Fatty liver often starts in the gut, not in the liver. Everything your bowel absorbs flows first to the liver through one vein. A leaky gut wall, bacteria that turn sugar into fat-building fuel, and small amounts of gut-made alcohol all reach the liver before the rest of your body does.
For years I told patients with prediabetes that their A1C was “not too bad.” I checked their liver enzymes, saw numbers inside the range, and moved on. I was reading the wrong end of the pipe. By the time insulin resistance shows up on a lab report, the liver has usually been taking deliveries from the gut for years.
The video above covers Chapter 5 of The Angry Gut, “The Fatty Liver Furnace.” Ami Michelle Grimes and I wrote it for the book released September 28, 2026. Here is the part that matters if you are reversing prediabetes or type 2 diabetes. If the gut feeds the liver, what changes about the plan?
Can fatty liver start in the gut?
A single layer of cells lines your intestine, renewed every few days. That layer is all that separates a bowel full of bacteria from the portal vein, which drains straight to your liver. When it loosens, bacterial fragments ride in with your dinner.
In 35 adults with biopsy-proven fatty liver, the bowel wall leaked more than it did in 24 healthy volunteers, and bacterial overgrowth in the small bowel was more common. The leak rose with the amount of fat in the liver.1
A 2024 study looked at people with type 2 diabetes. Some had liver scarring. Fluid from their stool cut the electrical resistance of a lab-grown sheet of gut cells to 185 units. In the comparison group it was 258. The loss tracked liver stiffness at a correlation of -0.88.2 Twelve people’s samples: a strong signal, not the last word.
How does sugar become liver fat by way of the gut?
Researchers deleted, in mice, the liver enzyme believed to supply the raw material for making fat from fructose. Fructose still built fat. Gut bacteria were converting fructose into acetate, and the liver was making fat out of the acetate.3
Speed chose the route. When fructose arrived slowly, the small bowel took up much of it. A sudden load pushed it past the small bowel and down to the bacteria.3 That is animal work, yet the kitchen version is simple: the sugar in a peach and the sugar in a bottle of soda do not travel the same road. (Why fructose differs from glucose is covered here.)
This is where the food system walks into your liver. Sugar sold as a drink is cheap, shelf-stable and gone in minutes: exactly the delivery that reaches the bacteria. Nobody picked that format for your liver. It was picked for the margin.
Can your gut make alcohol if you never drink?
A little, and everyone’s does. In a study of 1,557 people, ordinary blood alcohol ran 0.01 to 0.09 mg/dL, about a thousandth of the legal driving limit. In cirrhosis and diabetes it rose to about 4.85 mg/dL.4 Far below anything you would feel, but it reaches the liver first.
What you feed the gut decides how much it brews. Stool from patients with auto-brewery syndrome, grown on simple sugars, produced up to 35 mmol/L of alcohol. Given other foods, the same bacteria stayed below 10.5
Insulin resistance also appears to slow the cleanup. Take children with fatty liver. Their fasting blood alcohol was higher than in children without it. It climbed with insulin resistance. Yet diet and bacterial overgrowth were the same in both groups.6
Is insulin resistance the cause of fatty liver or the result?
Both, which is why it is so hard to break. Insulin resistance changes how the liver handles what the gut sends. A liver loaded with fat and bacterial alarm signals then joins the inflammatory crosstalk. That crosstalk keeps insulin resistance going. It is the loop described in metabolic inflammation as a cause of insulin resistance.
Waist size and weight matter in that loop, and we measure them. But body fat and a leaking bowel are not rival explanations. They are the same terrain seen from two rooms.
Why do my liver tests look normal?
Two blind spots. An ordinary ultrasound cannot see liver fat until it fills more than 30% of liver cells, so early disease looks normal on the scan.7 And blood drawn from your arm has already been through the liver’s filter.
One enzyme on your panel, GGT, follows the fat more closely than most people are told. Look at a nationwide Korean cohort. In the lowest third of GGT, 1.6% of people had a high fatty liver index. In the highest third, 47.7% did.8 A Korean national database tracked people who already have diabetes. It recorded 222,242 deaths over a median of 8.1 years. The top quarter of GGT carried 1.57 times the risk of death from any cause, compared with the bottom quarter.9 A GGT creeping upward inside the normal range deserves a question.
Will a probiotic fix fatty liver?
Not on the evidence so far. In the largest trial of its kind, 104 patients took a synbiotic or a placebo. On the synbiotic, liver fat dropped from 32.3% to 28.5%. On placebo it dropped further, from 31.3% to 25.2%. Only weight loss explained the change.10 Two small randomized trials of stool transplants, with 21 and 20 patients, shifted the gut community and left liver fat where it was.11,12
That does not make the gut the wrong target. It makes a capsule a poor way to hit it. The lever is what you send down the pipe, and when.
What does this mean for reversing insulin resistance?
It moves the work upstream, to the table:
- Keep sugar inside its food. Fructose in whole fruit arrives slowly. Fructose in a drink arrives as a flood that reaches the bacteria. Liquid sugar goes first.
- Eat on a rhythm. Gut bacteria keep time with your meals. When that rhythm broke, the disordered community made germ-free mice glucose intolerant and obese.13 A steady daily eating window is part of the treatment; see you are already intermittent fasting.
- Ask about choline. In a supervised study, some healthy women developed fatty liver on a low-choline diet. It went away when choline came back. Typical American intake sits near half the recommended amount: a median of 284 mg a day against 550 mg.14 That is a diet talk with your physician, not a supplement to buy.
- Track the trend. Collect every GGT result you have ever had. Five readings over ten years tell you more than one.
If you take glucose-lowering medication, make these changes with your prescriber involved. As your body answers insulin better, a dose that was right can become too strong.
Doing nothing costs you a liver that keeps taking deliveries a standard panel cannot see while your A1C drifts. Acting protects the organ that stands between your gut and everything downstream of it.
Reverse Diabetes MD sees patients at 4477 Woodson Rd, Suite 209, St. Louis, MO 63134. The chapter’s free technical supplement is at theangrygut.com, and the practice’s approach is on the type 2 diabetes page.
Frequently asked questions
What is MASLD, and is it the same as fatty liver?
MASLD stands for metabolic dysfunction-associated steatotic liver disease. It is the current name for what used to be called nonalcoholic fatty liver disease. The definition needs two things. You need fat in the liver. You also need at least one of five heart-and-metabolic risk factors. The name was set by 236 panelists from 56 countries.15
Should I get a leaky gut test?
