Neurons, that is brain and nerve cells, are primarily made out of what’s called ‘phosphorylated DHA’. That means the omega-3 fat DHA that is bound to a kind of fat called a phospholipid, as shown in the figure below.
Seafood contains phosphorylated DHA but DHA supplements, whether derived from fish oil or algae, is not phosphorylated. Hence, it needs to be attached to phospholipids to work. This attachment is done by a B vitamin dependent process called methylation.
There are several different kinds of phospholipids with strange names all starting with ‘phosphatidyl’ such as phosphatidyl choline, phosphatidyl serine, phosphatidyl inositol and phosphatidyl ethanolamine. To a large extent these can be made from phosphatidyl choline. As a group of nutrients they are classified as ‘semi-essential’ because we can make some, but not enough for optimal health and especially optimal brain health.
As a consequence there are moves afoot to classify choline (which can be easily attached to the ‘phosphatidyl’ part) as an essential nutrient with a recommended intake. This has come about due to the growing evidence that insufficient choline in pregnancy leads to cognitive impairment and developmental delay. This is particularly important for vegans because, like the omega-3 fatty acid DHA, there’s not much choline in plant-based foods, but there is some in foods such as quinoa, soya, beans, nuts and broccoli.
Currently an adequate intake of choline is defined as between 400mg and 520mg a day, the latter for pregnant and breast-feeding women. This is based on how much choline you need for healthy fat metabolism, liver function and reducing homocysteine levels. You also need choline to process cholesterol in the liver and brain. As you’ll see in the figure above, cholesterol is a vital brain component. But these levels don’t take into account what’s being learnt about choline’s role in brain development.. A good estimate of optimum daily choline intake would be at least 500mg and maybe double this in pregnancy.
Most important is choline’s role in building, and maintaining, a healthy brain. A pregnant woman’s intake defines the cognitive abilities of their child. Twenty years ago we knew that pregnant rats fed choline half way through their pregnancy have more connections between brain cells, plus improved learning ability and better memory recall. Now we know it’s true for babies with several recent trials showing similar results indicating that more choline in pregnancy enhances cognitive development.
An example of this is a study which gave women in their third trimester of pregnancy either 480mg of choline or almost double this – 930mg. They then tested the babies’ information processing speed at 4,7,10 and 13 months. Not only were the babies of the mothers given the higher dose faster but also the longer the mother had been given even the lower dose the faster were the child’s reactions. The authors concluded that “even modest increases in maternal choline intake during pregnancy may produce cognitive benefits for offspring ”. Seven years later, there will still memory advantages in the children whose mother had extra choline during pregnancy.
Babies are born with blood choline levels three times higher than their mother, illustrating how vital this nutrient is for building neuronal connections, which newborn babies do at a rate of up to a million new connections a second! An optimal intake for brain function is likely to be a lot higher than the 400 to 500mg recommended for adults, and higher still in pregnancy.
Since brain cells are made of a membrane containing choline (and other phospholipids) attached to the omega-3 fat DHA, without choline the omega-3 doesn’t work. The attaching of the two depends on methylation, a process that is dependent on B vitamins, especially B12, folate and B6. Choline helps methylation and healthy methylation, indicated by a low blood level of homocysteine, helps synthesize choline. You need all three – DHA, choline and B vitamins especially B12. So, if you are lacking in DHA, or in vitamin B12, then you’ll be doubly dependent on getting enough choline.
Choline rich foods – are vegans at risk of deficiency?
While the richest dietary sources are fish, eggs and organ meats there is significant amounts of choline in plant-based foods, notably soya as in tofu and soya milk, quinoa, nuts and seeds including flax seeds, almonds and peanuts, and cruciferous vegetables including broccoli, cauliflower and Brussels sprouts.
While, on the face of it, it does appear than vegans, especially those planning pregnancy, need to become choline focused in relation to choosing the right daily foods, and possibly supplementing, there is not yet conclusive evidence showing that vegan mothers are at risk, although it is likely that they are. One of the learnings that has come out of studies on omega-3 DHA is than vegan mothers may convert more vegan omega-3 ALA into DHA as an evolutionary imperative – not that a top up with supplementation isn’t still the recommendation. Could it be that vegan mothers make more choline if needed since it is so important for brain development? There are very few studies of vegans to know the answer to this question.
One recent study looked at choline levels in breast-milk of vegans, versus vegetarians and non-vegetarians. There was no significant difference with the author of the study concluding “This suggests that maternal plant-based diet by itself is not a risk factor for low breast-milk choline.”
The vegan community is certainly divided on this issue. Of course, the safe or cautious position, while the science unravels, is to supplement choline during pregnancy.
