Coffee and magnesium levels

Symptoms of poor magnesium intake can include muscle cramps, facial tics, poor sleep, and chronic pain. It pays to ensure that you get adequate magnesium before signs of deficiency occur.

But how can you know whether you’re getting enough?

According to population studies of average magnesium intake, there’s a good chance that you’re not.

Less than 30% of U.S. adults consume the Recommended Daily Allowance (RDA) of magnesium. And nearly 20% get only half of the magnesium they need daily to remain healthy.1 2 3

magnesium rda intake

Estimated U.S. Intake of Magnesium Recommended Daily Allowance

DO I GET ENOUGH MAGNESIUM?

One method of assessing your magnesium status is to simply contact your health care provider and request detailed magnesium testing. Yet magnesium assessment is typically done using blood serum testing, and these tests can be misleading. Only 1% of magnesium in the body is actually found in blood, and only .3% is found in blood serum, so clinical blood serum testing may not successfully identify magnesium deficiency.

What to do?

Fortunately, it’s possible to get a sense of where your intake may lie simply by asking yourself a few questions about your lifestyle, and watching for certain signs and signals of low magnesium levels.

Learn how to read your signs below, and find out what you can do to ensure magnesium balance and good health. If you answer yes to any of the following questions, you may be at risk for low magnesium intake.

1. Do you drink carbonated beverages on a regular basis?

Most dark colored sodas contain phosphates. These substances actually bind with magnesium inside the digestive tract, rendering it unavailable to the body. So even if you are eating a balanced diet, by drinking soda with your meals you are flushing magnesium out of your system.4 5 6

The average consumption of carbonated beverages today is more than ten times what it was in 1940.7This skyrocketing increase is responsible for both reduced magnesium and calcium availability in the body.8 9

2. Do you regularly eat pastries, cakes, desserts, candies or other sweet foods?

sugar and magnesium depletion

Refined sugar is not only a zero magnesium product but it also causes the body to excrete magnesium through the kidneys. The process of producing refined sugar from sugar cane removes molasses, stripping the magnesium content entirely.

And sugar does not simply serve to reduce magnesium levels. Sweet foods are known by nutritionists as “anti-nutrients”. Anti-nutrients like sweets are foods that replace whole nutritious foods in the diet, yet actually consume nutrients when digested, resulting in a net loss. Because all foods require vitamins and minerals to be consumed in order to power the process of digestion, it’s important to choose foods that “put back” vital nutrients, and then some.

The more sweet foods and processed baked goods you have in your diet, the more likely you are deficient in magnesium and other vital nutrients.

3. Do you experience a lot of stress in your life, or have you recently had a major medical procedure such as surgery?

Both physical and emotional stress can be a cause of magnesium deficiency.

Stress can be a cause of magnesium deficiency, and a lack of magnesium tends to magnify the stress reaction, worsening the problem. In studies, adrenaline and cortisol, byproducts of the “fight or flight” reaction associated with stress and anxiety, were associated with decreased magnesium.4

Because stressful conditions require more magnesium use by the body, all such conditions may lead to deficiency, including both psychological and physical forms of stress such as surgery, burns, and chronic disease.

4. Do you drink coffee, tea, or other caffeinated drinks daily?

coffee and magnesium loss

Magnesium levels are controlled in the body in large part by the kidneys, which filter and excrete excess magnesium and other minerals. But caffeine causes the kidneys to release extra magnesium regardless of body status.

If you drink caffeinated beverages such as coffee, tea and soda regularly, your risk for magnesium deficiency is increased.

5. Do you take a diuretic, heart medication, asthma medication, birth control pills or estrogen replacement therapy?

The effects of certain drugs have been shown to reduce magnesium levels in the body by increasing magnesium loss through excretion by the kidneys.

6. Do you drink more than seven alcoholic beverages per week?

alcohol and magnesium depletion

The effect of alcohol on magnesium levels is similar to the effect of diuretics: it lowers magnesium available to the cells by increasing the excretion of magnesium by the kidneys. In studies, clinical magnesium deficiency was found in 30% of alcoholics.10

Increased alcohol intake also contributes to decreased efficiency of the digestive system, as well as Vitamin D deficiency, both of which can contribute to low magnesium levels.11

7. Do you take calcium supplements without magnesium or calcium supplements with magnesium in less than a 1:1 ratio?

Studies have shown that when magnesium intake is low, calcium supplementation may reduce magnesium absorption and retention.12 13 14 And, whereas calcium supplementation can have negative effects on magnesium levels, magnesium supplementation actually improves the body’s use of calcium.7

calcium and magnesium absorption

Though many reports suggest taking calcium to magnesium in a 2:1 ratio, this figure is largely arbitrary. The ideal ratio for any individual will vary depending on current conditions as well as risk factors for deficiency.

However, several researchers now support a 1:1 calcium to magnesium ratio for improved bone support and reduced risk of disease. This is due not only to the increased evidence pointing to widespread magnesium deficiency, but also concerns over the risk of arterial calcification when low magnesium stores are coupled with high calcium intake.

According to noted magnesium researcher Mildred Seelig:

The body tends to retain calcium when in a magnesium-deficient state. Extra calcium intake at such a time could cause an abnormal rise of calcium levels inside the cells, including the cells of the heart and blood vessels… Given the delicate balance necessary between calcium and magnesium in the cells, it is best to be sure magnesium is adequate if you are taking calcium supplements.”8

8. Do you experience any of the following:

  • Anxiety?
  • Times of hyperactivity?
  • Difficulty getting to sleep?
  • Difficulty staying asleep?