Be careful with zonulin. When researchers checked the common commercial zonulin kit in 376 people, it did not detect the protein it claims to measure.16 Ask any gut test which molecule it detects, and what it was validated against.
Does “nonalcoholic” mean alcohol plays no part?
No. Gut-made alcohol reaches the liver in people who never drink. A study looked at 122 people who had liver biopsies. Some drank, but below the level that defines alcohol-related disease. That drinking was tied to the same bacterial bile acid shift seen in fatty liver.17
Related reading
Sources
- Miele L, et al. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Hepatology. 2009;49(6):1877-1887. doi:10.1002/hep.22848
- Forlano R, et al. Disruption of gut barrier integrity and host-microbiome interactions underlie MASLD severity in patients with type-2 diabetes mellitus. Gut Microbes. 2024;16(1):2304157. doi:10.1080/19490976.2024.2304157
- Zhao S, et al. Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. Nature. 2020;579(7800):586-591. doi:10.1038/s41586-020-2101-7
- Stamation R. Endogenous ethanol production in the human alimentary tract: A literature review. Journal of Gastroenterology and Hepatology. 2025;40(4):783-790. doi:10.1111/jgh.16869
- Xue G, et al. Three Klebsiella species as potential pathobionts generating endogenous ethanol in a clinical cohort of patients with auto-brewery syndrome: A case control study. EBioMedicine. 2023;91:104560. doi:10.1016/j.ebiom.2023.104560
- Engstler AJ, et al. Insulin resistance alters hepatic ethanol metabolism: Studies in mice and children with non-alcoholic fatty liver disease. Gut. 2016;65(9):1564-1571. doi:10.1136/gutjnl-2014-308379
- Newsome PN, et al. Guidelines on the management of abnormal liver blood tests. Gut. 2018;67(1):6-19. doi:10.1136/gutjnl-2017-314924
- Cho EJ, et al. Gamma-glutamyl transferase and risk of all-cause and disease-specific mortality: a nationwide cohort study. Scientific Reports. 2023;13(1):1751. doi:10.1038/s41598-022-25970-0
- Chung GE, et al. Gamma-glutamyl transferase and the risk of all-cause and disease-specific mortality in patients with diabetes: A nationwide cohort study. Journal of Diabetes. 2024;16(5):e13551. doi:10.1111/1753-0407.13551
- Scorletti E, et al. Synbiotics alter fecal microbiomes, but not liver fat or fibrosis, in a randomized trial of patients with nonalcoholic fatty liver disease. Gastroenterology. 2020;158(6):1597-1610.e7. doi:10.1053/j.gastro.2020.01.031
- Craven L, et al. Allogenic fecal microbiota transplantation in patients with nonalcoholic fatty liver disease improves abnormal small intestinal permeability: A randomized control trial. American Journal of Gastroenterology. 2020;115(7):1055-1065. doi:10.14309/ajg.0000000000000661
- Groenewegen B, et al. Consecutive fecal microbiota transplantation for metabolic dysfunction-associated steatotic liver disease: A randomized controlled trial. Gut Microbes. 2025;17(1):2541035. doi:10.1080/19490976.2025.2541035
- Thaiss CA, et al. Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. Cell. 2014;159(3):514-529. doi:10.1016/j.cell.2014.09.048
- Spencer MD, et al. Association between composition of the human gastrointestinal microbiome and development of fatty liver with choline deficiency. Gastroenterology. 2011;140(3):976-986. doi:10.1053/j.gastro.2010.11.049
- Rinella ME, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology. 2023;78(6):1966-1986. doi:10.1097/HEP.0000000000000520
- Scheffler L, et al. Widely used commercial ELISA does not detect precursor of haptoglobin2, but recognizes properdin as a potential second member of the zonulin family. Frontiers in Endocrinology. 2018;9:22. doi:10.3389/fendo.2018.00022
- Adams LA, et al. Bile acids associate with specific gut microbiota, low-level alcohol consumption and liver fibrosis in patients with non-alcoholic fatty liver disease. Liver International. 2020;40(6):1356-1365. doi:10.1111/liv.14453
- Padda GS, and Grimes AM. The Angry Gut: The First Brain: Older Than Thought, and Still in Charge. Chapter 5, “The Fatty Liver Furnace,” and its technical supplement. Nectar Media Group; 2026.
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed September 28, 2026
The bedtime psyllium trick for gut irritation is one tablespoon of psyllium fiber dissolved in a large glass of warm water. Take it about 30 minutes before bed.
Many people carry gut irritation and leaky gut. The thing that helps most is cheaper than anything in the supplement aisle.
How do you take psyllium husk before bed?
Psyllium fiber dissolved in a large glass of warm water, about 30 minutes before bed. Start with one tablespoon. Some people work up to two. Some do none at all and are fine — this is a dial, not a prescription.
What else should you change for gut irritation?
If you use a creamer, use a full-fat one — whole milk or actual cream — rather than a dried powdered creamer. And no caffeine after 3pm.
None of this is dramatic. It is the kind of change that shows up over weeks in how your gut behaves overnight.
Frequently asked questions
Is psyllium husk before bed okay?
Yes. This routine is built around bedtime: one tablespoon of psyllium fiber dissolved in a large glass of warm water, taken about 30 minutes before bed. A lot of people carry gut irritation and leaky gut, and this is the thing that helps most. It also costs less than anything in the supplement aisle.
Is 2 tablespoons of psyllium husk too much?
Start with one tablespoon. Some people work up to two, and some take none at all and are fine. Treat the amount as a dial, not a prescription. Begin with one tablespoon in a large glass of warm water about 30 minutes before bed, and adjust from there as you see how your gut responds.
Is it okay to have psyllium husk every day?
The routine is meant as a nightly evening habit, and none of it is dramatic. It is the kind of change that shows up over weeks in how your gut behaves overnight. Pair it with two simple changes: use a full-fat creamer, such as whole milk or actual cream, instead of a dried powdered one, and have no caffeine after 3pm.
Related reading
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed September 20, 2026
Altered cholesterol metabolism in the brain may have a role in Alzheimer’s. It is a different problem from the cholesterol on your blood test. In the adult brain, support cells called astrocytes make most of the cholesterol. They deliver it to neurons on a carrier protein, apoE. When that delivery runs high, neurons make more amyloid-beta. That is the protein that builds Alzheimer’s plaques.
If you live with insulin resistance or type 2 diabetes, this is worth knowing. That is because it recasts Alzheimer’s as one more place where a broken metabolism shows up.
Is brain cholesterol the same as blood cholesterol?
