How much thought do you give to your brain? Probably not much when everything is going well. But the actions we take throughout life can have a big impact not only on our brain health as we age, but also how we feel now, including how we cope with stress, deal with set-backs and enjoy life to the fullest.
Despite its diminutive size, your brain steals roughly 25% of your body’s energy. Like a performance car, it is highly dependent on the fuel you feed it as well as how well you sleep, your level of physical exercise, and the extent to which you keep your mind active throughout life.
We decided to research why brain health matters regardless of age and life stage, and created a brand new resource on our website. Read below for a snapshot of some key findings.
Please note that the life stages we have come up with are intended as signposts only and a way to organise information. We recognise the potential for overlap across life stages as well as individual diversity of experiences.
Pregnancy
The first 1,000 days of life, including 280 days of prenatal life, are a crucial stage of baby brain growth and development. Recent scientific evidence has identified that parental health and nutrition status at the time of conception and throughout pregnancy plays an important role in brain development.
Although rapidly growing foetal brains exhibit greater ability to adapt and change than adult brains, they are still vulnerable to injury. Optimising nutrition during pregnancy is one way of several to support foetal brain development. All nutrients are essential to neuroplasticity, but studies have highlighted the particular importance of glucose, fats, protein, iron, zinc, iodine, copper, folate and choline. Read more
Infancy
Infancy (0-3 years) is a time of rapid transition, growth and change. From the moment a child is born it should have all the brain cells that it will ever need (around 100 billion cells), although new brain cells can still be created into adulthood. Synapses, which facilitate the brain’s ability to send and receive information, are formed far quicker during these first three years of life compared to other stages of growth.
Within the first year of life, the cerebellum, involved with memory and movement, can triple in size to account for all the visual and physical experiences the infant encounters. Moreover, within the first three years of life the weight of the brain triples, as it undergoes profound growth. During these first three years of intense neurobiological growth, ketones (water-soluble molecules produced from fatty acids), are an infant’s primary fuel in the developing brain.
At this stage of life, vitamins A, C and D, omega-3 and omega-6, iron, folic acid, B12, iodine, copper, choline and zinc are important nutrients for development. Read more
Childhood
Childhood (4-11 years) is an important period of brain maturation, involving the shaping of cognitive function and resilience across the lifespan. Malnutrition amongst children is a worldwide issue. This encompasses two types of undernutrition: those in developing nations, where food scarcity has led to malnutrition and adverse health outcomes; and prevalence of obesity in developed nations, where abundance of high sugar, salt and fat processed foods at low prices has led to increased incidences of weight gain, reduced consumption of vegetables, fruit and other wholefoods, and therefore increased vitamin and mineral deficiency.
Childhood is a critical period of learning and memory. Nutrients that support this include omega-3, magnesium, vitamin D, zinc. Sleep, physical exercise, and fussy eating are additional factors that can influence a child’s neurological development. Read more
Teenager
Adolescence is a time of transition, change and increasing independence. During this important period of development, a healthy, varied diet is important to support learning and growth. Additionally, due to increased autonomy, it is essential that young people are educated and empowered regarding food choices and positive lifestyle habits.
Adolescence is also a time of increased susceptibility to mental health problems, and a lifestage where mental illnesses such as depression, anxiety, eating disorders, substance abuse disorders and psychosis may begin to develop. Moreover, schizophrenia and personality disorders may also begin to develop during adolescence. Globally, 1 in 7 10-19 year olds develop a mental health condition, and suicide is the fourth leading cause of death in 15-19 year olds. Key risk factors for the development of mental health conditions during adolescence include stress, the influence of media, lower socioeconomic status, and violence and abuse in the home.
Supporting health and wellbeing during adolescence is vitally important. Protective nutrients and dietary strategies include eating three healthy meals a day, exercising regularly, sleeping well, supporting bone health and promoting iron, B vitamin, omega-3 and vitamin D status. Read more
Young Adult
Young adulthood (18-30 years) is a life stage full of transition and change, characterised by increasing independence and autonomy typically. The brain continues to develop until the mid to late twenties, particularly areas responsible for reasoning and decision making, as well as emotional regulation.
Most mental health conditions emerge and are diagnosed during late adolescence. In fact, 75% of all mental illness diagnoses occur by age 24. During early adulthood, anxiety and depression remain prevalent and personality disorders may also be diagnosed. Early intervention in the form of psychological support, with nutrition as an adjunct, is crucial.
Research has identified a close link between the gut microbiome and mood/mood disorders. Fibre and probiotics help regulate the gut microbiota, which in turn helps produce neurotransmitters such as serotonin and GABA which influence mood. Read more
Middle Age
This life stage (30-50 years) is often characterised by progressions in careers and settling down. This may be accompanied by greater stress, which can influence neurological health. Building stress resilience through diet, sleep and adequate relaxation becomes key.
Many of the social, physical and psychological experiences of early life and young adulthood influence this life stage. For example, individuals who foster positive, meaningful relationships during their early adulthood have been observed to have better psychological outcomes during midlife.