The above symptoms may be neurological signs of magnesium deficiency. Adequate magnesium is necessary for nerve conduction and is also associated with electrolyte imbalances that affect the nervous system. Low magnesium is also associated with personality changes and sometimes depression.

9. Do you experience any of the following:

  • Painful muscle spasms?
  • Muscle cramping?
  • Fibromyalgia?
  • Facial tics?
  • Eye twitches, or involuntary eye movements?

Neuromuscular symptoms such as these are among the classic signs of a potential magnesium deficit.

Without magnesium, our muscles would be in a constant state of contraction.

Magnesium is a required element of muscle relaxation, and without it our muscles would be in a constant state of contraction. Calcium, on the other hand, signals muscles to contract. As noted in the book The Magnesium Factor, the two minerals are “two sides of a physiological coin; they have actions that oppose one another, yet they function as a team.”8

Chvostek’s Sign and Trousseau’s Sign are both clinical tests for involuntary muscle movements, and both may indicate either calcium or magnesium deficiency, or both. In fact, magnesium deficiency may actually appear as calcium deficiency in testing, and one of the first recommendations upon receiving low calcium test results is magnesium supplementation.

10. Did you answer yes to any of the above questions and are also age 55 or older?

Older adults are particularly vulnerable to low magnesium status. It has been shown that aging, stress and disease all contribute to increasing magnesium needs, yet most older adults actually take in less magnesium from food sources than when they were younger.

In addition, magnesium metabolism may be less efficient as we grow older, as changes the GI tract and kidneys contribute to older adults absorbing less and retaining less magnesium.15

If you are above 55 and also showing lifestyle signs or symptoms related to low magnesium, it’s particularly important that you work to improve your magnesium intake. When body stores of magnesium run low, risks of overt hypomagnesaemia (magnesium deficiency) increase significantly.

HOW CAN YOU KNOW FOR CERTAIN IF YOU HAVE A DEFICIENCY?

Magnesium’s impact is so crucial and far reaching that symptoms of its absence reverberate throughout the body’s systems. This makes signs of its absence hard to pin down with absolute precision, even for cutting edge researchers.  Doctors Pilar Aranda and Elena Planells noted this difficulty in their report at the International Magnesium Symposium of 2007:

The clinical manifestations of magnesium deficiency are difficult to define because depletion of this cation is associated with considerable abnormalities in the metabolism of many elements and enzymes. If prolonged, insufficient magnesium intake may be responsible for symptoms attributed to other causes, or whose causes are unknown.”

Among researchers, magnesium deficiency is known as the silent epidemic of our times, and it is widely acknowledged that definitive testing for deficiency remains elusive. Judy Driskell, Professor, Nutrition and Health Sciences at the University of Nebraska, refers to this “invisible deficiency” as chronic latent magnesium deficiency, and explains:

Normal serum and plasma magnesium concentrations have been found in individuals with low magnesium in [red blood cells] and tissues. Yet efforts to find an indicator of subclinical magnesium status have not yielded a cost-effective one that has been well validated.”16

Yet while the identification of magnesium deficiency may be unclear, its importance is undeniable.

Magnesium activates over 300 enzyme reactions in the body, translating to thousands of biochemical reactions happening on a constant basis daily. Magnesium is crucial to nerve transmission, muscle contraction, blood coagulation, energy production, nutrient metabolism and bone and cell formation.

Considering these varied and all-encompassing effects, not to mention the cascading effect magnesium levels have on other important minerals such as calcium and potassium, one thing is clear – long term low magnesium intake is something to be avoided.


Connie’s comments: I sometimes drink decaf coffee before I exercise and eat in the morning. I take 60:40 calcium:magnesium with Vitamin D and C in the afternoon and at night. And always choose whole foods rich in magnesium since I have difficulty sleeping and relieve muscle pain.

Email motherhealth@gmail.com for supplements personalized to your body composition. I get my supplements at Life Extension and I am a wholesaler.

Foods to eat and avoid when you have Gout and leg pains

Gout

Gout, a painful form of arthritis, occurs when high levels of uric acid in the blood cause crystals to form and accumulate around a joint.

Uric acid is produced when the body breaks down a chemical called purine. Purine occurs naturally in your body, but it’s also found in certain foods. Uric acid is eliminated from the body in urine.