No. Cholesterol does not cross freely from the bloodstream into the brain. The brain mostly makes its own, and it needs a great deal of it. A large part of the brain’s structure is cholesterol. Early in life, neurons make much of their own supply. With age, they lose much of that ability, and astrocytes take over.
Astrocytes are the most common cells in the brain. They outnumber neurons roughly five to one and cover almost the entire organ. Neurons cannot work without the support they give. Yet most talk about the brain skips them entirely (1). In the cholesterol story, they are the supplier.
How does the apoE carrier connect cholesterol to Alzheimer’s plaques?
Astrocytes load cholesterol onto apolipoprotein E, or apoE, and ship it to neurons. Gene experts have known for years that people with certain apoE variants carry a higher risk of Alzheimer’s. But no one could clearly explain why a cholesterol carrier would matter (2).
A 2021 study in PNAS offered one (3). Researchers found that more apoE meant more cholesterol reaching neurons. And more cholesterol in neurons meant more amyloid-beta. Neurons need cholesterol to make amyloid protein at all. Too much supply pushes production too high, and the excess clumps into plaques. When the researchers reduced apoE activity, less cholesterol reached the neurons and fewer plaques formed. In animal models, cutting astrocytes’ ability to make cholesterol, or to move it, had the same effect (3).
Brains of people with Alzheimer’s do show high cholesterol, which fits the picture.
Why not target amyloid directly?
Because amyloid protein is not simply waste. The brain controls how much it makes very tightly. That suggests it has normal jobs, and researchers still understand little about how neurons make it. Shutting it down directly risks results no one can predict. Turning down the cholesterol supply that drives overproduction is a more upstream target.
What does metabolic inflammation have to do with brain cholesterol?
Here the research and this practice’s view of disease meet. Over the last century, changes in how people eat and live have caused an epidemic of metabolic disorders. That includes broken cholesterol handling, and with it more heart disease and stroke. The brain is not exempt from that terrain.
There is also a second reading of the evidence. Amyloid-beta buildup may be a surrogate marker (a stand-in sign), not the root cause. Plaque may build up because local inflammation is high and the brain’s cleanup system is impaired. On that reading, astrocytes making too much cholesterol could be a reaction to underlying metabolic inflammation, not the first domino. Either way, the trail leads back to metabolism. For the mechanism behind that inflammation, see metabolic inflammation as a cause of insulin resistance and does overnutrition cause metabolic inflammation?
What should a person with insulin resistance take from this?
Three things.
- Alzheimer’s is not purely genetic bad luck. Even the best-known genetic risk factor, apoE, turns out to work through cholesterol transport. That is a metabolic process.
- A cholesterol number on a lab report does not tell you about your brain. Brain cholesterol is made and regulated locally.
- The upstream targets are the ones you can influence. Food, sleep, activity and blood sugar control shape inflammation and the metabolic state of the body. Controlling how brain cholesterol is made and moved may prove to be a key to preventing Alzheimer’s or slowing it. Lowering the metabolic inflammation that may drive it is available now.
Frequently asked questions
Do statins or a low-cholesterol diet lower brain cholesterol?
The research here is about cholesterol made inside the brain by astrocytes. The brain controls it apart from blood cholesterol. The studies did not test drugs or diets that lower cholesterol. So they do not show that lowering blood cholesterol changes brain cholesterol or Alzheimer’s risk.
If I carry a high-risk apoE gene, is Alzheimer’s certain?
No. ApoE variants raise risk. They do not decide the outcome. The newer research suggests apoE works through how much cholesterol it delivers to neurons. That places part of that risk inside a metabolic process rather than a fixed destiny.
Are type 2 diabetes and Alzheimer’s related?
They share ground. Both involve broken metabolism, and diabetes is an established risk factor for memory decline. Brain cholesterol transport is one more metabolic pathway now linked to Alzheimer’s plaques. That is why this practice treats brain health as part of reversing insulin resistance, not a separate subject.
Related reading
References
1. Sofroniew MV, Vinters HV. Astrocytes: biology and pathology. Acta Neuropathol. 2010;119(1):7-35. doi:10.1007/s00401-009-0619-8
2. Yamazaki Y, Painter MM, Bu G, Kanekiyo T. Apolipoprotein E as a Therapeutic Target in Alzheimer’s disease: A Review of Basic Research and Clinical Evidence. CNS Drugs. 2016;30(9):773-789. doi:10.1007/s40263-016-0361-4
3. Wang H, Kulas JA, Wang C, Holtzman DM, Ferris HA, Hansen SB. Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol. PNAS. 2021;118(33). doi:10.1073/pnas.2102191118
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Summary: The risk of dementia is higher in people with low socioeconomic status. Low income or financial insecurity is one of the major sources of chronic stress. A long stress response considerably raises the risk of dementia or age-related cognitive decline. Stress drives up the HPA-axis (the brain’s stress system). It raises cortisol and vasopressin. In the end that means wide metabolic changes, behavior changes, and a greater risk of cardiovascular events. All this also leads to a considerably greater risk of dementia.
Keywords: financial insecurity, dementia, cognitive decline, stress, chronic stress, cortisol, vasopressin
What raises the risk of dementia?
Dementia is now among the top 5 causes of death in the western world and the US. And as people live longer, they are also prone to cognitive decline that is not dementia. That leads to poorer quality of life and disability.
But not all adults get severe mental decline that causes disability. Genetics cannot explain most cases of severe mental decline. So researchers think it is related to lifestyle. There seem to be many factors behind a greater risk of dementia or faster cognitive decline. Low education and low income are among the leading risk factors.
Western nations are rich compared to many other parts of the world. Yet they have a higher dementia rate. So financial insecurity may appear to be the most unlikely factor behind the condition. But it is key to understand that financial insecurity is a psychological reaction. The financial insecurity people feel may be higher in certain parts of rich societies. Western nations also have a higher cost of living.
Does financial stress raise the risk of stroke and dementia?
Studies show that even minor stress from financial insecurity may raise the risk of neurological disorders (disorders of the brain and nerves). One large nationwide study in Hungary looked at 7880 cases of thrombolytic treatment (clot-busting drugs). They found that the risk of stroke was highest at the end of the month. That was due to greater financial insecurity at that time1.
The National Health and Aging Trends Study in the US found something similar. It looked at data from Medicare beneficiaries older than 65 years of age. It found that financial strain in older adults may raise the risk of dementia by 20% to 30%2.
How does financial stress lead to cognitive decline?
It appears that long-lasting financial insecurity leads to chronic stress. Chronic stress makes certain brain centers (HPA-axis) more active. That makes the pituitary gland trigger more stress hormones. So people living with chronic stress have higher levels of cortisol and vasopressin3.