Menopause normally occurs between the ages of 45-55, but premature menopause can affect 1 in 100 women. Decades of research supports a role for oestrogen in brain health. This hormone can function to produce energy within multiple brain regions involved in cognitive function. It is widely understood that oestrogen levels significantly decline when entering menopause, having a potentially negative impact on memory and cognition. Research has revealed the supportive role of diet and lifestyle factors through this period of transition, helping to attenuate the effects of menopause.
Midlife adults are generally less physically active and more at risk of unhealthy ageing related to sedentary lifestyle choices. Physical activity has positive effects not only on body composition but also mental health, sleep and menopause symptoms. Read more
Older Adult
Older adults (50-70 years old) are at increased risk of cognitive decline compared to their younger counterparts. Risk factors include cardiovascular disease, which has been correlated with increased incidence of cognitive decline and dementia, including Alzheimer’s disease. This intrinsic link between the heart and brain is further evidenced by how cardiac dysfunction has been identified as a predictor for cerebrovascular events. Coronary heart disease specifically has been associated with lower scores on cognitive function tests.
Novel nutritional and psychological approaches are constantly being explored to optimise brain health during the ageing process. Following a Mediterranean diet is supported by in-depth evidence demonstrating its benefits on cognitive health. This diet includes high intake of fats from fish and olive oil, and antioxidants from the consumption of fruit and vegetables.
Newer research has also highlighted the MIND diet, which recommends daily consumption of whole grains, fruits, vegetables, nuts and berries, and weekly consumption of beans, poultry and fish. Limited consumption of processed foods, meat, dairy and added sugars are suggested. Based on findings from a recent systematic review, researchers concluded that the MIND diet is superior to numerous other plant-rich diets for improving cognitive function and may possibly be associated with improved brain health in older adults.
Social interaction also becomes incrementally more important for health and wellbeing with age. Elderly people report improved self esteem and health and wellbeing outcomes when experiencing belonging in friendships, compared to those who reported loneliness and isolation. Finding ways to increase social interaction, via meeting up with friends for coffee, activities or hobbies are all ways to increase social interaction. Read more
Senior
This life stage is characterised by a slower pace of life for many people. It can be a time of great fulfilment, spending time with loved ones and having more time to pursue passions. However, it can also be a time of increased illness, loneliness and memory loss, as demonstrated in dementia.
Some individuals may be more at risk of developing memory loss and cognitive impairment. The APOE4 gene variation has been one of the most studied genetic risk factors with relation to Alzheimer’s disease. Telomeres, the protective ends of chromosomes, have also been observed to be shorter in individuals with the APOE4 gene variant. Telomeres shorten across the life span and are associated with the natural ageing process, but this can be accelerated due to oxidative stress caused by chronic stress, alcohol consumption and poor diet. Importantly, only 1 in a 100 cases of Alzheimer’s is caused by genes. Much of the risk comes from diet and lifestyle factors that we can change, highlighting the importance of prioritising brain health across the lifespan.
Maintaining physical exercise, increasing social interaction and eating well via the Mediterranean or MIND diet become important considerations at this stage of life. Read more
Final thoughts Tracking cognitive function at all stages of life empowers you to optimise your brain health for the long-term. Take our free Cognitive Function Test here for personalised feedback on how your cognitive function is performing and ways to improve it.
Brain Fats – Seafood, Omega-3 PUFAs, Phospholipids and Vitamin D
The omega-3 fat, docosahexaenoic acid (DHA) is the most abundant PUFA in the brain, concentrated in the grey matter and, particularly at the synapses.1 DHA is incorporated into membrane phospholipids, where it affects the properties of the membrane, for example, maintaining membrane fluidity. DHA, along with other omega-3 fats EPA, DPAn-3 and their mediators are involved in a wide variety of processes in the brain, such as making new neurons, synaptic connections and the regulation of inflammation.2
Fish, especially cold-water oily fish, contain high levels of DHA and EPA, and epidemiological studies consistently suggest that an elevated fish intake is associated with decreased risk of neurodegenerative diseases, such as Alzheimer’s disease.3 Recent estimates suggest that worldwide many populations are currently consuming DHA and EPA at levels well below the recommendations issued by many international authorities (GOED), with and blood levels of EPA and DHA have been estimated to be low to very low for most of the world, which may increase global risk for chronic disease.4
Interestingly, positive associations have also been found between walnut consumption and cognitive performance.5 Walnuts are a source of omega-3 fat, alpha-linolenic acid (ALA) and also a range of antioxidants.
