How sugar may damage the brain

Most people have heard that sugar is unhealthy, but how exactly does it work against your good mental health?

When you eat concentrated sources of rapidly-digestible carbohydrates such as sugar, flour, fruit juice, and processed cereal products, your blood sugar (glucose) can spike sharply, immediately triggering an equally strong spike in insulin, in an effort to bring blood glucose back down to normal.1

These dramatic fluctuations in glucose occur inside the brain as well, because brain glucose rises and falls in proportion to blood glucose.2 These steep spikes and drops in glucose and insulin levels can wreak havoc with your brain and body chemistry in the following three critical ways.

Refined carbohydrates can destabilize hormones and mood

The problem with unstable insulin levels is that insulin isn’t simply a blood sugar regulator. Insulin is a master metabolic hormone that orchestrates the levels of numerous other hormones throughout the body, including sex hormones like estrogen, the blood pressure regulating hormone aldosterone, and the stress hormones cortisol and adrenaline.3 Every time insulin peaks and plummets, these hormones follow suit, which can place you on an invisible internal hormonal roller coaster.

Let’s say you start off your morning with a food rich in refined carbohydrates — like orange juice, a bagel, or a bowl of corn flakes. Within a half hour, your blood sugar spikes, and your pancreas immediately releases insulin into your bloodstream to pull the extra sugar (glucose) out of your blood and squirrel it away into your cells. At about the 90-minute mark, as your blood sugar is dropping, you may experience a “sugar crash” and feel tired, unfocused, and hungry.

The body perceives plummeting glucose as an emergency, so it releases a mixture of hormones to keep glucose from falling below normal. This mixture includes the stress hormones cortisol and adrenaline — our “fight-or-flight” hormone. Adrenaline peaks between two and five hours after eating sugar, causing some to experience physical and emotional distress between meals, including panic symptoms such as anxiety, shakiness, and difficulty concentrating.

Many people consume refined carbohydrates at every meal and as snacks, which can place their hormones on a seesaw all day long and even well into the night. Age, metabolism, gender, genetics, and activity level all influence what your personal internal roller coaster feels like. Fluctuating energy levels, difficulty concentrating, mood swings, binge eating, irritability, anxiety attacks, and insomnia are all possibilities, depending on the individual.

Yet, even if you aren’t aware of any symptoms on the outside, this chaos may still be occurring on the inside, disrupting normal rhythms in ways that can slowly and silently lead to health problems down the road. For more information, including graphs of sugar and hormone roller coasters on different diets, read “Stabilize your mood with food.

Selection of bad sources carbohydrates

Refined carbohydrates can promote oxidation and inflammation

Unnaturally high spikes in blood sugar can be powerful promoters of oxidation and inflammation, which are features of many chronic diseases, including psychiatric disorders.

What is oxidation?

Oxidation happens. The chemical reactions our cells rely upon to turn food into energy require oxygen molecules that can break apart into reactive “free radicals” during glucose processing. Free radicals are like little bulls in a china shop — left unchecked, they bump into and react with neighboring structures and DNA, damaging cells from the inside out (oxidation). Since some amount of oxidation is normal and natural, Mother Nature has armed us with a variety of our very own internal antioxidants to mop up pesky free radicals. Under normal circumstances, these built-in antioxidants are sufficient to keep oxidation and anti-oxidation forces in balance and prevent cellular damage.4

The problem with high-sugar foods and beverages is that they can flood chemical pathways with too much glucose at once, generating more free radicals than our internal antioxidants can neutralize.5 Excess free radicals are then free to randomly destroy whatever they encounter. Depression, bipolar disorder, schizophrenia and obsessive-compulsive disorder are all associated with excess oxidation.6 We are often told that the solution to our oxidation problem is to consume colorful, anti-oxidant-rich fruits and vegetables to bring our systems back into balance, but the truth is that most plant “superfood” antioxidants, when consumed in their natural form, are very poorly absorbed by the human body and are therefore of little use to us.7

It is not the lack of superfoods that tilts our cells too far towards oxidation, it is the presence of refined carbohydrates that deplete our natural antioxidants and make it appear as if we need more antioxidant power than we already have. Instead of buying antioxidants, wouldn’t it make a lot more sense to simply stop eating pro-oxidants? For more information about the pros and cons of antioxidants, including superfood examples, read the “The antioxidant myth.

What is inflammation?