Studies confirm that people diagnosed with Alzheimer’s or dementia from other causes have higher cortisol than healthy adults4.
Cortisol is a complex hormone. It may not cause any side effects in the short run. But it may cause major metabolic problems in the long run. That is why chronic stress may raise the risk of dementia.
Cortisol raises blood glucose levels. It raises the risk of insulin resistance (when cells stop answering insulin). It suppresses the immune system and boosts appetite. It also causes a wide range of behavior changes. Together these raise the risk of cognitive decline in older adults5.
Chronic stress also raises levels of vasopressin. This hormone narrows blood vessels and makes the body hold water. Higher levels may raise the risk of hypertension (high blood pressure). It also considerably raises the risk of cardiovascular diseases. This means a greater risk of stroke and cognitive decline5.
But it is key to know that cortisol and vasopressin are important hormones we need to stay healthy. In small amounts, cortisol helps the stress response. So at normal levels it does no harm. A short rise now and then is not always bad either. It is levels that stay high for months or even years that raise the risk of cognitive decline.
Financial insecurity tends to be a long-term problem. For many, it may start at a young age and may last for the rest of their life. Frequent worries and feeling insecure in the end cause metabolic disorders, unhealthy lifestyle choices, and a slow decline in thinking.
To sum up, high stress from financial insecurity is one of the factors that may speed up cognitive decline. This is most true in older adults. It means that managing stress through behavior and lifestyle changes may help lower the risk of cognitive decline and dementia.
Frequently asked questions
Can stress cause dementia?
Chronic stress raises the risk. Stress that lasts months or years keeps the HPA axis switched on. So cortisol and vasopressin stay high. Cortisol raises blood sugar and insulin resistance, suppresses the immune system and boosts appetite. Vasopressin raises blood pressure and cardiovascular risk. People with Alzheimer’s or other dementia have higher cortisol than healthy adults. Short bursts of stress are not the problem.
What are some possible causes of dementia?
Genetics cannot explain most cases of severe mental decline, which points to lifestyle. Low education and low income are among the leading risk factors. Chronic stress, including long-running money worries, adds high cortisol, insulin resistance, high blood pressure and cardiovascular disease. Each of those raises the risk of stroke and cognitive decline. In US adults over 65, financial strain raised dementia risk by 20% to 30%.
Can anxiety cause dementia?
Constant worry works through the same stress pathway. Frequent worries and feeling insecure keep cortisol and vasopressin high. This often goes on for years or starts at a young age. Over time that drives metabolic disorders, unhealthy lifestyle choices and a slow decline in thinking. Managing stress through behavior and lifestyle changes may help lower the risk of cognitive decline and dementia.
Related reading
References
1. Folyovich A, Biczó D, Bajnok A, et al. Higher Incidence of Stroke on the Last Day of the Month in Hungary—a Role for Psychosocial Factors and Financial Insecurity? Journal of Stroke and Cerebrovascular Diseases. 2016;25(5):1192-1195. doi:10.1016/j.jstrokecerebrovasdis.2016.02.010
2. Samuel LJ, Szanton SL, Wolff JL, Ornstein KA, Parker LJ, Gitlin LN. Socioeconomic disparities in six-year incident dementia in a nationally representative cohort of US older adults: an examination of financial resources. BMC Geriatrics. 2020;20(1):156. doi:10.1186/s12877-020-01553-4
3. Magri F, Cravello L, Barili L, et al. Stress and dementia: the role of the hypothalamic-pituitary-adrenal axis. Aging Clin Exp Res. 2006;18(2):167-170. doi:10.1007/BF03327435
4. Ouanes S, Popp J. High Cortisol and the Risk of Dementia and Alzheimer’s Disease: A Review of the Literature. Frontiers in Aging Neuroscience. 2019;11:43. doi:10.3389/fnagi.2019.00043
5. Lee DY, Kim E, Choi MH. Technical and clinical aspects of cortisol as a biochemical marker of chronic stress. BMB Rep. 2015;48(4):209-216. doi:10.5483/BMBRep.2015.48.4.275
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Linoleic acid, the main omega-6 fat in vegetable oils such as soybean oil, drives abdominal obesity more than total fat does. In mice, an 8% linoleic acid diet caused severe abdominal obesity on medium- and high-fat diets alike. Adding omega-3 (EPA and DHA) prevented it.
Summary: Eating less total fat did not considerably cut the rate of abdominal fat buildup, and obesity has gone up. Studies suggest this rise is due more to eating more linoleic acid (LA), an omega-6 fatty acid. It happened as people switched from animal fats to eating more vegetable oils. That switch also meant less omega-3 in the diet. Experimental studies confirm that eating less LA may considerably help lower the risk of obesity. Adding omega-3 to the diet may bring an extra benefit by countering the harmful effects of LA. That would help lower obesity rates.
Keywords: linoleic acid (LA), omega-6 fatty acids, omega-3 fatty acids, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), endocannabinoid system
Do vegetable oils cause obesity?
New experimental data indicate that a high intake of omega-6 and a fairly low intake of omega-3 have more to do with obesity than total fat intake does. The same goes for buildup of visceral fat (fat packed around the organs) and insulin resistance (when cells stop answering insulin). Correcting the omega-6: omega-3 ratio in the diet may be the key to countering obesity.
Abdominal obesity has grown at an alarming rate in the last 40-50 years in the US. Historical data shows that in men, it rose from 12.7% to 38.3%. In women, it grew from 19.4% to almost 60% between 1960 and 2000. This tripling of abdominal obesity is hard to explain by the total fat in the diet alone1.
Researchers think the rise in abdominal obesity has more to do with the quality of the fats people eat. Some researchers suggest that humans evolved to eat omega-6 and omega-3 fatty acids in almost equal amounts. But in the modern diet, the ratio runs from ~10:1 to 25:1. That’s a severe imbalance2.
If that is the case, correcting the omega-6 to omega-3 ratio may solve much of the obesity problem. That means eating more omega-3 and less omega-6. But before making any firm recommendation, there has to be strong evidence for the theory.
Researchers think some evidence comes from tracking how diets changed over history. For example, data shows that omega-6 intake rose sharply from 1900 onwards. That is when people in the western world switched from butter or lard to more vegetable oils, like soybean oil. This brought a two-fold increase in linoleic acid (LA), the main omega-6 fatty acid in vegetable oils. It now makes up 8 to 10% of total calorie intake3.
A systematic review of studies further supports this. It indicates that LA content in subcutaneous tissues (the fat under the skin) in the US has gone up 2.5 times.