Omega-3 Supplementation and cognitive decline
DHA supplementation appears to show the greatest promise in the early stage before the onset of memory loss symptoms,1 and at levels at or above 1000 mg per day (Ismail 2015).6
A study of healthy 50-75 year olds were given 2,200 mg a day of omega 3 fish oils for six months not only reported significant increase in executive function, one aspect of cognition that is a hallmark of Alzheimer’s, but also beneficial structural changes in white matter integrity and grey matter volume in the brain. The cognitive improvement correlated with blood levels of omega-3 PUFAs.7
A randomized, double-blind, placebo-controlled, clinical study, gave 900 mg of DHA a day for 24 weeks and reported an improvement in learning and memory function in those with age-related cognitive decline.8 In a further trial by the same research group, giving 2,000 mg a day of DHA or placebo to 402 people with mild to moderate Alzheimer’s disease, therefore further along the disease process, for a period of 18 months found no cognitive improvement.9
Phospholipids
Phospholipids, rich in eggs and seafood, are abundant in the brain. They make up the membranes of the different types of cells in the brain. These include Phosphatidylethanolamine (PE) and phosphatidylserine (PS) phosphatidylcholine (PC) and phosphatidylinositol (PI). They become attached to omega-3 DHA. (see film ‘Build Your Brain‘) Phosphatidylethanolamine (PE) and phosphatidylserine (PS) are enriched in DHA, whereas much lower levels are found in phosphatidylcholine (PC) and phosphatidylinositol (PI).3 Attaching DHA to phospholipids is a process that requires methylation, which is dependent on B vitamins.9 Interestingly, although DHA is typically found high in PS, levels have been found to be low in PS in post-mortem samples from Alzheimer’s disease patients.10 PS supplementation may benefit cognition in the elderly,11 but as PS is highly enriched with DHA, it is currently unclear whether the potential beneficial effects of PS on cognition are due to the intact PS or DHA. Although PC is not highly enriched in DHA, higher plasma concentrations of PC-DHA are associated with reduced risk of dementia and AD,12 and post mortem samples from AD shows depletion of PC-DHA in grey matter.13
Supplementation
A number of trials have investigated the effects of providing multinutrient supplements containing a range of nutritional factors with the aim of supporting phospholipid biosynthesis. Our recent systematic review identified that omega-3 PUFAs and B vitamins as part of these multinutrient formulas confers benefits on cognition in older adults across a range of different types of measures of cognition in older adults.14 Furthermore, 12-week trial of citicoline has shown cognitive benefits in healthy older adults.15
Vitamin D
The primary source of vitamin D is exposure to sunlight. Seafood provides the most dietary vitamin D. Vitamin D deficiency increases risk of AD.161,17,18 Supplements of vitamin D can be derived from animal or fungal sources (mushrooms and yeast). Supplementing 800iu (20mg) a day for 12 months has been shown to improve cognitive function and lessen amyloid protein markers.19
In a study in France involving 912 elderly patients followed for twelve years, a total of 177 dementia cases (124 AD) occurred: 25(OH)D deficiency was associated with a nearly three-fold increased risk of AD.20
References
1.Dyall, S. C. (2015, 2015-April-21). Long-chain omega-3 fatty acids and the brain: A review of the independent and shared effects of EPA, DPA and DHA [Review]. Frontiers in Aging Neuroscience, 7(52). https://doi.org/10.3389/fnagi.2015.00052
2. Dyall, S. C., Balas, L., Bazan, N. G., Brenna, J. T., Chiang, N., da Costa Souza, F., Dalli, J., Durand, T., Galano, J. M., Lein, P. J., Serhan, C. N., & Taha, A. Y. (2022, Apr). Polyunsaturated fatty acids and fatty acid-derived lipid mediators: Recent advances in the understanding of their biosynthesis, structures, and functions. Prog Lipid Res, 86, 101165. https://doi.org/10.1016/j.plipres.2022.101165
4. Stark, K. D., Van Elswyk, M. E., Higgins, M. R., Weatherford, C. A., & Salem, N., Jr. (2016, Jul). Global survey of the omega-3 fatty acids, docosahexaenoic acid and eicosapentaenoic acid in the blood stream of healthy adults. Prog Lipid Res, 63, 132-152. https://doi.org/S0163-7827(15)30033-3 [pii]10.1016/j.plipres.2016.05.001 Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16
5. Theodore LE, Kellow NJ, McNeil EA, Close EO, Coad EG, Cardoso BR. Nut Consumption for Cognitive Performance: A Systematic Review. Adv Nutr. 2021 Jun 1;12(3):777-792. doi: 10.1093/advances/nmaa153. PMID: 33330927; PMCID: PMC8166568.
6. Ismail
7. A. Veronica Witte, Lucia Kerti, Henrike M. Hermannstädter, Jochen B. Fiebach, Stephan J. Schreiber, Jan Philipp Schuchardt, Andreas Hahn, Agnes Flöel, Long-Chain Omega-3 Fatty Acids Improve Brain Function and Structure in Older Adults, Cerebral Cortex, Volume 24, Issue 11, November 2014, Pages 3059–3068, https://doi.org/10.1093/cercor/bht163
8. Yurko-Mauro K, McCarthy D, Rom D, et al; Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimers Dement. 2010; 6, 456-64
9. Quinn JF, Raman R, Thomas RG, et al; Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial. JAMA, 2010; Nov 3;304(17):1903-11.
10. A David Smith, Fredrik Jernerén, Helga Refsum, ω-3 fatty acids and their interactions, The American Journal of Clinical Nutrition, Volume 113, Issue 4, April 2021, Pages 775–778, https://doi.org/10.1093/ajcn/nqab013
11. Cunnane, Stephen & Schneider, Julie & Tangney, Christine & Tremblay-Mercier, Jennifer & Fortier, Mélanie & Bennett, David & Morris, Martha. (2012). Plasma and Brain Fatty Acid Profiles in Mild Cognitive Impairment and Alzheimer’s Disease. Journal of Alzheimer’s disease : JAD. 29. 691-7. 10.3233/JAD-2012-110629.