What intake of choline can you achieve from a vegan diet alone? Here’s a list of the best plant-based food for choline, compared to egg and fish as a yardstick, listed in order of how much you could get in a reasonable serving*:
*Many foods have not been analysed for choline, and measurements do vary, so this is a guide rather than a definitive list.
What does this mean for your daily diet? Here’s a typical vegan daily menu aimed to maximise choline intake and how much it would give you (I’m not including all foods and recipes, just those ingredient that deliver significant amount of choline):
BREAKFAST
A cup of soya milk 57mg
Small handful of nuts or seeds 20mg
(Flax, chia, almonds etc)
LUNCH
A cup of cooked quinoa (1/3 cup raw) 43mg
A serving (100g) of either broccoli, 36mg
cauliflower or Brussels sprouts
Avocado (1/2) 14mg
SNACKS
A tablespoon of almond or peanut butter 10mg
Hummus (1/2 cup) 34mg
Two slices of wholegrain bread 17mg
DINNER
A serving of tofu (125g) or beans 35-40mg
Half a cup of shiitake mushrooms 27mg
A serving (100g) of either broccoli, 36mg
cauliflower or Brussels sprouts
TOTAL 332mg
In reality you are unlikely to achieve this every day, and it would be quite limiting on your food choices, so a realistic target would be to achieve 300mg of choline from food. If you are aiming to achieve 500mg, which is the low end of optimal – more than this may be optimal in pregnancy – that leaves a shortfall of around 200mg of choline, suggesting the need for supplementation.
The most direct source of choline is from soya-derived lecithin granules and capsules. A flat tablespoon of lecithin granules (7.5g), which has a neutral and pleasant taste and can be sprinkled on cereals, in shakes and soups or eaten as is, provides 1,500 mg of phosphatidylcholine and around 200mg (13 per cent) of choline. Some ‘high phosphatidyl choline’ lecithin, sometimes called ‘high PC lecithin’ is 18 per cent choline, thus you need less – approximately a flat dessertspoon.
One tablespoon of lecithin granules equals three 1,200mg lecithin capsules (if ‘high PC’ two capsules would suffice). We suggest that this is a sensible addition to a completely vegan diet. (If you aspire to be plant-based most, but not all of the time the addition of two eggs, or an egg and a fish serving, would achieve 500mg a day of choline.)
You can also find ‘brain food’ supplements providing a combination of different kinds of phospholipids, not just choline, but its hard to get enough choline from these if your only other food sources are plant-based foods.
In summary, we need both omega-6 and omega-3 fats, as well as phospholipids.
Have one or two servings a day of dark green, leafy veg – especially those that grow in colder climates such a kale, broccoli, brussels sprouts, or a serving of seaweed as sources of both choline and omega-3.
Have a serving of quinoa, beans or tofu every day, if not two, for choline.
Have a dessertspoon of high PC lecithin, or two capsules of high PC lecithin granules every day. These guidelines are especially important if you are planning a pregnancy, pregnant or breast-feeding.
If you are not completely vegan the best food source for phospholipids and choline are eggs. Eat six eggs a week. The choline is in the yolk. The advice regarding omega-3 – eat three servings of fish a week, is good for choline too but it is present in all fish, not just oily fish high in omega-3 fats.
Have you taken the Cognitive Function Test to find out your Dementia Risk Index score? It’s completely FREE and you can choose to pay for the COGNITION programme afterwards if you need personalised recommendations to help you put diet and lifestyle tips into action.
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 you can take one of our at-home, pin-prick, DRIfT blood test so you can know exactly how sugar is impacting your body and also become a part 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
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Findings to date suggest that the oral microbiome, via interactions with the gut and brain (a network called the oral-gut-brain axis), may be a key consideration for brain health, and multiple associated conditions. This post will focus on three key areas where there is present research: autism, Down’s syndrome, and Alzheimer’s disease.
Supporting the oral-gut-brain axis is an area of research that is undeveloped, however, it seems logical that many of the measures employed for supporting gut and brain health would also be salient.
Far from being distant organs, the gut and brain communicate through a complex network of neural, hormonal and immune pathways and messengers, called the “gut-brain axis”. The integrity of our digestive system directly impacts the information our brain receives, and the quality of the building blocks of the brain tissue itself.
Our mood can also be impacted by poor vagal tone. The vagus nerve connects our digestive system to our brain and is the major nerve in our ‘rest and digest’ nervous system. With busy and stressful lifestyles regularly triggering our ‘fight or flight’ response, this vagus nerve may not be functioning well, which can contribute to depression and indigestion.
Much of the immune system is housed in our gut, making sense when much of our environmental risk exposure enters the body through our food. Our gut, therefore, needs to be in good shape for our immune system to be working well.