Can cutting omega-6 or adding omega-3 prevent obesity?
Researchers ran lab experiments in mice to understand the effect of LA on obesity. They also wanted to learn more about the role of a high-fat diet4.
Firstly, they split mice into two groups. One was fed a medium-fat diet (35% of total calorie intake). The other got a high-fat diet (65% of the total calorie intake). They split the mice into two groups again. One was fed a diet with 1% LA and the other an 8% LA diet. That means 1% and 8% of energy came from LA.
Interestingly, they found that eating more fat was not much related to obesity. There was not much difference between the 1% LA groups on the medium-fat and high-fat diets.
But there was a clear and high association between obesity and high LA intake, no matter the total fat intake. Thus, the 8% LA mice on both the medium-fat and high-fat diets developed severe abdominal obesity.
Next, they wanted to understand the role of omega-3 fatty acids in the diet. So they added omega-3 (eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA)) to the diet of the mice in the 8% LA group.
They found that a diet rich in omega-3 may help prevent obesity and so metabolic disorders. To their surprise, omega-3 could help control obesity in mice on an 8% LA diet. Total fat in the diet did not have much impact on it. So omega-3 fatty acids prevented fat buildup in the 8% LA and medium-fat diet group. They did the same in the 8% LA and high-fat diet group.
It confirmed the following things:
• LA is the primary cause of abdominal obesity, on a low fat or a high-fat diet. So LA intake needs to be limited.
• Eating a diet rich in omega-3 fatty acids (EPA+DHA) may help counter the obesity-causing effects of LA.
How does linoleic acid cause weight gain?
Researchers think this power of LA to cause obesity can be explained by changes inside cells from eating a lot of LA. It mainly stimulates the endocannabinoid system (a body signaling system). That leads to impaired fat storage and changes in behavior and appetite. So it raises the risk of obesity.
Total calorie intake counts. But perhaps how many calories the body gets from fat matters less. Even a high-fat diet will not cause obesity if it is low in LA-containing fats. And adding omega-3 fatty acids rich in EPA and DHA may help counter these obesity-causing effects of LA.
Frequently asked questions
Are seed oils bad for you?
Yes, at the levels Americans now eat them. Linoleic acid, the main omega-6 fat in vegetable oils such as soybean oil, drives abdominal obesity more than total fat does. In mice, an 8% linoleic acid diet caused severe abdominal obesity on both medium- and high-fat diets, whatever the total fat. Linoleic acid now supplies 8 to 10% of total calories.
Why is everyone suddenly against seed oils?
Because the timing fits. From 1900 on, people in the western world swapped butter and lard for vegetable oils like soybean oil. That doubled linoleic acid intake and lowered omega-3. Between 1960 and 2000, abdominal obesity rose from 12.7% to 38.3% in men and from 19.4% to almost 60% in women. Total fat alone does not explain that jump.
Should I stop using seed oils?
Yes. Cut them out. Cutting linoleic acid is the main lever this research points to. That is because even a high-fat diet did not cause obesity when it was low in linoleic acid. Adding omega-3 fats, EPA and DHA, helps counter what omega-6 does. Our ancestors ate omega-6 and omega-3 in roughly equal amounts. The modern diet runs from about 10:1 to 25:1.
References
1. Okosun IS, Chandra KMD, Boev A, et al. Abdominal adiposity in US adults: prevalence and trends, 1960–2000. Preventive Medicine. 2004;39(1):197-206. doi:10.1016/j.ypmed.2004.01.023
2. Simopoulos AP. Evolutionary Aspects of the Dietary Omega-6/Omega-3 Fatty Acid Ratio: Medical Implications. In: Alvergne A, Jenkinson C, Faurie C, eds. Evolutionary Thinking in Medicine: From Research to Policy and Practice. Advances in the Evolutionary Analysis of Human Behaviour. Springer International Publishing; 2016:119-134. doi:10.1007/978-3-319-29716-3_9
3. DiNicolantonio JJ, O’Keefe JH. Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart. 2018;5(2):e000898. doi:10.1136/openhrt-2018-000898
4. Alvheim AR, Malde MK, Osei-Hyiaman D, et al. Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity (Silver Spring). 2012;20(10):1984-1994. doi:10.1038/oby.2012.38
Related reading
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
A two-hour glucose tolerance test can flag future memory decline years before it shows. A Finnish study followed 961 adults aged 45 to 74. The higher their blood sugar two hours after a glucose drink, the more their recall of new information slipped over the next decade. This held even after other risk factors were accounted for.
That makes the two-hour number more than a diabetes label. It reads how well your body clears a sugar load, and the brain appears to keep score.
Why the two-hour reading catches what a fasting test misses
A fasting glucose test shows where your blood sugar sits after a night without food. It says little about what happens after a meal. In early insulin resistance, the pancreas makes up for it by pouring out extra insulin. So fasting sugar can stay normal for years, while every meal produces a long, high spike.
The oral glucose tolerance test (OGTT) exposes that gap. You drink a measured glucose solution, and your blood sugar is checked two hours later. The American Diabetes Association reads the result this way (3):
- Under 140 mg/dL: outside the prediabetes and diabetes ranges.
- 140 to 199 mg/dL: prediabetes.
- 200 mg/dL or higher: diabetes.
The OGTT measures the response to a load rather than a resting value. Because of that, it is particularly good at finding diabetes early. It is also good at settling the question when a fasting test is borderline.
What did the Finnish glucose tolerance study find?
The researchers drew on the Health 2000 Survey, a national Finnish population study, and its 2011 follow-up (2). Between 2001 and 2002, 961 middle-aged and older adults took an OGTT. Their average age was about 56, and a little over half of them were women. They also did memory and language tests. They named words in a category, learned a word list, and recalled that list after a delay. About 10 years later they repeated the tests.
A higher two-hour glucose value at the start predicted a worse score on delayed word recall a decade later. It also predicted a steeper drop in that score over the 10 years. Delayed recall measures episodic memory. This is the memory for specific events and new information: what you were told at the doctor’s office, where you parked, the date of a graduation or a wedding. The link held after the analysis adjusted for risk factors already known for cognitive decline (2).
Does a high glucose tolerance result mean Alzheimer’s is coming?
No. The study measured memory decline, not dementia diagnoses. It did not track who went on to develop Alzheimer’s disease. Diabetes is an established risk factor for poorer memory later in life. But that is not the same as a diagnosis of dementia (4). Whether a poor OGTT in midlife predicts Alzheimer’s itself still needs longer follow-up.
What the study does establish is useful on its own. A routine, low-cost test given in midlife carries information about the brain ten years out.