12. Richter Y, Herzog Y, Lifshitz Y, Hayun R, Zchut S. The effect of soybean-derived phosphatidylserine on cognitive performance in elderly with subjective memory complaints: a pilot study. Clin Interv Aging. 2013;8:557-63. doi: 10.2147/CIA.S40348. Epub 2013 May 21. PMID: 23723695; PMCID: PMC3665496.
13. Schaefer EJ, Bongard V, Beiser AS, Lamon-Fava S, Robins SJ, Au R, Tucker KL, Kyle DJ, Wilson PW, Wolf PA. Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study. Arch Neurol. 2006 Nov;63(11):1545-50. doi: 10.1001/archneur.63.11.1545. PMID: 17101822.
14. Yuki D, Sugiura Y, Zaima N, Akatsu H, Takei S, Yao I, Maesako M, Kinoshita A, Yamamoto T, Kon R, Sugiyama K, Setou M. DHA-PC and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer’s disease. Sci Rep. 2014 Nov 20;4:7130. doi: 10.1038/srep07130. PMID: 25410733; PMCID: PMC5382699.
15. Fairbairn, P., Dyall, S. C., & Tsofliou, F. (2022, Apr 27). The Effects of Multi-Nutrient Formulas containing a Combination of Omega-3 Polyunsaturated Fatty Acids and B vitamins on Cognition in the older adult: A Systematic Review and Meta-analysis. Br J Nutr, 1-42. https://doi.org/10.1017/S0007114522001283
16. Nakazaki E, Mah E, Sanoshy K, Citrolo D, Watanabe F. Citicoline and Memory Function in Healthy Older Adults: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial. J Nutr. 2021 Aug 7;151(8):2153-2160. doi: 10.1093/jn/nxab119. PMID: 33978188; PMCID: PMC8349115.
17. Sommer I, Griebler U, Kien C, Auer S, Klerings I, Hammer R, Holzer P, Gartlehner G. Vitamin D deficiency as a risk factor for dementia: a systematic review and meta-analysis. BMC Geriatr. 2017 Jan 13;17(1):16. doi: 10.1186/s12877-016-0405-0. PMID: 28086755; PMCID: PMC5237198;
18. Jayedi A, Rashidy-Pour A, Shab-Bidar S. Vitamin D status and risk of dementia and Alzheimer’s disease: A meta-analysis of dose-response †. Nutr Neurosci. 2019 Nov;22(11):750-759. doi: 10.1080/1028415X.2018.1436639. Epub 2018 Feb 15. PMID: 29447107;
19. Chai B, Gao F, Wu R, Dong T, Gu C, Lin Q, Zhang Y. Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis. BMC Neurol. 2019 Nov 13;19(1):284. doi: 10.1186/s12883-019-1500-6. PMID: 31722673; PMCID: PMC6854782.
20. Jia J, Hu J, Huo X, Miao R, Zhang Y, Ma F. Effects of vitamin D supplementation on cognitive function and blood Aβ-related biomarkers in older adults with Alzheimer’s disease: a randomised, double-blind, placebo-controlled trial. J Neurol Neurosurg Psychiatry. 2019 Dec;90(12):1347-1352. doi: 10.1136/jnnp-2018-320199. Epub 2019 Jul 11. PMID: 31296588.
21. Feart C, Helmer C, Merle B, Herrmann FR, Annweiler C, Dartigues JF, Delcourt C, Samieri C. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: 10.1016/j.jalz.2017.03.003. Epub 2017 May 16. PMID: 28522216.
Robert Lustig is Professor Emeritus of Pediatrics in the Division of Endocrinology, and Member of the Institute for Health Policy Studies at the University of California, San Francisco. He is a pediatric neuroendocrinologist,and an international authority on obesity, diabetes,nutrition,and neuroscience. He is the author of three books that have changed our understanding of the danger of sugar on our metabolism – Fat Chance, The Hacking of the American Mind, and Metabolical.
Most people know that refined sugar is not good for you, but what is it about sugar that’s particularly bad for your brain? Why is it essential, not only for brain health and dementia prevention, to reduce your intake of not only sugar but refined carbohydrates in general? (By refined, I mean those whose fiber has been processed away – not ‘whole’ as in vegetables, whole fruit (not juice), beans, and whole grains.
Let’s start at the extreme. What happens if you lived at the North Pole, and ate virtually no carbohydrates, or at least so little as to force your body and brain to switch to a kind of fuel, ketones, produced from fat? This is often called a “very low carb high fat” (LCHF) or “ketogenic” diet. Would you get sick? This is what Vilhjamur Steffanson did, when his Arctic exploration shipwrecked in 1913, and he was forced to live amongst the Inuit for two years. He noted that there was no diabetes, no cancer — and no Alzheimer’s. In 1928, he and his colleague checked themselves into Bellvue hospital, and ate only meat for one year.[1]They were healthier than the researchers who studied them!
