Late-Night Eating And Melatonin May Impair Insulin Response (#GotBitcoin?)
When most people think about what raises blood glucose levels, they think about dietary composition or what you eat. And rightfully so. Eating a meal consisting of highly processed, refined sugars that are lacking a fiber matrix can quickly raise blood sugar levels. However, what most people do not realize is that in addition to what you eat…when you eat is also a very important determinant of blood glucose levels. Late-Night Eating And Melatonin May Impair Insulin Response (#GotBitcoin?)
The Importance Of When You Eat
Time-restricted eating implies eating all of your meals in a specified time-window, such as an 8-12-hour period and then fasting for the remaining 16-12 hours. Obviously, there is an intermittent fasting component to time-restricted eating, but it also has a circadian component to it because you try and eat all your meals during a time when metabolism is optimal.
The body’s circadian rhythms – the 24-hour cycles of biological, hormonal, and behavioral patterns – are optimized to promote our survival. These rhythms modulate a wide array of physiological processes, including the body’s production of hormones that regulate sleep, hunger, and metabolism, ultimately influencing body weight, performance, and susceptibility to disease. Roughly 10 to 40 percent of gene expression in mammals is under circadian control including genes in the brain, liver, and muscle. As such, circadian rhythmicity may have profound implications for human healthspan.
Metabolism changes throughout the day. For example, when healthy adults eat meals that are identical in terms of both their macronutrient and caloric content at breakfast, lunch, or dinner, the postprandial glucose increase is lowest after breakfast (in the morning) and highest after an evening dinner even though the meals were 100% identical. Melatonin shuts down insulin productionA key player in the body’s circadian metabolic processes is melatonin, a hormone produced deep within the center of the brain, in the pea-sized pineal gland. Melatonin plays an important role in our physiology by regulating the expression of more than 500 genes, but we rightly think of it as a sleep inducer with its increased production being tied to both our natural sleep time and our light exposure. In fact, the greatest influence on its secretion is light: generally, melatonin levels are low during the day and high during the night. But melatonin doesn’t regulate sleep alone. It sends messages to other parts of the body in preparation for sleep, including the pancreas, where it binds to receptors and signals the temporary (overnight) cessation of insulin production. This wasn’t a problem in our pre-industrial past, but in today’s environment of 24-hour food availability, it can have far-reaching effects on health. When food consumption regularly occurs outside normal daylight hours, the risk of hyperglycemia – higher than optimal blood glucose levels – increases. Chronic exposure to elevated glucose increases our risk of developing diabetes and other metabolic disorders. But it might also cause brain volume. Studies have shown an association of even high normal fasting blood glucose associated with losses in the hippocampus and the amygdala, areas involved in memory and cognition. In other words, healthy people without diabetes. Humans are the only species that disobeys their biological clocks, uncoupling the natural rhythms of light and dark around us. In this brief episode, we learn how restoring our dietary and sleep pattern to one that more closely syncs with those imposed by nature, especially by avoiding eating within 2-3 hours before bed and onset of melatonin production, may improve our health and potentially prolong our healthspan. Watch this short episode on how late-night eating may suffer from an impaired insulin response thanks to melatonin.
|Circadian Report v3 (updated 3/7/19)|
|If you have used one of the consumer genetic testing services like 23andMe, your raw data may contain some of the single nucleotide polymorphisms that affect circadian rhythm and sleep. As of 3/7/19, the circadian report has been updated! The new updates includes updates for SNPs in the following genes:CRY2 – SNP involved in the regulation of the circadian rhythm have been associated with fasting glucose levels.ADA – SNP involved in adenosine degradation may be related to sleep depth.MTNR1B – SNP in a melatonin receptor have been associated with the risk for type-2 diabetes and may have implications for meal timing.To learn more…|
Visit the genetics page on my website
Did you enjoy this article?
Maybe you’d like to support more like it!
This post and all of my newsletters, videos, and podcasts are brought to you by people like you through pay-what-you-can crowdfunding.
- Pledging your support comes with a few benefits…
- Occasional early content previews
- Periodic updates letting you know what’s going on with FoundMyFitness and what I have planned ahead.
- A monthly hangout for my top pledgers (or a more sporadic one for everyone else)
… other ways I sometimes conspire to show my supporters appreciation
And last but not least…
The opportunity to be one of the people I strive to, every single month, make the beneficiary of the very best I have to offer.
Perciavalle Patrick has a Ph.D. in biomedical science from the University of Tennessee Health Science Center, Memphis TN and St. Jude Children’s Research Hospital, Memphis TN. She also has a Bachelor’s of Science degree in biochemistry/chemistry from the University of California, San Diego. She has done extensive research on aging, cancer, and nutrition. She did her graduate research at St. Jude Children’s Research Hospital where she investigated the link between mitochondrial metabolism, apoptosis, and cancer. Her groundbreaking work discovered that a protein that is critical for cell survival has two distinct mitochondrial localizations with disparate functions, linking its anti-apoptotic role to a previously unrecognized role in mitochondrial respiration and maintenance of mitochondrial structure. Her dissertation findings were published in the 2012 issue of Nature Cell Biology.
Dr. Patrick trained as a postdoctoral fellow at Children’s Hospital Oakland Research Institute with Dr. Bruce Ames. She investigated the effects of micronutrient (vitamins and minerals) inadequacies on metabolism, inflammation, DNA damage, and aging and whether supplementation can reverse the damage. In addition, she also investigated the role of vitamin D in brain function, behavior, and other physiological functions and has published papers in FASEB on how vitamin D regulates serotonin synthesis and how this relates to autism and other neuropsychiatric disorders.
Dr. Patrick has also done research on aging at the Salk Institute for Biological Sciences. At the Salk, she investigated what role insulin signaling played in protein misfolding, which is commonly found in neurodegenerative diseases such as Alzheimer’s disease.
She frequently engages the public on topics including the role micronutrient deficiencies play in diseases of aging, the role of genetics in determining the effects of nutrients on a person’s health status, benefits of exposing the body to hormetic stressors, such as through exercise, fasting, sauna use or heat stress, or various forms of cold exposure, and the importance of mindfulness, stress reduction, and sleep. It is Dr. Patrick’s goal to challenge the status quo and encourage the wider public to think about health and longevity using a proactive, preventative approach.
* Vitamin D and the Omega-3 Fatty Acids Control Serotonin Synthesis and Action, Part 2: Relevance for ADHD, Bipolar, Schizophrenia, and Impulsive Behavior FASEB Journal
* Vitamin D Hormone Regulates Serotonin Synthesis. Part 1: Relevance for Autism FASEB Journal
* Requirement for Anti-Apoptotic MCL-1 in the Survival of BCR-ABL B-Lineage Acute Lymphoblastic Leukemia Blood
* Delving Deeper: MCL-1′s Contribution to Normal and Cancer Biology Trends in Cell Biology
* Anti-Apoptotic MCL-1 Localizes to the Mitochondrial Matrix and Couples Mitochondrial Fusion to Respiration Nature Cell Biology
* Ubiquitin-Independent Degradation of Anti-Apoptotic MCL-1 Molecular and Cellular Biology
* Opposing Activities Protect Against Age-Onset Proteotoxicity Science
Your Questions And Comments Are Greatly Appreciated.
Monty H. & Carolyn A.Go back