Maintaining Balance
Our blood sugar levels also impact our mood. Our brain is an energy hungry organ, using 25% of our total energy stores and preferring glucose to carbohydrates to keep it going. If our blood glucose levels are unstable, say from a high carbohydrate diet, this can be stressful for the brain to cope with and can cause mood swings or feeling ‘hangry’.
Blood sugar swings can also make us feel fatigued and have a detrimental impact on an important protein, BDNF (brain-derived neurotrophic factor) essential for the survival and growth of brain cells. BDNF helps our brain cells communicate and promotes the calming neurotransmitter GABA, levels of which may be low in anxiety sufferers. It also supports how our body makes energy, and therefore if levels of BDNF are low, we are more likely to feel fatigued, listless and at risk of experiencing mental ill health.
Top Tip
Keeping our gut healthy with a Mediterranean style diet, abundant in fibre-rich fruit and vegetables, oily Omega-3 rich fish, and wholegrains enriched with B-vitamins, translates into increased brain health, in turn improving our mood and mental health.
With thanks to Julie Pichler at Vagus Wellbeing for this article.Julie is a registered Nutritional Therapist and delivers our Workplace Wellbeing programme, offering educational and empowering webinars. Julie’s specialism is the gut-brain connection and how food impacts our mood and brain health.
Find out more about our webinars here and how they can support your employees’ mental wellbeing.
Methylation and mental health are intricately related. We take a deeper look into the association and why it is important.
What is methylation?
Methylation has been a buzzword in the integrative health sphere for some time now. This is unsurprising considering its importance to our overall health and wellbeing. You may have heard of it before – or even googled it… Were you then promptly turned off by it after just one glance at its complexity?
We don’t blame you; understanding methylation is not for the faint-hearted.
However, let us break it down for you into bite sized chunks. Hopefully you can finally make sense of it and apply this knowledge to your everyday life.
Think of it as a biological switch
Methylation is a critical biochemical process that happens billions of times in every single cell of the human body. It’s responsible for a vast range of biological functions such as:
Detoxification
DNA expression
Neurotransmitter production
Hormone regulation
Whilst it can be complex in nature, the process of methylation simply entails the transfer of four atoms: one carbon atom and three hydrogen atoms. These are transferred from one substance to another.
Let’s say that methylation is a type of biological switch that turns on and off to help keep our health in check.
How does methylation impact mental health?
While we know that methylation plays an intrinsic role in many important body functions, for the purpose of this article, we will focus on its role in mental well-being and brain health.
Put simply, methylation helps us make neurotransmitters, such as serotonin, dopamine, adrenaline, norepinephrine and melatonin.
Methylation does this in a number of ways. It helps:
Convert tryptophan (building block for serotonin) to 5-HTP (precursor to serotonin)
Transport dopamine, norepinephrine and adrenaline
Convert norepinephrine to adrenaline (important for focus and attention)
Lastly, convert serotonin to melatonin (sleep neurohormone)
So as you can see, it’s pretty vital to a balanced mood and overall brain health.
What impacts methylation?
Unfortunately there are many things that can negatively impact methylation, such as our diet, exposure to environmental toxins, genetic factors and lifestyle habits.
Let’s look at this in a little more detail.
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Anything that triggers oxidative stress can have a negative effect on methylation. Oxidative stress is a natural biological process that’s usually offset by our body’s own endogenous antioxidant production. But when there’s an imbalance between the two, and factors in our environment generating oxidative stress are tipping the scale in their favour, that’s when we can see prolonged inflammation and problems with methylation.
What specific environmental factors can impact methylation?
Our modern environment is plagued with reactive oxygen species ROS that generate oxidative stress in the body. Key examples are environmental endocrine disruptors, like PCBs, herbicides, pesticides and plasticisers, as well as air pollution.
Whilst we can’t necessarily fully control these aspects in our environment, we can control our defence against them, as well as making wise dietary choices that will have less of these substances in them.
But first, let’s talk about what else can impact methylation.
Dietary factors and methylation
What you eat can impact how well you methylate, especially the intake of processed foods and sugars, which has been shown to play a negative role in methylation.
Perhaps unsurprisingly, research shows that eating a wholefood diet that includes wholemeal cereals, fish, legumes, fruits and vegetables can have a positive effect on methylation.
Aside from dietary factors, there are a few nutrients that play a critical role in methylation.
Folate
Perhaps the most important nutrient is folate or B9. Methylation is almost entirely dependent on the availability of folate in the diet. It uses this nutrient to create the methyl donors – SAMe and methionine – to spark enzymatic reactions that are required for neurotransmitter production and transport.
A large body of research (1) confirms that folate deficiency – something that is incredibly common – is frequently seen in those with depression, and is remediated with the supplementation of this nutrient.
When we consider the role that optimal methylation plays in producing serotonin and other neurotransmitters, it’s easy to see why folate is so important.
What about folic acid?