Your brain likes ketones
Ketones are made in the liver from fat – either breaking down your own fat (for example, if you were fasting, eating very little or exercising a lot), or from ingestion of a type of fat containing ‘medium chain triglycerides’ (MCTs). Coconut oil is approximately 54% MCTs and contains all 4 MCTs (C6, C8, C10, C12), but it turns out that one particular kind of MCT, called C8 because it is 8 carbons long, is the best fat for the liver to convert into ketones.
You may be surprised to know that your brain can run well on glucose (the kind of sugar that is fuel for our cells), but even better on ketones. The reason is that ketones cross into the brain easily, rapidly, and without a biochemical transporter. This is why children with severe epilepsy improve on a ketogenic diet. Watch this short film ‘Fuel your Brain’.
Brain benefits of a low-carb ketogenic diet
In fact, brain cells prefer ketones. In two studies, one on people with Alzheimer’s and the other on those with pre-dementia or mild cognitive impairment, giving 2 tablespoons of C8 oil (called capricin or caprylic acid triglyceride), brain energy derived from ketones went up by 230% and memory and mental acuity improved in those with Minimal Cognitive Impairment (MCI).[2,3]
A ketogenic diet has been shown to reduce schizophrenia symptoms, help reduce shaking in Parkinson’s, and slow down cognitive decline in those with dementia or pre-dementia. In fact, the ketogenic diet has been used to effectively treat childhood epilepsy for over 100 years! There’s a good review on the current status of the ketogenic diet in psychiatry here.[4]
Ketogenic diets may help in many ways. Firstly, when a person eats too much carbohydrate, sugar, but especially fructose, damages the energy burning factories in cells, called mitochondria, so their ability to produce chemical energy for the neuron is greatly reduced. Switching to burning ketones instead can increase mitochondria number and function. A recent study also shows that a ketogenic diet has a positive effect on the gut microbiome,[5] and this might be one way the diet helps reduce fits in people with epilepsy.[6] Fructose, on the other hand, disrupts the gut microbiome in a negative way.
How sugar damages your brain
But what is it about a ketogenic diet that is good for your brain? Is it the ketones, the lowering of insulin, the type of fat, the elimination of carbohydrate, or specifically the elimination of sugar? We don’t yet know – I ask this question of every Alzheimer’s and metabolic researcher I know, and no one can tell me – just that it works.
There are a few possible mechanisms. First, the more carbs and sugar you eat, the more resistant you become to the hormone insulin. Insulin not only drives glucose into cells (including brain cells), but also sends excess sugar to the liver to turn into fat. When a person becomes insulin resistant, ironically, glucose transport is negatively impacted, reducing brain energy availability. Insulin resistance is a major driver of depression.[7] A ketogenic diet can reverse that.
Fructose, which comprises half of sucrose (‘white’ or ‘table’ sugar), and half of ‘high-fructose corn syrup’ (added to numerous processed foods), damages our mitochondria, which leads to less brain energy availability. One study showed that fructose reduces liver mitochondrial function, while glucose stimulates it.[8]“The most important takeaway of this study is that high fructose in the diet is bad,” said Dr. C. Ronald Kahn from the Joslin Diabetes Center. “It’s not bad because it’s more calories, but because it has effects on liver metabolism to make it worse at burning fat. As a result, adding fructose to the diet makes the liver store more fat, and this is bad for the liver and bad for whole body metabolism.”
Fructose is the main sugar in most fruits. People then extrapolate, “oh fruit must be bad for you.” Not true. Whole fruit has fibre (both soluble and insoluble); together they slow down glucose and fructose absorption in the GI tract limiting both liver and brain exposure, and they also help feed the gut bacteria (microbiome), so actually you get less fructose entering the bloodstream. Juicing the fruit removes the protective fiber, and juice has been shown to be just as dangerous to metabolism as is soda. So, eat your fruit — don’t drink it!
Carbohydrates and fructose age your brain
There’s another reason why sugar, and especially fructose, is bad for your brain and body. They produce Advanced Glycation Endpoints or AGEs, which damage the brain. These ‘oxidise’ proteins (so does cigarette smoke), rendering them useless , allowing them to aggregate into clumps, and use up valuable antioxidants in your diet such as vitamin C and E.
Fructose acts on your liver to switch your metabolism away from fat burning to fat making and storing, and inhibits an anti-ageing process called ‘autophagy’ which helps clean up and remove damaged mitochondria in order to regenerate new, healthier cells.
Why sweet foods are so addictive
So far we’ve only explored why sugar is bad for your “physical” brain. Knowing this is a good start. But why does your “emotional” brain keep telling you that you want it? Why do people find it so hard to resist, and so many become sugar addicts? The answer is that fructose activates the “reward system” in the brain. It causes dopamine release, the motivational neurotransmitter associated with ‘reward’. Any chemical that does so can be addictive – cocaine, heroin, alcohol, nicotine, or example. The trouble is the more you have, the more your brain ‘down-regulates’, i.e. becomes less responsive to your own natural feel-good dopamine, so you end up needing more sugar to get the hit and, in the end, you get no hit at all but feel thoroughly awful without it. That’s the Law of Diminishing Returns. That’s addiction.