How could post-meal sugar spikes damage memory?
Think of the two-hour value as a stress test for your metabolism. Some bodies cannot clear a glucose drink in two hours. Such a body is running high insulin and repeated sugar surges through every meal, every day. The brain’s memory centers are among the most energy-hungry tissues in the body. And they sit downstream of that same blood supply.
The Diabetes Care study was not designed to prove a mechanism. But the direction of the finding fits what this practice sees in the clinic: insulin resistance is not a blood sugar problem with side effects; it is a whole-body problem, and the brain is part of the body. For the background, see what exactly is insulin resistance and insulin resistance and hyperinsulinemia: the actual disease.
Can memory decline from insulin resistance be prevented?
Much of it, if it is caught early. The CDC notes that dementia is not a normal part of aging. It also notes that a substantial share of cases, around 40%, may be delayed or prevented by addressing risk factors that can be changed (1). Diabetes, depression and smoking are among them.
That is the practical value of a two-hour result above 140 mg/dL in your 40s or 50s. It gives you a decade or more of lead time. Steps that improve how your body handles glucose are the same steps that protect the brain. They are bringing post-meal sugar down, quitting smoking, staying physically active and getting enough sleep. Food choices matter most for the post-meal spike. Start with foods that improve insulin sensitivity.
Frequently asked questions
Should I ask my doctor for a glucose tolerance test if my fasting sugar is normal?
It is a reasonable request if you have risk factors. These include extra weight around the belly, a family history of type 2 diabetes, high triglycerides or a history of gestational diabetes. A normal fasting glucose can hide years of insulin resistance. In the Finnish study, the two-hour value was the reading that tracked with memory decline a decade later.
How should I prepare for a two-hour glucose tolerance test?
You come in fasting and drink a measured glucose solution. Then you stay put until blood is drawn two hours later. Follow your clinic’s instructions on how long to fast and which medications to take that morning. Plan for the wait.
Is forgetfulness a sign of high blood sugar?
Not on its own; some forgetfulness comes with age. But diabetes is a known risk factor for poorer memory later in life. In the Finnish study, higher two-hour glucose predicted greater loss of episodic memory over 10 years. If forgetfulness comes with weight gain around the middle, fatigue after meals or rising blood sugar, get your metabolism checked.
Related reading
References
1. Centers for Disease Control and Prevention. The Truth About Aging and Dementia. Published September 8, 2021. Accessed October 2, 2021. https://www.cdc.gov/aging/publications/features/dementia-not-normal-aging.html
2. Toppala S, Ekblad LL, Viitanen M, Rinne JO, Jula A. Oral Glucose Tolerance Test Predicts Episodic Memory Decline: A 10-Year Population-Based Follow-up Study. Diabetes Care. 2021;44(10):2435-2437. doi:10.2337/dc21-0042
3. American Diabetes Association. Diagnosis. Accessed October 2, 2021. https://www.diabetes.org/a1c/diagnosis
4. Arvanitakis Z, Tatavarthy M, Bennett DA. The Relation of Diabetes to Memory Function. Curr Neurol Neurosci Rep. 2020;20(12):64. doi:10.1007/s11910-020-01085-9
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Important Points:
- Weight Loss
- Benefits
- Diabetes
- Cancer
- Pain
- Cognitive function
What are the health benefits of losing weight?
Losing weight lowers blood pressure, strengthens the heart and reduces your cancer risk. Losing just 5 to 7 percent of body weight delays the onset of type 2 diabetes. It also improves mood, memory, fertility, sexual function, skin, and joint and back pain.
1. It will improve your cognitive function
Losing weight is not just a physical change. It can also affect the way a person thinks. A study published in The Journal of Clinical Endocrinology & Metabolism found that intentional weight loss improves verbal memory, verbal fluency, executive function (planning and self-control), and global cognition (overall thinking). If you feel you need help in this area, losing weight would give you a boost.
2. It helps with your mood
Losing weight through exercise not only makes you healthier. It can also make you happier. According to the Journal of Clinical Psychiatry, exercise can help mental health by reducing anxiety, depression, and negative mood. It can also improve self-esteem.
3. It can improve your sex life.
A study published in the journal Obesity showed that people with obesity are more prone to erectile dysfunction. It has also been reported that the quality of sex is lower in people with obesity than in people without a weight problem. So with regular exercise and weight loss, penile function will improve. You can get back a satisfying sex life.
4. It can increase reproductive functioning.
Losing weight can help improve fertility in women, especially those with polycystic ovary syndrome or PCOS. In men, weight loss helps improve semen health, which raises the chances of having a child.
5. You sweat less
Body fat acts as a natural insulator. So losing weight through losing body fat will keep you feeling cooler and make you less likely to sweat.
6. Your blood pressure will become lower
As little as a loss of ten pounds can bring a person’s blood pressure back to normal. The effect is so strong that weight loss is recommended along with medication in treating hypertension (high blood pressure).
7. It strengthens the heart
Losing weight makes it easier for your heart to pump blood through the body, while exercise strengthens your heart muscles. Losing weight is generally better for your cardiovascular health.
8. It prevents Type 2 Diabetes
According to the National Institute of Diabetes and Digestive and Kidney Diseases, losing just 5 to 7 percent of your body weight delays the onset of type 2 diabetes.
9. It helps prevent cancer
Obesity is a risk factor for many forms of cancer, from breast to colorectal cancer. Losing weight removes this risk factor. That lowers your risk of developing cancer.
10. It is good for the kidneys.
Because losing weight can reduce high blood pressure, it prevents renal (kidney) damage and kidney diseases. Losing weight also prevents diabetes, a common cause of kidney failure. That gives you two great perks of losing weight.
11. It prevents pancreatitis and pancreatic stones.
Obesity is associated with a higher risk of pancreatitis and gallstones. Both are surgical risks and can cause a person a lot of pain. By losing weight, you lower the chance that stones will form and keep your pancreas in tip-top shape.
12. Your skin will be clearer
Psoriasis is a chronic inflammatory skin disease closely associated with obesity. Keeping a normal weight has been shown to lessen how severe psoriasis is and how often it flares up. Psoriasis aside, people who are obese are generally more prone to skin problems than those with normal weight.
13. It improves oral health
Losing weight has been correlated with fewer inflammatory gum conditions, and so with better oral health.
14. It helps with body pain
Being overweight puts extra work on your joints. This leads to joint pain and inflammation. Losing weight lightens the load on your knees and back, which helps ease joint pain.