  • High-purine vegetables. Studies have shown that vegetables high in purines do not increase the risk of gout or recurring gout attacks. A healthy diet based on lots of fruits and vegetables can include high-purine vegetables, such as asparagus, ginger spinach, peas, cauliflower or mushrooms. You can also eat beans or lentils, which are moderately high in purines but are also a good source of protein.  Greens rich in sulfur such as asparagus, broccoli, parsley, celery , carrots, cucumbers, red onion, tomatoes, bell peppers, lettuce ,zucchini, squash ,pumpkin , watermelon, green beans, cinnamon, black currants berries for tea, nettle soup, coffe (black and green), and probiotics such as pickled greens and yogurt.
  • Eat high potassium rich foods.  Potassium citrate helps alkalize your urine and improves the excretion of uric acid. Potassium is widely available in fruits and vegetables. The most beneficial sources include broccoli, celery, avocado, spinach and romaine lettuce. If you want to supplement, consider using potassium bicarbonate, which is probably the best potassium source to use as a supplement.
  • Avoid sugar. Uric acid is a byproduct of fructose metabolism. In fact, fructose is the ONLY type of sugar that will raise your uric acid levels and will typically generate uric acid within minutes of ingestion. The ideal range for uric acid is between 3 to 5.5 mg/dL. The connection between fructose consumption and increased uric acid is so reliable that a uric acid level taken from your blood can actually be used as a marker for fructose toxicity.
  • Avoid Organ and glandular meats, high in purines. Avoid meats such as liver, kidney and sweetbreads, which have high purine levels and contribute to high blood levels of uric acid.  Organ meats, brewer’s yeast, sardines and tuna packed in oil, chicken livers and beef fillet all have over 100 mg of purine per 100 g of product.24 Foods high in purine will breakdown to uric acid.
  • Avoid Selected seafood. Avoid the following types of seafood, which are higher in purines than others: anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel and tuna.
  • Avoid Alcohol. The metabolism of alcohol in your body is thought to increase uric acid production, and alcohol contributes to dehydration. Beer is associated with an increased risk of gout and recurring attacks, as are distilled liquors to some extent. The effect of wine is not as well-understood. If you drink alcohol, talk to your doctor about what is appropriate for you.
  • Vitamin C. Vitamin C may help lower uric acid levels. Talk to your doctor about whether a 500-milligram vitamin C supplement fits into your diet and medication plan.  Vit C rich citrus fruits such as lemon, digestive enzymes from pineapple, papaya and mangoes. Good fats in avocado, coconut and fruits such as apples, kiwi,plums, pomelo, pears, cherries, peaches, blackberries.
  • Coffee. Some research suggests that moderate coffee consumption may be associated with a reduced risk of gout, particularly with regular caffeinated coffee. Drinking coffee may not be appropriate for other medical conditions. Talk to your doctor about how much coffee is right for you.
  • Cherries. There is some evidence that eating cherries is associated with a reduced risk of gout attacks.
  • Avoid: Prescription drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs), which are the norm when it comes to treating gout, have been proven to do you more harm than good.
  • Reduce stress, sleep more and Practice Grounding.  Grounding or earthing is the process of walking or standing barefoot on bare earth, permitting free electrons from the earth to enter your body. These powerful antioxidants combat free radicals in your system.

    Grounding may reduce your risk of cardiovascular disease and may thin your blood, both good things when you want to reduce your risk for gout. If you want to try grounding, start by walking in a dewy, grassy area barefoot.

    If you live near a large body of water, that’s a great location for walking barefoot, as seawater is a good conductor.

  • Here are the most popular natural home remedies voted by gout sufferers:

    1. Apple Cider Vinegar: ACV is considered king when it comes to a gout natural home remedy and it’s my most popular post voted by social media. ACV helps your body become more alkaline and the acidity helps relieve acute gout pain. Many gout sufferers report drinking 1-2  tablespoons of raw unfiltered and organic apple cider vinegar in a glass of at least 8 ounces of water. Some will drink this 2-3 times a day for better results. ACV can also be used as topical treatment. You you can soak your foot for about 30 minutes in a bucket full of 4 cups of hot water and 1 cup of apple cider vinegar. You can also soak a clean, dry cloth in apple cider vinegar and wrap it around the affected area for about 15 minutes.

    2. Baking Soda: Another extremely popular natural home remedy for gout sufferers is baking soda. Like apple cider vinegar, it makes your body more alkaline. Many consume ½ a teaspoon in a glass of 8 oz. water.Many will repeat this throughout the day until they have consumed at least 3 teaspoons of baking soda. It helps lower uric acid providing with relief from the pain at the same time. Avoid this home remedy if suffering from high blood pressure and try to limit salt intake in your meals during the day when taking baking soda. Baking soda is very high in sodium. The maximum recommended dose is 4 teaspoons throughout the day.

    3. Cherries: Whether sweet or sour, cherries have been known to be extremely effective in treating gout and lowering uric acid due to their high antioxidant properties. In one study conducted with 600 people suffering from gout, it was concluded that eating half a cup serving of cherries daily (10-12 cherries) resulted in a 35% reduced risk of a successive gout attack. For those eating 2 or even 3 servings in a day, their risk dropped to 50%! But that is too much sugar as well which can cause other health ailments. Best recommendation is to use a tart cherry extract supplement and avoid the sugar intake if you can!

    4. Ginger and/or Turmeric: The powerful anti-inflammatories present in ginger root and turmeric can be very helpful in easing gout pain and inflammation. I basically chop off a little piece the size of an inch and boil it for about 20 minutes and drink it as tea. You can also add ginger root and/or turmeric in cooking recipes. Some may also eat a small piece raw daily. Others use it topically to reduce swelling by making a paste of ginger root with water and then apply it to the affected area, leaving it on for about 30 minutes.

  • ———-
  • Connie’s comments: My 80 yr old mother has been taking zyflamend capsule, combo of turmeric and ginger for her leg pains in the past.

Genetics Link Sleep Disturbances With Restless Leg Syndrome, Schizophrenia and Obesity

Summary: Researchers have identified a genetic link between a diverse array of health disorders and sleep problems.

Source: Mass General.

A team of American and British scientists have for the first time discovered genetic connections between sleep disturbance and a range of medical disorders including obesity.