Blood sugar control reduces dementia risk
Keeping blood glucose levels in the low-normal range is reflected by a low blood glycosylated haemoglobin (HbA1C) level, which means ‘sugar-coated red blood cells’. A low HbA1c is good and is a proxy for improved insulin sensitivity, associated with reduced risk for dementia in several studies.[9,10,11,12,13,14]
A new study also shows that, in 40 year old adults with so-called normal glucose levels but at the higher end of the normal range, have increased their risk of Alzheimer’s by 15% [37]
Type 2 diabetes, the net result of losing blood sugar control, almost doubles the risk for dementia.[15,16] Diabetes is also associated with more rapid brain shrinkage.[17,18] Even people in the upper normal range of blood glucose have increased brain atrophy, impaired cognition, and increased risk of dementia.[19,20]
For instance, one trial measured HbA1c and glucose levels in several thousand elderly people over the course of almost seven years.In that time, slightly more than a quarter of the participants developed dementia, and the bottom line was that rising glucose levels were associated with increased risk of developing the condition, irrespective of whether the participants also had diabetes. Non-diabetics who experienced a modest increase in blood sugar levels had an 18% increased risk of dementia, as compared to those who already had diabetes at the start of the study or developed it within the trial period, who had a 40% increased risk.[21]
Insulin resistance is strongly related to cognitive decline
But even more important than loss of glucose control is the loss of insulin control. Back in 2004, researchers at Columbia University showed that people with high insulin levels – the principal hallmark of metabolic dysfunction – were twice as likely to develop dementia as those with healthy levels. Moreover, those with the highest insulin levels had the worst memory retrieval.[22] The same year, an Italian study established a link between heightened insulin levels and declining mental function.[23] Similarly, a Puerto Rican study found that people who consumed the large amounts of sugar doubled their risk of suffering poor cognitive function,[24] while another US study discovered a strong correlation between blood sugar level and memory loss.[25]
Two studies – one in Ireland,[26] and the other in the United States,[27] – established a link between high dietary glycemic load (GL; how high does your blood glucose rise when you eat carbohydrate) and cognitive decline. Indeed, both of these reports suggested that high GL is even more predictive of the pathological changes associated with Alzheimer’s than either high carb or high sugar intake. A high GL diet is also associated with more amyloid plaque[28] and more cognitive decline, especially in those who carry the ApoE4 gene, a regulator of fat metabolism.[29]
A long-term study found evidence that this sort of shrinkage is more common among people with high blood glucose levels, even when those levels are still within what are considered ‘normal’ (i.e. non-diabetic) limits.[30] This cognitive decline starts young. Cognitive decline in overweight children is associated with a high GL diet[31], and adolescents with metabolic dysfunction driven by a high GL diet have been shown to have shrinkage of the hippocampal area of the brain, as well as other structural changes and cognitive deficits. [32,33]
Prevention action – how to cut down your sugar load
In practical terms, preventing dementia today means avoiding sugar as much as possible. If you’re going to eat carbohydrate, eat ‘whole’ carbohydrate foods such as whole vegetables, fruits (not juice), beans, only wholegrain bread (labelled as ‘100% wholegrain’, or pasta in small quantities.
Starchy carbohydrates such as pasta, rice and potatoes benefit from being cooked and cooled, then eaten cold or re-heated, as some of the carbohydrate is converted into resistant starch – a type of fibre we can’t digest but which has the added benefit of fermenting and feeding our gut bacteria.
Make sure the carbohydrate comes with its inherent fibre. Oat cakes would be better than bread since the fibre in these foods helps ‘slow release’ the sugars. Eating white bread is associated with a poorer cognitive test performance, whereas high fibre bread is associated with better performance.[34] Eating carbohydrate foods with protein, for example brown rice with fish, or porridge oats with seeds, or fruit with nuts, further reduces the glycemic load (GL) of a meal. The best fruits in this respect are low-sugar high-fiber fruits like berries, cherries, and plums.
These kinds of foods are consistent with a Mediterranean diet which has also been shown to reduce risk.[35] Conversely, grapes, raisins, and bananas are high GL. A study in Finland and Sweden compared those with a healthy versus unhealthy diet, including the above criteria, in mid-life for future risk of developing Alzheimer’s disease and dementia 14 years later. Those who ate the healthiest diet had an 88% decreased risk of developing dementia and a 92% decreased risk of developing Alzheimer’s disease.[36]
The take-home message is, if you are going to eat complex carbohydrates, eat them with fibre, fat and protein.
However, if you want to go one step further, you can switch to eating a ketogenic low-carb, high fat diet. The problem with the ketogenic diet is staying on it – there’s so much carbohydrate out there it’s hard to avoid it. But there are now breath monitors (e.g. Ketoscan, BioSense from ReadOut Health) that can help you stay in ketosis. A good book to help you explore and put into practice either a low carb ketogenic diet or a low GL diet is ‘The Hybrid Diet’ by Patrick Holford & Jerome Burne. And to understand how processed food is your enemy, take a look at my book ‘Metabolical’.