Our immune system reacts to oxidative damage sugar can cause by mounting an inflammatory response. This isn’t the kind of inflammation that makes your brain swollen, red, or sore — it’s inflammation on a microscopic level. Multiple lines of evidence point to a strong connection between inflammation and many cases of depression, bipolar disorder, and schizophrenia. 8

When cells are in distress, they release tiny cries for help in the form of “inflammatory cytokines” such as IL-6 and TNF-alpha that can be measured in the blood. Levels of these molecules are often higher in people with mood and psychotic disorders. Inflammatory cytokines can trigger damage to nearby brain cells and cause chemical imbalances in the brain by disrupting normal production of serotonin, dopamine, and glutamate — key neurotransmitters involved in psychiatric disorders. While we don’t yet have clinical studies cementing a causal relationship, paths leading from sugar to oxidation to inflammation may help to connect the dots between modern diets and mental illnesses.

Refined vegetable oils like soybean and sunflower oil may also contribute to excess inflammation, because they are unnaturally high in omega-6 fatty acids. Industrially-produced seed oils are found in all kinds of processed foods — from high-carbohydrate foods like chips and baked goods to popular low-carbohydrate foods like mayonnaise and salad dressings. Omega-6 fatty acids are responsible for mounting the inflammatory response to oxidative damage, injuries and infections, whereas omega-3 fatty acids are responsible for initiating the healing response that follows.

These two forces work best when they are roughly in balance. Unfortunately, modern diets are not only extremely high in omega-6 fatty acids, they are also often too low in omega-3 fatty acids, tilting our immune system too far towards inflammation and away from healing.9 Imbalances in these essential fatty acids are seen in most psychiatric disorders.10

Numerous studies have tested whether anti-inflammatory drugs can be used to treat mood and psychotic disorders (and they do sometimes help to some extent),11 but rather than taking drugs to simply mask symptoms — drugs which cost money and can cause side effects — why not stop inflammation at its source by eliminating processed foods instead? For more about how to help cool brain inflammation without medication, including a chart listing the omega-6 content of various oils, see “Cooling brain inflammation naturally with food.

Vegetable oils

Vegetable oils: What we know and what we don’t

GuideVegetable oils have quickly become a major source of calories in our food supply. Is that a good thing? To find out, let’s review what we know, and what we don’t know.

Too much sugar contributes to insulin resistance

Insulin resistance, which now affects more than 50% of Americans and has reached epidemic proportions in many other countries around the world, is emerging as a potentially important factor in the development of most of the mental health problems we fear — from straightforward conditions such as depression to complex brain degeneration disorders like schizophrenia and Alzheimer’s disease.12 As tragic as this may seem, understanding that insulin resistance of the brain strongly influences our risk for psychiatric disorders is tremendously empowering, because insulin resistance is a familiar beast we already know how to tame.

High-sugar diets flood the bloodstream with too much glucose, placing pressure on the pancreas to produce high amounts of insulin to process it all. Over time, if insulin levels run too high too often, your delicate insulin signaling system can break down from overuse. The receptors that transmit insulin’s instructions can become damaged and dwindle in number, making it increasingly difficult for cells to respond to insulin’s important messages. The pancreas tries to overcome this “resistance” by releasing even more insulin into the bloodstream, creating a vicious cycle of climbing insulin levels and worsening insulin resistance.

In people with insulin resistance, the insulin receptors responsible for escorting insulin from the bloodstream into the brain’s interior can malfunction and shrink in number, restricting insulin flow into the brain. If you have insulin resistance or even type 2 diabetes, glucose will continue to waltz easily into the brain, but insulin will struggle to gain access.

Without adequate insulin, brain cells can’t process glucose properly, and will start to slow down. This sluggish glucose processing problem is called “cerebral glucose hypometabolism” and is a key feature of many brain disorders, particularly Alzheimer’s disease.13

For simple ways to figure out whether you have insulin resistance, see “How to diagnose, prevent and treat insulin resistance.” 

How low-carbohydrate diets can improve brain metabolism

If high blood sugar and insulin jeopardize brain health through inflammation, oxidation, and insulin resistance, then reducing blood glucose and insulin levels should help improve brain health. A growing body of scientific literature supports the idea that ketogenic diets have the potential to address all of these underlying biochemical disturbances, and therefore hold great promise for the dietary treatment of psychiatric disorders.14

As carbohydrates tend to raise glucose and insulin levels the most and fats raise insulin the least, it stands to reason that a low-carbohydrate, high-fat diet could be one of the best ways to target these root causes of brain malfunction, improve brain metabolism, and protect the brain from further damage.15 It has been known for nearly a century that ketogenic diets have the power to completely eliminate seizures in some children with epilepsy and significantly reduce the frequency of seizures in others.16 If that isn’t an indication that low-carbohydrate diets can stabilize brain chemistry, what is?