Lead author Jacqueline Lane, PhD, postdoctoral fellow at Massachusetts General Hospital (MGH), and joint senior authors Richa Saxena, PhD, assistant professor of Anæsthesia at MGH and Harvard Medical School, and Martin K Rutter, MD, FRCP, senior lecturer in Cardiometabolic Medicine from The University of Manchester, publish their groundbreaking research in Nature Genetics today.

The study looked at the biological controllers of sleep duration, insomnia and excessive daytime sleepiness and how they linked to the health and life histories of more than 112,000 people taking part in the world-leading UK Biobank study. Study participants reported their sleep duration, the degree of insomnia and daytime sleepiness, and then had their genes mapped. Other information about them, such as their weight and any diseases they suffered from, was also collected.

The researchers identified for the first time areas of the genome that are associated with sleep disturbance – including insomnia and excessive daytime sleepiness – and also discovered novel genetic links with several medical conditions, including restless legs syndrome, schizophrenia and obesity. The strongest genetic association for insomnia symptoms fell within a gene previously linked to restless legs syndrome – a nervous system disorder affecting around 1 in 20 people that leads to a strong urge to move one’s legs, which is often worse at night. Other gene regions were important for insomnia, but selectively in either men or women.

The team also identified genetic links between longer sleep duration and schizophrenia risk and between increased levels of excessive daytime sleepiness and measures of obesity (body mass index and waist circumference). The research also suggested that insomnia has shared underlying biology with major depression and abnormal glucose metabolism.

Funded by the U.S. National Institutes of Health and The University of Manchester’s Research Innovation Fund, the study marks a major advance in understanding the biology of sleep.

One in four British adults are obese, according to the U.N. Food and Agriculture Organization, prompting fears that the U.K. has become the “fat man of Europe.” And at any one time, about 280,000 people are being treated for schizophrenia by the National Health Service. Individuals with schizophrenia have a 1 in 10 chance of dying by their own hand within ten years of diagnosis.

Rutter says, “This clinical science is an important step forwards in understanding the biological basis for these conditions; so it’s very exciting. Scientists have long observed a connection between sleep disorders and these conditions in epidemiological studies. But this is the first time these biological links have been identified at a molecular level.”

Image shows a DNA strand.

UK Biobank aims to improving the prevention, diagnosis and treatment of a wide range of serious and life-threatening illnesses. Lane says, “We’re particularly pleased to be able to use UK Biobank data in this way; it’s an amazing resource for scientists.”

Saxena adds, “It’s important to remember there is no molecular targeting available for conditions which affect sleep: all we really have are sedatives. So we hope that this research will enable scientists to develop new ways to intervene on a range of conditions in a much more fundamental way. We acknowledge these findings will need further study, but we believe this knowledge amounts to a key advance in our understanding of the biology behind sleep – a major influence on our health and behaviour.”

ABOUT THIS GENETICS RESEARCH ARTICLE

Funding: Funding provided by National Institutes of Health, University of Manchester Research Innovation Fund.

Source: Terri Ogan – Mass General
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits” by Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter and Richa Saxena in Nature Genetics. Published online December 19 2016 doi:10.1038/ng.3749

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Mass General. “Genetics Link Sleep Disturbances With Restless Leg Syndrome, Schizophrenia and Obesity.” NeuroscienceNews. NeuroscienceNews, 19 December 2016.
<http://neurosciencenews.com/sleep-genetics-obesity-schizophrenia-5776/&gt;.

Abstract

Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits

Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality, affect 25–30% of adults worldwide. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7).

“Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits” by Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter and Richa Saxena in Nature Genetics. Published online December 19 2016 doi:10.1038/ng.3749

Gut Microbe Movements Regulate Host Circadian Rhythms

Summary: Study exposes a new dynamic between the mammalian organism and the microbes that live inside their gut.

Source: Cell Press.

Even gut microbes have a routine. Like clockwork, they start their day in one part of the intestinal lining, move a few micrometers to the left, maybe the right, and then return to their original position. New research in mice now reveals that the regular timing of these small movements can influence a host animal’s circadian rhythms by exposing gut tissue to different microbes and their metabolites as the day goes by. Disruption of this dance can affect the host. The study appears December 1 in Cell.

“This research highlights how interconnected the behavior is between prokaryotes and eukaryotes, between mammalian organisms and the microbes that live inside them,” says Eran Elinav, an immunologist at the Weizmann Institute of Science, who led the work with co-senior author Eran Segal, a computational biologist also at the Weizmann. “These groups interact with and are affected by each other in a way that can’t be separated.”

The new study had three major findings:

  • The microbiome on the surface layer of the gut undergoes rhythmical changes in its “biogeographical” localization throughout the day and night; thus, the surface cells are exposed to different numbers and different species of bacteria over the course of a day.
  • “This tango between the two partners adds mechanistic insight into this relationship,” Elinav says.
  • The circadian changes of the gut microbiome have profound effects on host physiology, and unexpectedly, they affect tissue that is far away from the gut, such as the liver, whose gene expression changes in tandem with the gut microbiome rhythmicity. “As such,” adds Elinav, “disturbances in the rhythmic microbiome result in impairment in vital diurnal liver functions such as drug metabolism and detoxification.”
  • The circadian rhythm of the host is deeply dependent on the gut microbiota oscillations. Although some circadian machinery in the host was maintained by its own internal clock, other components of the circadian clock had their normal rhythms destroyed. Most surprising, another set of genes in the host that normally exhibit no circadian rhythms stepped in and took over after the microbial rhythms were disrupted.