And if you want to know how sugar is impacting your body and brain then upi can take one of our at-home, pin-prick, HbA1c (sugar) blood test so you can know exactly how sugar is impacting your body and also become apart of our vital research into this area.
Food for the Brain is a non-for-profit educational and research charity that offers a freeCognitive Function Testand assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing theCognitive Function Testyou are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices
1. Heinbecker P. STUDIES ON THE METABOLISM OF ESKIMOS. Journal of Biological Chemistry. 1928 Dec;80(2):461–75.
2. Fortier M, Castellano C-A, St-Pierre V, Myette-Côté É, Langlois F, Roy M, et al. A ketogenic drink improves cognition in mild cognitive impairment: Results of a 6-month RCT. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association [Internet]. 2020 Oct 26; Available from: https://pubmed.ncbi.nlm.nih.gov/33103819/
3. Croteau E, Castellano C-A, Richard MA, Fortier M, Nugent S, Lepage M, et al. Ketogenic Medium Chain Triglycerides Increase Brain Energy Metabolism in Alzheimer’s Disease. Journal of Alzheimer’s disease: JAD [Internet]. 2018;64(2):551–61. Available from: https://pubmed.ncbi.nlm.nih.gov/29914035/
4. Bostock ECS, Kirkby KC, Taylor BVM. The Current Status of the Ketogenic Diet in Psychiatry. Frontiers in psychiatry [Internet]. 2017;8:43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28373848
5. Paoli A, Mancin L, Bianco A, Thomas E, Mota JF, Piccini F. Ketogenic Diet and Microbiota: Friends or Enemies? Genes. 2019 Jul 15;10(7):534
6. Olson CA, Vuong HE, Yano JM, Liang QY, Nusbaum DJ, Hsiao EY. The Gut Microbiota Mediates the Anti-Seizure Effects of the Ketogenic Diet. Cell [Internet]. 2018 Jun [cited 2019 Apr 17];173(7):1728-1741.e13. Available from: https://www.cell.com/cell/pdf/S0092-8674(18)30520-8.pdf
7. Watson K, Nasca C, Aasly L, McEwen B, Rasgon N. Insulin resistance, an unmasked culprit in depressive disorders: Promises for interventions. Neuropharmacology [Internet]. 2018 Jul 1 [cited 2022 Aug 5];136(Pt B):327–34. Available from: https://pubmed.ncbi.nlm.nih.gov/29180223/
8. Softic S, Meyer JG, Wang G-X, Gupta MK, Batista TM, Lauritzen HPMM, et al. Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins. Cell Metabolism [Internet]. 2019 Oct;30(4):735-753.e4. Available from: https://www.cell.com/cell-metabolism/pdfExtended/S1550-4131(19)30504-2
9. Luchsinger JA, Tang M-X ., Shea S, Mayeux R. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 11;63(7):1187–92.
10. Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, et al. Insulin Resistance and Executive Dysfunction in Older Persons. Journal of the American Geriatrics Society. 2004 Oct;52(10):1713–8.
11. Xu WL, von Strauss E, Qiu CX, Winblad B, Fratiglioni L. Uncontrolled diabetes increases the risk of Alzheimer’s disease: a population-based cohort study. Diabetologia. 2009 Mar 12;52(6):1031–9.
12. Hassing Lb, Grant Md, Hofer Sm, Pedersen Nl, Nilsson Se, Berg S, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: A longitudinal population-based study. Journal of the International Neuropsychological Society. 2004 Jul;10(4):599–607.
13. Yaffe K, Blackwell T, Whitmer RA, Krueger K, Barrett Connor E. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. The Journal of Nutrition, Health & Aging [Internet]. 2006 Jul 1 [cited 2022 Aug 5];10(4):293–5. Available from: https://pubmed.ncbi.nlm.nih.gov/16886099/
14. Roberts RO, Knopman DS, Cha RH, Mielke MM, Pankratz VS, Boeve BF, et al. Diabetes and Elevated Hemoglobin A1c Levels Are Associated with Brain Hypometabolism but Not Amyloid Accumulation. Journal of Nuclear Medicine. 2014 Mar 20;55(5):759–64.
15. Arvanitakis Z, Wilson RS, Bienias JL, Evans DA, Bennett DA. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol. 2004 May;61(5):661-6. doi: 10.1001/archneur.61.5.661. PMID: 15148141.
16. Yaffe K, Blackwell T, Kanaya AM, Davidowitz N, Barrett-Connor E, Krueger K. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology [Internet]. 2004 Aug 24 [cited 2022 Mar 16];63(4):658–63. Available from: https://n.neurology.org/content/63/4/658
17. Tiehuis AM, van der Graaf Y, Visseren FL, Vincken KL, Biessels GJ, Appelman APA, et al. Diabetes Increases Atrophy and Vascular Lesions on Brain MRI in Patients With Symptomatic Arterial Disease. Stroke. 2008 May;39(5):1600–3.