The brain is a highly-active electrical organ that demands a constant supply of high-quality fuel, and while it’s true that some of its fuel must be in the form of glucose, that glucose does not need to come from carbohydrates in the diet. In 2005, the (American) Institute of Medicine and the Food and Nutrition Board acknowledged that “the lower limit of dietary carbohydrate compatible with life is apparently zero, provided that adequate amounts of protein and fat are consumed.”17 Through a natural process called “gluconeogenesis” (making glucose from scratch), the liver can make all the glucose we need from fat and protein and release it into the bloodstream for any cells that require it, including brain cells.18

When carbohydrate intake is sufficiently low and intakes of protein and fat are adequate, such as on a standard LCHF (low-carbohydrate/high-fat) diet, blood (and brain) glucose levels will typically stabilize in a healthy range.19 If insulin levels are sufficiently low, the body switches from primarily burning sugar to primarily burning fat. This shift is called “ketosis” because fat breaks down into fatty acids and “ketones” that are released into the blood to serve as sources of fuel for hungry cells. You can test to see if you are generating ketones with a blood ketone meter.

Although most cells in the body can burn fatty acids, brain cells aren’t equipped to burn them.20 So, they burn ketones instead. Ketones are an excellent fuel source for the brain — they burn more cleanly and efficiently than glucose, with much less oxidation and inflammation.21 Although some rapid-fire brain cells always require some glucose (because it burns faster than ketones do), ketones can meet up to a remarkable two-thirds of the brain’s total energy requirements.22 In fact, given the option, most brain cells will burn ketones over glucose, making ketones the preferred energy source for large portions of the human brain.23

Although insulin resistance of the brain makes it difficult for insulin to cross into the brain, it doesn’t interfere with the flow of ketones.24 Therefore the more ketones you have in your blood, the higher your brain ketone levels will be, and the more ketones your brain cells can absorb and use for energy. As an added bonus, it just so happens that ketones burn beautifully in a low-insulin environment, making ketones an ideal fuel source for the insulin-resistant brain.

The food-mood connection

From glucose and insulin spikes to oxidation, inflammation, and insulin resistance, a modern diet full of refined carbohydrates and vegetable oils is indeed a potential driver of psychological distress. For more details about how a whole-food, low-carbohydrate diet can help with specific psychiatric disorders, please visit our guide, The food-mood connection.

If you are struggling with mental health issues and taking medication, we have a lot more information on this topic in our guide, Low carb and mental health: Getting started and managing medications. We also have an FAQ that addresses many common questions and concerns about the links between diet and mental health.

/ Dr. Georgia Ede, MD



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Comments

  1. These are just three examples of human clinical studies illustrating how blood sugar and insulin respond to high-carbohydrate foods; many other examples exist.

    The American Journal of Clinical Nutrition 1998: Acute effects on insulin sensitivity and diurnal metabolic profiles of a high-sucrose compared with a high-starch diet [strong evidence]

    Journal of Nutrition 2003: Physiological validation of the concept of glycemic load in lean young adults [strong evidence]

    American Journal of Clinical Nutrition 2008: Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals [strong evidence]

  2. New England Journal of Medicine 2012: Relationship between cerebrospinal fluid glucose and serum glucose [strong evidence]

  3. Neuroscience & Biobehavioral Reviews 2002: Carbohydrate ingestion, blood glucose and mood [moderate evidence]

    Journal of Pediatrics 1995: Enhanced adrenomedullary response and increased susceptibility to neuroglycopenia: mechanisms underlying the adverse effects of sugar ingestion in healthy children [moderate evidence]

  4. Cellular Physiology and Biochemistry 2017: Antioxidants maintain cellular redox homeostasis by elimination of reactive oxygen species [discusses mechanism; ungraded]

  5. Medicinal Research Reviews 2015: Postprandial dysmetabolism and oxidative stress in type 2 diabetes: pathogenetic mechanisms and therapeutic strategies [discusses mechanism; ungraded]

  6. Review article of multiple lines of evidence including clinical trials and observational studies. Journal of Neuroinflammation 2013: Neuroinflammation and psychiatric illness [weak to moderate evidence]

  7. Antioxidants & Redox Signaling 2013: Dietary (poly)phenolics in human health: structures, bioavailability, and evidence of protective effects against chronic diseases [strong evidence]