Previous work by Elinav and Segal revealed that our biological clocks work in tandem with the biological clocks in our microbiota and that disrupting sleep-wake patterns and feeding times in mice induced changes in the microbiome in the gut.

“Circadian rhythms are a way of adapting to changes in light and dark, metabolic changes, and the timing of when we eat,” says Segal. “Other studies have shown the importance of the microbiome in metabolism and its effect on health and disease. Now, we’ve shown for the first time how circadian rhythms in the microbiota have an effect on circadian rhythms in the host.”

Image shows a visual abstract for the research.

The investigators say their work has potential implications for human health in two important ways. First of all, because drugs ranging from acetaminophen to chemotherapy are metabolized in the liver, understanding — and potentially being able to manipulate — the circadian rhythms of our microbiota could affect how and when medications are administered.

Second, understanding more about this relationship could help to eventually intervene in health problems like obesity and metabolic syndrome, which are more common in people whose circadian rhythms are frequently disrupted due to shift work or jet lag.

“What we learned from this study is that there’s a very tight interconnectivity between the microbiome and the host. We should think of it now as one supraorganism that can’t be separated,” Segal says. “We have to fully integrate our thinking with regard to any substance that we consume.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This research was primarily funded by Yael and Rami Ungar, Israel; Leona M. and Harry B. Helmsley Charitable Trust; the Gurwin Family Fund for Scientific Research; Crown Endowment Fund for Immunological Research; estate of Jack Gitlitz; estate of Lydia Hershkovich; the Benoziyo Endowment Fund for the Advancement of Science; Adelis Foundation; John L. and Vera Schwartz, Pacific Palisades; Alan Markovitz, Canada; Cynthia Adelson, Canada; CNRS (Centre National de la Recherche Scientifique); estate of Samuel and Alwyn J. Weber; Mr. and Mrs. Donald L. Schwarz, Sherman Oaks; grants funded by the European Research Council; the German-Israel Binational foundation; the Israel Science Foundation; the Minerva Foundation; the Rising Tide foundation; the Alon Foundation scholar award; the Rina Gudinski Career Development Chair; and the Canadian Institute For Advanced Research (CIFAR).

Source: Joseph Caputo – Cell Press
Image Source: NeuroscienceNews.com image is credited to Thaiss et al/Cell 2016.
Original Research: Full open access research for “Microbiota Diurnal Rhythmicity Programs Host Transcriptome Oscillations” by Christoph A. Thaiss, Maayan Levy, Tal Korem, Lenka Dohnalová, Hagit Shapiro, Diego A. Jaitin, Eyal David, Deborah R. Winter, Meital Gury-BenAri, Evgeny Tatirovsky, Timur Tuganbaev, Sara Federici, Niv Zmora, David Zeevi, Mally Dori-Bachash, Meirav Pevsner-Fischer, Elena Kartvelishvily, Alexander Brandis, Alon Harmelin, Oren Shibolet, Zamir Halpern, Kenya Honda, Ido Amit, Eran Segal, and Eran Elinav for correspondence informationemail in Cell. Published online December 1 2026 doi:10.1016/j.cell.2016.11.003

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Cell Press “Gut Microbe Movements Regulate Host Circadian Rhythms.” NeuroscienceNews. NeuroscienceNews, 2 December 2026.
<http://neurosciencenews.com/cut-microbes-circadian-rhythm-5663/&gt;.

Abstract

Microbiota Diurnal Rhythmicity Programs Host Transcriptome Oscillations

Highlights
•Intestinal microbiota biogeography and metabolome undergo diurnal oscillations
•Circadian oscillations of serum metabolites are regulated by the microbiota
•Microbiota rhythms program the circadian epigenetic and transcriptional landscape
•The microbiota regulates the circadian liver transcriptome and detoxification pattern

Summary
The intestinal microbiota undergoes diurnal compositional and functional oscillations that affect metabolic homeostasis, but the mechanisms by which the rhythmic microbiota influences host circadian activity remain elusive. Using integrated multi-omics and imaging approaches, we demonstrate that the gut microbiota features oscillating biogeographical localization and metabolome patterns that determine the rhythmic exposure of the intestinal epithelium to different bacterial species and their metabolites over the course of a day. This diurnal microbial behavior drives, in turn, the global programming of the host circadian transcriptional, epigenetic, and metabolite oscillations. Surprisingly, disruption of homeostatic microbiome rhythmicity not only abrogates normal chromatin and transcriptional oscillations of the host, but also incites genome-wide de novo oscillations in both intestine and liver, thereby impacting diurnal fluctuations of host physiology and disease susceptibility. As such, the rhythmic biogeography and metabolome of the intestinal microbiota regulates the temporal organization and functional outcome of host transcriptional and epigenetic programs.

“Microbiota Diurnal Rhythmicity Programs Host Transcriptome Oscillations” by Christoph A. Thaiss, Maayan Levy, Tal Korem, Lenka Dohnalová, Hagit Shapiro, Diego A. Jaitin, Eyal David, Deborah R. Winter, Meital Gury-BenAri, Evgeny Tatirovsky, Timur Tuganbaev, Sara Federici, Niv Zmora, David Zeevi, Mally Dori-Bachash, Meirav Pevsner-Fischer, Elena Kartvelishvily, Alexander Brandis, Alon Harmelin, Oren Shibolet, Zamir Halpern, Kenya Honda, Ido Amit, Eran Segal, and Eran Elinav for correspondence informationemail in Cell. Published online December 1 2026 doi:10.1016/j.cell.2016.11.003

THE LINK BETWEEN CIRCADIAN RHYTHMS AND AGING

MIT study finds that a gene associated with longevity also regulates the body’s circadian clock.