18. Samaras K, Lutgers HL, Kochan NA, Crawford JD, Campbell LV, Wen W, et al. The impact of glucose disorders on cognition and brain volumes in the elderly: the Sydney Memory and Ageing Study. AGE [Internet]. 2014 Jan 9 [cited 2022 Aug 5];36(2):977–93. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039246/
19. Mortby ME, Janke AL, Anstey KJ, Sachdev PS, Cherbuin N. High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through life study. PLoS One. 2013 Sep 4;8(9):e73697. doi: 10.1371/journal.pone.0073697. PMID: 24023897; PMCID: PMC3762736.
20. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.
21. Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zheng H, Haneuse S, Craft S, Montine TJ, Kahn SE, McCormick W, McCurry SM, Bowen JD, Larson EB. Glucose levels and risk of dementia. N Engl J Med. 2013 Aug 8;369(6):540-8. doi: 10.1056/NEJMoa1215740. Erratum in: N Engl J Med. 2013 Oct 10;369(15):1476. PMID: 23924004; PMCID: PMC3955123.
22. Luchsinger JA, Tang MX, Shea S, Mayeux R. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004 Oct 12;63(7):1187-92. doi: 10.1212/01.wnl.0000140292.04932.87. PMID: 15477536.
23. Abbatecola AM, Paolisso G, Lamponi M, Bandinelli S, Lauretani F, Launer L, Ferrucci L. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc. 2004 Oct;52(10):1713-8. doi: 10.1111/j.1532-5415.2004.52466.x. PMID: 15450050.
24. Ye X, Gao X, Scott T, Tucker KL. Habitual sugar intake and cognitive function among middle-aged and older Puerto Ricans without diabetes. Br J Nutr. 2011 Nov;106(9):1423-32. doi: 10.1017/S0007114511001760. Epub 2011 Jun 1. PMID: 21736803; PMCID: PMC4876724.
25. Seetharaman S, Andel R, McEvoy C, Dahl Aslan AK, Finkel D, Pedersen NL. Blood glucose, diet-based glycemic load and cognitive aging among dementia-free older adults. J Gerontol A Biol Sci Med Sci. 2015 Apr;70(4):471-9. doi: 10.1093/gerona/glu135. Epub 2014 Aug 22. PMID: 25149688; PMCID: PMC4447796.
26. Power SE, O’Connor EM, Ross RP, Stanton C, O’Toole PW, Fitzgerald GF, Jeffery IB. Dietary glycaemic load associated with cognitive performance in elderly subjects. Eur J Nutr. 2015 Jun;54(4):557-68. doi: 10.1007/s00394-014-0737-5. Epub 2014 Jul 18. PMID: 25034880.
27. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
28. Taylor MK, Sullivan DK, Swerdlow RH, Vidoni ED, Morris JK, Mahnken JD, Burns JM. A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults. Am J Clin Nutr. 2017 Dec;106(6):1463-1470. doi: 10.3945/ajcn.117.162263. Epub 2017 Oct 25. PMID: 29070566; PMCID: PMC5698843.
29. Gentreau M, Raymond M, Chuy V, Samieri C, Féart C, Berticat C, Artero S. High Glycemic Load Is Associated with Cognitive Decline in Apolipoprotein E ε4 Allele Carriers. Nutrients. 2020 Nov 25;12(12):3619. doi: 10.3390/nu12123619. PMID: 33255701; PMCID: PMC7761247.
30. M.E. Mortby et al., ‘High “normal” blood glucose is associated with decreased brain volume and cognitive performance in the 60s: the PATH through Life Study’, PLoS One (2013), vol 8:e73697.
31. Lakhan, S.E., Kirchgessner, A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 12, 114 (2013). https://doi.org/10.1186/1475-2891-12-114
32. Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescence. Pediatrics. 2012 Oct;130(4):e856-64. doi: 10.1542/peds.2012-0324. Epub 2012 Sep 3. PMID: 22945407; PMCID: PMC3457620.
33. Mangone A, Yates KF, Sweat V, Joseph A, Convit A. Cognitive functions among predominantly minority urban adolescents with metabolic syndrome. Appl Neuropsychol Child. 2018 Apr-Jun;7(2):157-163. doi: 10.1080/21622965.2017.1284662. Epub 2017 Feb 22. PMID: 28631969.
34. Loef M, Walach H. Fruit, vegetables and prevention of cognitive decline or dementia: a systematic review of cohort studies. J Nutr Health Aging. 2012 Jul;16(7):626-30. doi: 10.1007/s12603-012-0097-x. PMID: 22836704.
35. Martínez-Lapiscina EH, Clavero P, Toledo E, Estruch R, Salas-Salvadó J, San Julián B, Sanchez-Tainta A, Ros E, Valls-Pedret C, Martinez-Gonzalez MÁ. Mediterranean diet improves cognition: the PREDIMED-NAVARRA randomised trial. J Neurol Neurosurg Psychiatry. 2013 Dec;84(12):1318-25. doi: 10.1136/jnnp-2012-304792. Epub 2013 May 13. PMID: 23670794.
36. Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M. Midlife healthy-diet index and late-life dementia and Alzheimer’s disease. Dement Geriatr Cogn Dis Extra. 2011 Jan;1(1):103-12. doi: 10.1159/000327518. Epub 2011 Apr 27. PMID: 22163237; PMCID: PMC3199886.
37. Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.