metabolites. ¹⁵ This chronic low-grade inflammation can compromise gut barrier function, leading to increased intestinal permeability ("leaky gut") and systemic inflammation that interferes with optimal light utilization. ¹⁶
When the gut barrier is compromised, lipopolysaccharides (LPS) from gut bacteria can enter systemic circulation, triggering inflammatory responses that can interfere with mitochondrial function and photobiomodulation responses. ¹⁷ This creates a vicious cycle where poor dietary choices reduce the body's ability to benefit from sunlight exposure.
ME: We know enough to go on a probiotic regimen when prescribed antibiotics, but what type of gut bacteria are we cultivating on a daily basis?
◆CAI: G. Microbiome Interactions. The gut microbiome both influences and is influenced by circadian rhythms, with light exposure playing a role in maintaining microbial diversity and beneficial bacterial populations. ¹⁸ Certain bacterial strains can produce metabolites that enhance the body's response to light exposure, while others may produce compounds that interfere with circadian function. ¹⁹
High PUFA intake and low-fat diets can negatively alter gut microbiome composition, reducing beneficial bacteria that support circadian health and increasing populations associated with inflammation and metabolic dysfunction. ²⁰ This microbial dysbiosis can further impair the body's ability to derive maximum benefit from sunlight exposure.
ME: If you have been on a low-fat diet and consuming high levels of seed oils (ultra-processed foods) you will probably sunburn easily. Ease into the sun regime, but ease out of the poor diet.
◆CAI: H. Practical Implications for Optimal Sunlight Utilization. To optimize the body's ability to utilize sunlight for health benefits, dietary considerations should include prioritizing stable fats (saturated and monounsaturated) while minimizing industrial seed oils high in omega-6 PUFAs. Adequate total fat intake ensures proper absorption of fat-soluble vitamins and supports healthy bile acid production.
Traditional diets that evolved in sunny climates often emphasized stable fats like coconut oil, olive oil, and animal fats, while providing adequate cholesterol for vitamin D synthesis. These dietary patterns supported optimal membrane composition for light exposure while providing the nutritional building blocks necessary for the body's photobiological systems to function effectively.
The integration of proper sunlight exposure with appropriate dietary fat intake represents a synergistic approach to health that acknowledges the co-evolution of our photobiological and metabolic systems.
Understanding these connections helps explain why the modern combination of excessive seed oil consumption, low-fat dieting, and indoor living creates a perfect storm of metabolic dysfunction that undermines our innate ability to thrive with appropriate sun exposure.
-◆-
1. Hoogerwerf, W. A. (2010). Role of clock genes in gastrointestinal motility. American Journal of Physiology-Gastrointestinal and Liver Physiology, 299(3), G549-G555.
2. Thaiss, C. A., Zeevi, D., Levy, M., Zilberman-Schapira, G., Suez, J., Tengeler, A. C., ... & Elinav, E. (2014). Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. Cell, 159(3), 514-529.
3. Yano, J. M., Yu, K., Donaldson, G. P., Shastri, G. G., Ann, P., Ma, L., ... & Hsiao, E. Y. (2015). Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell, 161(2), 264-276.
4. Calder, P. C. (2015). Functional roles of fatty acids and their effects on human health. Journal of Parenteral and Enteral Nutrition, 39(1), 18S-32S.
5. Yin, H., Xu, L., & Porter, N. A. (2011). Free radical lipid peroxidation: mechanisms and analysis. Chemical Reviews, 111(10), 5944-5972.
6. Stillwell, W., & Wassall, S. R. (2003). Docosahexaenoic acid: membrane properties of a unique fatty acid. Chemistry and Physics of Lipids, 126(1), 1-27.
7. Hoppel, C. L., Tandler, B., Fujioka, H., & Riva, A. (2009). Dynamic organization of mitochondria in human heart and in myocardial disease. International Journal of Biochemistry & Cell Biology, 41(10), 1949-56.
8. Hamblin, M. R. (2013). Mechanisms and applications of the anti-inflammatory effects of photobiomodulation. AIMS Biophysics, 4(3), 337361.
9. Karu, T. (1999). Primary and secondary mechanisms of action of visible to near-IR radiation on cells. Journal of Photochemistry and Photobiology B: Biology, 49(1), 1-17.
10. Holick, M. F. (2007). Vitamin D deficiency. New England Journal of Medicine, 357(3), 266-81.
11. Dawson-Hughes, B., Heaney, R. P., Holick, M. F., Lips, P., Meunier, P. J., & Vieth, R. (2005). Estimates of optimal vitamin D status. Osteoporosis International, 16(7), 713-716.
12. Bikle, D. D. (2014). Vitamin D metabolism, mechanism of action, and clinical applications. Chemistry & Biology, 21(3), 319-29.
13. Chiang, J. Y. (2013). Bile acid metabolism and signaling. Comprehensive Physiology, 3(3), 1191-1212.
14. Pathak, P., Xie, C., Nichols, R. G., Ferrell, J. M., Boehme, S., Krausz, K. W., ... & Chiang, J. Y. (2018). Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism. Hepatology, 68(4), 1574-88.
15. Simopoulos, A. P. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomedicine & Pharmacotherapy, 56(8), 365-79.
16. Bischoff, S. C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J. D., Serino, M., ... & Wells, J. M. (2014). Intestinal permeability–a new target for disease prevention and therapy. BMC Gastroenterology, 14(1), 189.
17. Cani, P. D., Amar, J., Iglesias, M. A., Poggi, M., Knauf, C., Bastelica, D., ... & Burcelin, R. (2007). Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes, 56(7), 1761-72.
18. Liang, X., Bushman, F. D., & FitzGerald, G. A. (2015). Rhythmicity of the intestinal microbiota is regulated by gender and the host circadian clock. Proceedings of the National Academy of Sciences, 112(33), 10479-84.
19. Schroeder, B. O., & Bäckhed, F. (2016). Signals from the gut microbiota to distant organs in physiology and disease. Nature Medicine, 22(10), 1079-89.
20. Patterson, E., Wall, R., Fitzgerald, G. F., Ross, R. P., & Stanton, C. (2012). Health implications of high dietary omega-6 polyunsaturated fatty acids. Journal of Nutrition and Metabolism, 2012, 539426.
◆
ME: Claude Antrhopic AI provided a great summary in consonance with the observation that the trifecta of low-fat diet, high seed oil & fructose consumption with sun avoidance are linked to metabolic dysfunction.
The mitochondrial turmoil induced by elevated seed oil consumption, fatty acids that rapidly go rancid, whilst eliminating the thousands of phospholipids provided by animal fats also appears to be exacerbated by high sugar, especially fructose consumption. We’ll delve into this topic in Sunlight Sonata V.