15. It improves your nail health
A study published in the journal Nutrients found that obesity has been strongly linked to iron deficiency anemia. This type of anemia can wreak havoc on your nails and make them brittle and fragile.
Cognitive Effects of Intentional Weight Loss in Elderly Obese Individuals With Mild Cognitive Impairment
https://academic.oup.com/jcem/article/101/3/1104/2804876
Exercise for Mental Health
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470658/
Sexual Functioning and Obesity: A Review
https://onlinelibrary.wiley.com/doi/full/10.1038/oby.2012.104
Sexual Quality of Life Lower for the Obese
https://corporate.dukehealth.org/NEWS-LISTING/SEXUAL-QUALITY-LIFE-LOWER-OBESE
Weight loss before fertility treatment may improve pregnancy odds for women with PCOS
Your Guide To Lowering Blood Pressure
https://www.nhlbi.nih.gov/files/docs/public/heart/hbp_low.pdf
Health Risks of Being Overweight
https://www.niddk.nih.gov/health-information/weight-management/health-risks-overweight
Obesity and Cancer
https://www.cancer.gov/ABOUT-CANCER/CAUSES-PREVENTION/RISK/OBESITY/OBESITY-FACT-SHEET
Obesity and pancreatitis.
https://www.ncbi.nlm.nih.gov/pubmed/28719397
Psoriasis and Obesity.
https://www.ncbi.nlm.nih.gov/pubmed/28226326
Skin problems in people with obesity
https://journals.rcni.com/DOI/ABS/10.7748/NS2004.05.18.35.38.C3609
Obesity and oral health–is there an association?
https://www.ncbi.nlm.nih.gov/pubmed/23213928
Obesity as an Emerging Risk Factor for Iron Deficiency
http://www.mdpi.com/2072-6643/6/9/3587
Related reading
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Important Points:
- Parkinson’s disease
- Gut bacteria
- Gastrointestinal
What role does gut bacteria play in Parkinson’s disease?
Gut bacteria are tied to how the brain functions in Parkinson’s disease. In a California Institute of Technology study, stool from Parkinson’s patients was transplanted into sterile mice, and it produced the disease’s symptoms. Researchers point to alpha-synuclein, a protein found in both the gut and the brain, as the link.
Parkinson’s disease is a progressive neurologic disorder marked by tremors and stiff muscles. It affects more than 10 million people worldwide. Almost 200 years have passed since Parkinson’s disease was first identified as an observable medical condition. Yet today, we still do not know the exact cause of this disabling condition.
However, we have made some progress in identifying some risk factors associated with Parkinson’s. In a recent study published by the California Institute of Technology, researchers identified a new possible cause of Parkinson’s disease. They found a link between gut bacteria and how the brain functions.
Researchers took stool samples from patients with Parkinson’s disease and transplanted them into sterile mice. This produced the symptoms of the disease in a previously healthy subject. Researchers hypothesize that this may be due to a protein called alpha-synuclein (αSyn). This protein is present in both the brain and the gut of patients with Parkinson’s disease. It may play a key role in the development of the disease.
This study seems to confirm what other researchers noticed long ago. Gut problems have always been associated with Parkinson’s. Constipation, ulcers, and bloating are significantly more frequent in people with the disease. This points to a bigger role for gut problems in the disease pathophysiology (how the disease works in the body). In fact, a previous study looked at people who had their vagus nerve severed as treatment for a gastric ulcer. It showed they had a lower chance of developing Parkinson’s. This is not that surprising, since 70 percent of the peripheral nervous system innervates (supplies nerves to) the gut. With this in mind, the nervous system and the gastrointestinal system may not be as far apart as we first thought. Evidence of their strong link keeps mounting. So understanding this relationship has now sparked a lot of interest.
The research is promising, but there is still a lot of work to be done. Mice experiments may not translate to human test subjects, but the researchers are optimistic. Hopefully, once this hypothesis is proven and better understood, it will pave the way for more effective treatments for Parkinson’s disease. These treatments would aim at modifying gut bacteria instead of being directed at the brain.
Statistics on Parkinson’s
http://www.pdf.org/en/parkinson_statistics
Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease
http://www.cell.com/cell/fulltext/S0092-8674(16)31590-2
Parkinson’s disease may start in the Stomach
http://sciencenordic.com/parkinsons-disease-may-start-stomach
Related reading
- Can Probiotics Treat GI Conditions?
- How Gut Bacteria Affect Brain Health
- Brain Cholesterol and Alzheimer’s
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Important Points:
- Walking
- Exercise
- Endorphins
- Cardiovascular health
What are the benefits of walking?
Walking protects the heart, increases blood flow to the brain, relieves stress and lifts mood. Walking for as little as 15 minutes after a meal also produces smaller blood sugar spikes.
Few physical activities can be as easy and as natural as walking. It is simple and easy to access. And walking has been shown to have benefits you can use to help improve your health. Here are a few benefits you can gain by walking for as little as 30 minutes per day.
- It helps improve cardiovascular health
Anyone who cares about their health knows by now that exercise is a key to a healthy heart. But did you know that as little as 30 minutes of walking a day can reduce a person’s chance of dying of cardiovascular disease by as much as 24 percent? This comes from a study published in the journal Clinical Epidemiology. It shows that even low-impact exercise can contribute greatly to cardiovascular health.
- It increases blood flow to the brain
In a study presented at the Experimental Biology meeting, researchers found that walking does your body good not only through its cardiovascular and muscle benefits but also through its brain benefits. Walking has been proven to increase blood flow to the brain. That explains why walking helps people who feel sluggish feel energized. So whenever you feel dull or listless, give walking a shot. It might help.
- It is a natural stress reliever and mood elevator
A study from the University of Michigan found that group walking helps lower symptoms of depression. It also helps people cope with stress and improves overall mental health and well-being. This might be related to the fact that exercise helps our body release endorphins, which lift mood naturally.
- Walking helps regulate blood sugar levels
In one small study published by the American Diabetes Association, some people walked for as little as 15 minutes after a meal. They had smaller blood sugar spikes than those who did not walk. This lowers the risk of heart disease, kidney disease and other complications tied to diabetes.
Frequently asked questions
How long should you walk each day?
Thirty minutes a day is enough to make a difference. A study in the journal Clinical Epidemiology linked as little as 30 minutes of daily walking to as much as a 24 percent lower chance of dying from cardiovascular disease. For blood sugar, even 15 minutes of walking after a meal helps.
Does walking after eating lower blood sugar?
Yes. A small study published by the American Diabetes Association looked at walking after meals. Walking for as little as 15 minutes after a meal produced smaller blood sugar spikes than not walking. Smaller spikes lower the risk of heart disease, kidney disease and the other complications that come with diabetes.