Human sleeping and waking patterns are largely governed by an internal circadian clock that corresponds closely with the 24-hour cycle of light and darkness. This circadian clock also controls other body functions, such as metabolism and temperature regulation.

Studies in animals have found that when that rhythm gets thrown off, health problems including obesity and metabolic disorders such as diabetes can arise. Studies of people who work night shifts have also revealed an increased susceptibility to diabetes.

A new study from MIT shows that a gene called SIRT1, previously shown to protect against diseases of aging, plays a key role in controlling these circadian rhythms. The researchers found that circadian function decays with aging in normal mice, and that boosting their SIRT1 levels in the brain could prevent this decay. Conversely, loss of SIRT1 function impairs circadian control in young mice, mimicking what happens in normal aging.

Since the SIRT1 protein itself was found to decline with aging in the normal mice, the findings suggest that drugs that enhance SIRT1 activity in humans could have widespread health benefits, says Leonard Guarente, the Novartis Professor of Biology at MIT and senior author of a paper describing the findings in the June 20 issue of Cell.

The image shows a brain attached to a tree in day time.

“If we could keep SIRT1 as active as possible as we get older, then we’d be able to retard aging in the central clock in the brain, and health benefits would radiate from that,” Guarente says.

Staying on schedule

In humans and animals, circadian patterns follow a roughly 24-hour cycle, directed by the circadian control center of the brain, called the suprachiasmatic nucleus (SCN), located in the hypothalamus.

“Just about everything that takes place physiologically is really staged along the circadian cycle,” Guarente says. “What’s now emerging is the idea that maintaining the circadian cycle is quite important in health maintenance, and if it gets broken, there’s a penalty to be paid in health and perhaps in aging.”

Last year, Guarente found that a robust circadian period correlated with longer lifespan in mice. That got him wondering what role SIRT1, which has been shown to prolong lifespan in many animals, might play in that phenomenon. SIRT1, which Guarente first linked with aging more than 15 years ago, is a master regulator of cell responses to stress, coordinating a variety of hormone networks, proteins and genes to help keep cells alive and healthy.

To investigate SIRT1’s role in circadian control, Guarente and his colleagues created genetically engineered mice that produce different amounts of SIRT1 in the brain. One group of mice had normal SIRT1 levels, another had no SIRT1, and two groups had extra SIRT1 — either twice or 10 times as much as normal.

Mice lacking SIRT1 had slightly longer circadian cycles (23.9 hours) than normal mice (23.6 hours), and mice with a 10-fold increase in SIRT1 had shorter cycles (23.1 hours).

In mice with normal SIRT1 levels, the researchers confirmed previous findings that when the 12-hour light/dark cycle is interrupted, younger mice readjust their circadian cycles much more easily than older ones. However, they showed for the first time that mice with extra SIRT1 do not suffer the same decline in circadian control as they age.

The researchers also found that SIRT1 exerts this control by regulating the genes BMAL and CLOCK, the two major keepers of the central circadian clock.

Enhancing circadian function

A growing body of evidence suggests that being able to respond to large or small disruptions of the light/dark cycle is important to maintaining healthy metabolic function, Guarente says.

“Essentially we experience a mini jet lag every day because the light cycle is constantly changing. The critical thing for us is to be able to adapt smoothly to these jolts,” Guarente says. “Many studies in mice say that while young mice do this perfectly well, it’s the old mice that have the problem. So that could well be true in humans.”

If so, it could be possible to treat or prevent diseases of aging by enhancing circadian function — either by delivering SIRT1 activators in the brain or developing drugs that enhance another part of the circadian control system, Guarente says.

“I think we should look at every aspect of the machinery of the circadian clock in the brain, and any intervention that can maintain that machinery with aging ought to be good,” he says. “One entry point would be SIRT1, because we’ve shown in mice that genetic maintenance of SIRT1 helps maintain circadian function.”

Some SIRT1 activators are now being tested against diabetes, inflammation and other diseases, but they are not designed to cross the blood-brain barrier and would likely not be able to reach the SCN. However, Guarente believes it could be possible to design SIRT1 activators that can get into the brain.

Roman Kondratov, an associate professor of biology at Cleveland State University, says the study raises several exciting questions regarding the potential to delay or reverse age-related changes in the brain through rejuvenation of the circadian clock with SIRT1 enhancement.

“The importance of this study is that it has both basic and potentially translational applications, taking into account the fact that pharmacological modulators of SIRT1 are currently under active study,” Kondratov says.

Researchers in Guarente’s lab are now investigating the relationship between health, circadian function and diet. They suspect that high-fat diets might throw the circadian clock out of whack, which could be counteracted by increased SIRT1 activation.

Notes about this aging and circadian rhythm research

The research was funded by the National Institutes of Health and the Glenn Foundation for Medical Research.