  8. Current Topics in Behavioral Neurosciences 2017: Evidence for inflammation-associated depression [strong evidence]

    Psychiatric Clinics of North America 2016: Bipolar disorder and inflammation [strong evidence]

    International Journal of Molecular Sciences 2017: Neuroinflammation and oxidative stress in psychosis and psychosis risk [strong evidence]

  9. A review of observational studies, animal studies, and human clinical trials: Experimental Biology and Medicine 2008: The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases [ungraded]

  10. Psychoneuroendocrinology 2018: Omega-3 and omega-6 fatty acid levels in depressive and anxiety disorders [strong evidence]

    Journal of Clinical Psychiatry 2016: Omega-3 and omega-6 polyunsaturated fatty acids in bipolar disorder: a review of biomarker and treatment studies [strong evidence]

    Journal of the Canadian Academy of Child and Adolescent Psychiatry 2016: Omega-6 to omega-3 fatty acid ratio in patients with ADHD: a meta-analysis [strong evidence]

    Psychiatry Research 2013: Red blood cell polyunsaturated fatty acids measured in red blood cells and schizophrenia: a meta-analysis [strong evidence]

    Nutrients 2017: Relationship between long chain n-3 polyunsaturated fatty acids and autism spectrum disorder: systematic review and meta-analysis of case-control and randomized controlled trials [strong evidence]

  11. (strong evidence)Current Topics in Behavioral Neurosciences 2017: Evidence for inflammation-associated depression [strong evidence]

    Lancet Psychiatry 2015: Inflammation and immunity in schizophrenia: implications for pathophysiology and treatment [strong evidence]

  12. Insulin resistance in Americans

    JAMA Network 2015: Prevalence of and trends in diabetes among adults in the United States, 1988-2012

    Insulin resistance around the world

    Current Hypertension Reports 2018: The global epidemic of the metabolic syndrome

    Depression

    Neuropharmacology 2018: Insulin resistance, an unmasked culprit in depressive disorders: promises for interventions [weak evidence]

    Schizophrenia

    JAMA Psychiatry 2017: Impaired glucose homeostasis in first-episode schizophrenia: a systematic review and meta-analysis [strong evidence]

    Alzheimer’s disease

    Journal of Diabetes Science and Technology 2008: Alzheimer’s disease is type 3 diabetes: evidence reviewed [strong evidence]

  13. Journal of Neuroscience Research 2017: Cerebral hypoperfusion and glucose hypometabolism: key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer’s disease [discusses mechanism; ungraded]

  14. Neuroscience and Biobehavioral Reviews 2018: Ketogenic diet as a metabolic therapy for mood disorders: evidence and developments [reviews multiple lines of evidence; ungraded]

    Frontiers in Psychiatry 2017: The current status of the ketogenic diet in psychiatry [Narrative review of mechanisms, animal studies and case reports; ungraded]

  15. American Journal of Clinical Nutrition 2009: Food insulin index: physiologic basis for predicting insulin demand evoked by composite meals

  16. Cochrane Database Systematic Review 2016: Ketogenic diet and other dietary treatments for epilepsy [strong evidence]

  17. U.S. Institute of Medicine of the National Academies 2005: Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids 2005

  18. U.S. Institute of Medicine of the National Academies 2005: Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids 2005

  19. Molecular Cellular Biochemistry 2007: Beneficial effects of ketogenic diet in obese diabetic subjects [year-long, non-randomized clinical trial, weak evidence]

    European Journal of Clinical Nutrition 2013: Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets [narrative literature review; ungraded]

  20. Neurochemistry International 2017: Brain energy metabolism spurns fatty acids as fuel due to their inherent mitotoxicity and potential capacity to unleash neurodegeneration [reviews of mechanisms; ungraded]

  21. Journal of Lipid Research 2014: Ketogenic diets, mitochondria, and neurological diseases [discusses mechanism, ungraded]

  22. Journal of Neurochemistry 2015: Effects of ketone bodies in Alzheimer’s disease in relation to neural hypometabolism, ß-amyloid toxicity, and astrocyte function [discusses mechanism, ungraded]

  23. Frontiers in Molecular Neuroscience 2016: Can ketones help rescue brain fuel supply in later life? Implications for cognitive health during aging and the treatment of Alzheimer’s disease [reviews of mechanisms; ungraded]

  24. Annals of the New York Academy of Sciences 2016: Can ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer’s disease [multiple controlled human clinical trials; moderate evidence]