How does walking improve your mood?
Exercise helps your body release endorphins, which lift mood naturally. A University of Michigan study found that group walking lowered symptoms of depression. It also improved coping with stress and boosted overall mental health and well-being. Walking also increases blood flow to the brain. That is why a walk helps people who feel sluggish feel energized.
Related reading
- What Is Cotton-Mouth and Why Does It Happen?
- Health Benefits of Losing Weight
- How Gut Bacteria Affect Brain Health
- What Are Psychobiotics? Gut Bacteria, Mood and Blood Sugar
- Vagus Nerve Stimulation Benefits
Sources
Replacing sedentary time with physical activity: a 15-year follow-up of mortality in a national cohort
How walking benefits the brain
https://www.sciencedaily.com/releases/2017/04/170424141340.htm
Walking off depression and beating stress outdoors? Nature group walks linked to improved mental health
Three 15-min Bouts of Moderate Postmeal Walking Significantly Improves 24-h Glycemic Control in Older People at Risk for Impaired Glucose Tolerance
http://care.diabetesjournals.org/content/36/10/3262
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Important Points:
- Vagus nerve
- Stimulation
- Nervous system
- Anxiety
What are the benefits of Vagus Nerve Stimulation?
Vagus nerve stimulation calms the body. It lowers heart rate and blood pressure, relaxes muscles, improves mood and tones down inflammation. It has also been used to treat anxiety disorders and depression.
Feeling tense? Do you often feel stressed out by today’s hectic, fast-paced life? If you are like most people, your answer is most likely yes. Oddly enough, you do not need to look very far for a solution. Your own body has a built-in way of handling stress, and there is a secret to using it.
Our nervous system is split into two working parts: the sympathetic and the parasympathetic. The sympathetic nervous system is the excitatory (revving-up) part. Its main job is to trigger the body’s fight-or-flight response. An overactive sympathetic nervous system could leave you restless and always stressed. To balance things out, the parasympathetic nervous system runs the body’s restoring functions, like resting and digesting. This is the system we need to tap into to relax.
The key lies in hijacking the powerful function of the vagus nerve. The word vagus shares its origin with the word vague. Both come from the Latin root that means wandering. Why? The vagus nerve was named that way because it controls a wide range of organs in the body. Think of it as the boss of the eyes, mouth, heart, lungs, stomach, and gut when it comes to letting loose and relaxing. A second reason the vagus nerve is powerful is its direct link to our control center, the brain. It uses 80 percent of its nerve conduction to carry information from the body to the brain.
There are a number of ways to stimulate the vagus nerve. Deep breathing and yoga are known for their calming effect. That is because stretching out the lungs and chest muscles stimulates the vagus nerve.
Meditation is another method worth exploring. A study published in the International Journal of Yoga found that chanting the sound “Om” stimulates the vagus nerve. A new way to stimulate the vagus nerve is to grow a healthy gut microbiota (the bacteria living in your gut). The study from Arizona State University suggests that taking a probiotic containing Lactobacillus casei boosts vagal stimulation. This improved mood in those who took part in the study.
When the vagus nerve is stimulated on purpose, it has a deep therapeutic effect on our health. Vagal stimulation can decrease heart rate, lower blood pressure, relax muscles, improve mood and even tone down inflammation. A study published in the journal Science found that vagal stimulation suppresses the inflammatory response that starts in the spleen.
Anxiety raises blood pressure and pulse rate. Vagal stimulation lowers both. That is why it has been used to treat anxiety disorders with significant success. A study by the Department of Psychiatry of the Medical University of South Carolina looked at people with anxiety. It found that vagal stimulation produced not only acute (short-term) but also long-term improvement.
The effects of vagal stimulation go beyond calming an overactive nervous system. It has also worked in treating depression. Depression shows up as a lack of motivation and excitement. The China Academy of Chinese Medical Sciences saw significant improvement in people with depressive symptoms just by stimulating the vagus nerve.
So next time you feel burned out and could use some rest and relaxation, do not forget to give vagus nerve stimulation a try.
Frequently asked questions
How can you stimulate your vagus nerve naturally?
Deep breathing and yoga work because stretching the lungs and chest muscles stimulates the vagus nerve. Meditation helps too: a study in the International Journal of Yoga found that chanting “Om” stimulates it. Your gut plays a part as well. A probiotic containing Lactobacillus casei enhanced vagal stimulation and improved mood in the people who took part in one study.
What does the vagus nerve do?
The vagus nerve is the key to the parasympathetic nervous system. That is the rest-and-digest side that balances the fight-or-flight response. Its name comes from the Latin for “wandering” because it reaches the eyes, mouth, heart, lungs, stomach and gut. About 80 percent of its nerve traffic carries information from the body up to the brain.
Can vagus nerve stimulation help anxiety and depression?
Yes. Anxiety raises blood pressure and pulse, and vagal stimulation lowers both. That is why it has been used to treat anxiety disorders with significant success. A Medical University of South Carolina study found improvement right away and over the long term. Researchers at the China Academy of Chinese Medical Sciences also saw significant improvement in people with depressive symptoms.
Does vagus nerve stimulation reduce inflammation?
Yes. A study published in the journal Science found that vagal stimulation suppresses the inflammatory response that starts in the spleen. It also lowers heart rate and blood pressure, relaxes muscles and lifts mood. Toning down inflammation is one of the main therapeutic effects of stimulating the vagus nerve on purpose.
Related reading
Sources
Viva vagus: Wandering nerve could lead to range of therapies
Neurohemodynamic correlates of ‘OM’ chanting: A pilot functional magnetic resonance imaging study. Int J Yoga. 2011 Jan-Jun; 4(1): 3–6.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099099/
University of California, San Francisco (UCSF). (2014, August 15). Do gut bacteria rule our minds? In an ecosystem within us, microbes evolved to sway food choices. ScienceDaily. Retrieved August 10, 2016 from www.sciencedaily.com/releases/2014/08/140815192240.htm
Science. Acetylcholine-Synthesizing T Cells Relay Neural Signals in a Vagus Nerve Circuit
http://science.sciencemag.org/content/334/6052/98
A pilot study of vagus nerve stimulation (VNS) for treatment-resistant anxiety disorders.
http://www.ncbi.nlm.nih.gov/pubmed/20633378#
Elsevier. (2016, February 4). New non-invasive form of vagus nerve stimulation works to treat depression. ScienceDaily. Retrieved August 10, 2016 from www.sciencedaily.com/releases/2016/02/160204111728.htm
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026