Contact: Anne Trafton – MIT
Source: MIT press release
Image Source: The brain image is available in the public domain.
Original Research: Abstract for “SIRT1 Mediates Central Circadian Control in the SCN by a Mechanism that Decays with Aging” by Hung-Chun Chang, Leonard Guarente in Cell. Published online June 20 2013 doi: 10.1016/j.cell.2013.05.027

Brain Metabolism Predicts Fluid Intelligence in Young Adults

A healthy brain is critical to a person’s cognitive abilities, but measuring brain health can be a complicated endeavor. A new study by University of Illinois researchers reports that healthy brain metabolism corresponds with fluid intelligence – a measure of one’s ability to solve unusual or complex problems – in young adults.

The results are reported in the journal Cerebral Cortex.

“Fluid intelligence is one of the most useful cognitive measures available,” said U. of I. Ph.D. candidate Aki Nikolaidis, who led the research with Ryan Larsen, a research scientist at the Beckman Institute for Advanced Science and Technology, and Beckman Institute director Arthur Kramer.

“This domain relates to an individual’s job satisfaction and salary level, among other real-world outcomes,” he said.

The researchers measured concentrations of the molecule N-acetyl aspartate, a known marker of metabolic activity in the brain, using magnetic resonance spectroscopy. Nikolaidis then looked at the relationship between NAA concentrations in different regions of the brain and fluid intelligence.

“MR spectroscopy allows us to go beyond simply imaging the structures of the brain. It allows us to image the capacity of the brain to produce energy,” Larsen said.

Previous research relating MR spectroscopy data to cognition has been inconsistent. One explanation may be that researchers fail to account for all relevant factors that relate to cognition, including brain size, in their analyses, Nikolaidis said. One goal of the current study was to address these previous contradictions.

“We wanted to do a more definitive study with a large sample size and with a higher quality methodological approach of acquiring the data,” Nikolaidis said. The researchers were able to create a more detailed map of NAA concentration in the brain than previous studies had, he said.

Image shows a girl reading a book.

The team found that NAA concentration in an area of the brain linked to motor abilities in the frontal and parietal cortices was specifically linked to fluid intelligence but not to other closely related cognitive abilities. The brain’s motor regions have a role in planning and visualizing movements as well as carrying them out, Nikolaidis said. Mental visualization is a key element of fluid intelligence, he said.

The researchers concluded that fluid intelligence depends on brain metabolism and health. While overall brain size is genetically determined and not readily changed, NAA levels and brain metabolism may respond to health interventions including diet, exercise or cognitive training, Nikolaidis said.

ABOUT THIS NEUROSCIENCE RESEARCH

Funding: This research was funded by the Office of Naval Research; Abbott Nutrition through the Center for Nutrition, Learning, and Memory at the U. of I.; and the National Science Foundation.

Source: Sarah Banducci – University of Illinois at Urbana Champaign
Image Source: The image is in the public domain.
Original Research: Abstract for “Multivariate Associations of Fluid Intelligence and NAA” by Aki Nikolaidis, Pauline L. Baniqued, Michael B. Kranz, Claire J. Scavuzzo, Aron K. Barbey, Arthur F. Kramer, and Ryan J. Larsen in Cerebral Cortex. Published online March 22 2016 doi:10.1093/cercor/bhw070


Multivariate Associations of Fluid Intelligence and NAA

Understanding the neural and metabolic correlates of fluid intelligence not only aids scientists in characterizing cognitive processes involved in intelligence, but it also offers insight into intervention methods to improve fluid intelligence. Here we use magnetic resonance spectroscopic imaging (MRSI) to measure N-acetyl aspartate (NAA), a biochemical marker of neural energy production and efficiency. We use principal components analysis (PCA) to examine how the distribution of NAA in the frontal and parietal lobes relates to fluid intelligence. We find that a left lateralized frontal-parietal component predicts fluid intelligence, and it does so independently of brain size, another significant predictor of fluid intelligence. These results suggest that the left motor regions play a key role in the visualization and planning necessary for spatial cognition and reasoning, and we discuss these findings in the context of the Parieto-Frontal Integration Theory of intelligence.

“Multivariate Associations of Fluid Intelligence and NAA” by Aki Nikolaidis, Pauline L. Baniqued, Michael B. Kranz, Claire J. Scavuzzo, Aron K. Barbey, Arthur F. Kramer, and Ryan J. Larsen in Cerebral Cortex. Published online March 22 2016 doi:10.1093/cercor/bhw070

Researchers Discover Sandman’s Role in Sleep Control

Summary: A new study brings researchers one step closer to unlocking the mysteries of sleep.

Source: University of Oxford.

Oxford University researchers have discovered what causes a switch to flip in our brains and wake us up. The discovery, published in the journal Nature, brings us closer to understanding the mystery of sleep.

Sleep is governed by two systems—the circadian clock and the sleep homeostat. While the circadian clock is quite well understood, very little is known about the sleep homeostat.

Professor Gero Miesenböck, in whose laboratory the new research was conducted, explained: ‘The circadian clock allows us to anticipate predictable changes in our environment that are caused by the Earth’s rotation. As such, it makes sure we do our sleeping when it hurts us least, but it doesn’t speak to the mystery of why we need to sleep in the first place.

‘That explanation will likely come from understanding the second controller—called the sleep homeostat. The homeostat measures something—and we don’t know what that something is—that happens in our brains while we are awake, and when that something hits a certain ceiling, we go to sleep. The system is reset during sleep, and the cycle begins anew when we wake up.’

Image shows a dial.

The team studied the sleep homeostat in the brain of fruit flies—the animal that also provided the first insights into circadian timekeeping, some 45 years ago. Each fly has around two dozen sleep-control neurons, brain cells that are also found in other animals and believed to exist in people. These neurons convey the output of the sleep homeostat: If the neurons are electrically active, the fly is asleep, and when they are silent, the fly is awake.

To switch the neurons the team relied on a technique called optogenetics, discovered by Miesenböck in 2002, in which pulses of light are used to switch on and off the activity of brain cells. In the current work, optogenetics was used to stimulate the production of the messenger chemical dopamine.

In people, drugs that act as psychostimulants (such as cocaine) increase dopamine levels in the brain, and this effect was also seen in the flies. When the dopaminergic system was activated, the sleep-control neurons fell silent and the fly woke up. If the team stopped the dopamine delivery and waited for a while, the sleep-control neuron flipped back to the electrically active state and the fly went back to sleep.

The sleep switch is a ‘hard’ switch, meaning that it is either on or off. ‘That makes sense,’ said Miesenböck. ‘You want to be either asleep or awake but not drift through twilight states.’

Dr Diogo Pimentel, one of the two lead authors of the study, said: ‘Being able to operate the sleep switch at will has given us a chance to find out how it works.’

When sleep-control neurons are electrically active, an ion channel the researchers discovered and called Sandman is kept inside. Ion channels control the electrical impulses through which brain cells communicate. When dopamine is present, it causes Sandman to move to the outside of the cell. Sandman then effectively short-circuits the neurons and shuts them off—leading to wakefulness.

Lead author Dr Jeff Donlea said: ‘In principle, this is a device that’s similar to the thermostat on the wall of your living room. But instead of measuring temperature and turning on the heat when it is too cold, this device turns on sleep when your sleep need exceeds a set point.’

As Prof. Miesenböck explained: ‘The billion-dollar question in all of this is: what is the equivalent of temperature in this system? In other words, what does the sleep homeostat measure? If we knew the answer, we’d be one giant step closer to unraveling the mystery of sleep.’

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: University of Oxford
Image Source: This NeuroscienceNews.com image is credited to Centre for Neural Circuits and Behaviour.
Video Source: The video is credited to CNCB.
Original Research: Abstract for “Operation of a homeostatic sleep switch” by Diogo Pimentel, Jeffrey M. Donlea, Clifford B. Talbot, Seoho M. Song, Alexander J. F. Thurston and Gero Miesenböck in Nature. Published online August 3 2016 doi:10.1038/nature19055

Operation of a homeostatic sleep switch

Sleep disconnects animals from the external world, at considerable risks and costs that must be offset by a vital benefit. Insight into this mysterious benefit will come from understanding sleep homeostasis: to monitor sleep need, an internal bookkeeper must track physiological changes that are linked to the core function of sleep. In Drosophila, a crucial component of the machinery for sleep homeostasis is a cluster of neurons innervating the dorsal fan-shaped body (dFB) of the central complex. Artificial activation of these cells induces sleep, whereas reductions in excitability cause insomnia. dFB neurons in sleep-deprived flies tend to be electrically active, with high input resistances and long membrane time constants, while neurons in rested flies tend to be electrically silent3.

Correlative evidence thus supports the simple view that homeostatic sleep control works by switching sleep-promoting neurons between active and quiescent states3. Here we demonstrate state switching by dFB neurons, identify dopamine as a neuromodulator that operates the switch, and delineate the switching mechanism. Arousing dopamine caused transient hyperpolarization of dFB neurons within tens of milliseconds and lasting excitability suppression within minutes. Both effects were transduced by Dop1R2 receptors and mediated by potassium conductances. The switch to electrical silence involved the downregulation of voltage-gated A-type currents carried by Shaker and Shab, and the upregulation of voltage-independent leak currents through a two-pore-domain potassium channel that we term Sandman.

Sandman is encoded by the CG8713 gene and translocates to the plasma membrane in response to dopamine. dFB-restricted interference with the expression of Shaker or Sandman decreased or increased sleep, respectively, by slowing the repetitive discharge of dFB neurons in the ON state or blocking their entry into the OFF state. Biophysical changes in a small population of neurons are thus linked to the control of sleep–wake state.

“Operation of a homeostatic sleep switch” by Diogo Pimentel, Jeffrey M. Donlea, Clifford B. Talbot, Seoho M. Song, Alexander J. F. Thurston and Gero Miesenböck in Nature. Published online August 3 2016 doi:10.1038/nature19055


Potassium and Sleep

The featured article by LiveScience 1 highlights three nutrients tied to three common sleep problems. To this, I would add melatonin, which is both a hormone and an antioxidant: Magnesium deficiency can cause insomnia. Lack of potassium can lead to difficulty staying asleep throughout the night.

Potassium Rich Foods

1) Avocado
1 whole: 1068 mg (30% DV)

2) Spinach
1 cup: 839mg (24% DV)

3) Sweet potato
1 medium: 952 mg (27% DV)

4) Coconut Water
1 cup 600 mg (17% DV)

5) Kefir or Yogurt
1 cup: 579 mg (15% DV)

6) White Beans
½ cup: 502 mg (15% DV)

7) Banana
1 large: 422 mg (12% DV)

8) Acorn squash
1 cup: 899 mg (26% DV)

9) Dried apricots
½ cup: 755 mg (22% DV)

10) Mushrooms
1 cup: 428 mg (27% DV)