Many are drawn to supplementing folate in the form of folic acid, the synthetic version of this nutrient. You can often find folic acid in fortified foods such as breakfast cereals and breads.
However, what people don’t realise is that this version of folate needs to be converted in the body to l-methylfolate and many people lack the ability to do this efficiently due to gene variations.
This means the body is unable to utilise the folic acid properly. We go into gene variants in a little more depth further down, so hold on for more information.
Where can we get folate in our diet?
The best food sources of folate are dark leafy greens (like spinach and kale), legumes (such as lentils and chickpeas), liver, asparagus, Brussels sprouts, and fortified grains, so be sure to be getting these in your diet frequently.
B12
Whereas folate is important to initiate the methylation cycle, B12 is required for the activation of folate from dietary folate to 5-methyltetrahydrofolate, so that it can go on to create the methyl groups – SAMe and methionine.
If there isn’t enough B12 in the diet, folate can get stuck in the cycle, which halts methylation.
B12 is a nutrient that’s found in animal foods, such as meats, fish, eggs, poultry and dairy products. This means that if you’re vegan or vegetarian, you will likely need to supplement your B12 and consider eating fortified foods, such as plant milks.
Choline
Choline – plays an important role in various junctions in the methylation cycle. It is widely known that when folate is low, the body uses choline as its back up methyl donor to help keep methylation ticking along.
It helps with activation of folate, as well as the recycling of homocysteine to methionine – a critical step in methylation.
The test that shows how well you are methylating…
Having high homocysteine is a key way of indicating whether your methylation is struggling and whether this recycling process isn’t functioning properly.
We don’t want accumulating levels of homocysteine as it is a neurotoxin that has been linked to psychiatric disorders such as depression, schizophrenia, bipolar and Alzheimer’s disease (2).
This is why if mental health is a concern, testing for homocysteine is a great way to find out whether you may have issues methylating. You can order and test your homocysteine level accurately from the comfort of your own home. Join our research and order your homocysteine test.
(Bear in mind that levels are not static and can change based on how well you’re methylating, as well as certain dietary factors, such as caffeine and alcohol consumption, which have been shown in some cases to tax methylation.)
Testing methylation
In addition to homocysteine, which is explained in further detail below, you can also take a DNA test to see whether you have any mutations on the MTHFR gene – the primary gene that is responsible for folate activation and homocysteine recycling – both of which are necessary for optimal methylation and therefore neurotransmitter production.
Testing for MTHFR
Variants or mutations on the MTHFR gene are inherited from your parents and can either be heterozygous (meaning you have one mutation) or homozygous (two mutations).
It’s well known that having a homozygous mutation is more likely to cause health problems and having a heterozygous mutation is unlikely to cause issues.
Common variants are:
C677T
A1298C
Testing for these variants is done by a simple saliva test and is usually done privately. Here in the UK, there are various providers such as Lifecode GX, however, if you’re not based in the UK there are likely many more providers globally.
How do we optimise methylation?
As well as eating a wholefood diet that is devoid of sugar and processed foods, if you suspect methylation may be an issue for you, it’s important to take the environmental factors listed above into consideration.
In order to avoid toxins and pollutants you can:
Eat organic produce as much as possible and wash any inorganic vegetables properly before consumption.
Drink filtered water
Buy toxin free cosmetics that don’t include typical endocrine disruptors such as parabens, benzophenones, bisphenols, and phthalates
Key takeaway: there is so much you can do to support your methylation pathways and support your mental health!
Eating a healthy, balanced diet, as well as engaging in healthy lifestyle practices as we outline in our COGNITION Programme, is key. We cannot change our genes but we can create the right environment for them.
When you become a FRIEND and gain access to your personalised 6-month COGNITION programme you will learn how to create the right environment to ‘upgrade your brain’.
Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.
By completing the Cognitive Function Test you 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. Please support our research by becoming a Friend of Food for the Brain.
Despite the festivities and joy that Christmas celebrations can bring for some, for many, it can be a particularly painful time with heightened feelings of loneliness and despair. This may be especially true for those who are isolated or disconnected from their loved ones. With the extra pressures that this year brings, it’s important to have some strategies in place to help us find a sense of connection.
An interesting recent study, offers some key information on how the brain is wired to seek social connection as if our survival depended on it, which helps us to understand why many of us feel such despair when we’re lonely. Neuroscientists at the University of Cambridge observed 40 participants in complete isolation for 10 hours, after which they were shown images of people socialising or playing sport. In response to these images, neurons in the midbrain – which is the part of the brain that is responsible for producing dopamine, our reward neurotransmitter – were stimulated. Interestingly, the same thing happened when these same participants – on a different day – were made to fast for 10 hours and then shown images of appetising food, like pizza and cake. This demonstrates how when we are lonely, we crave social connection in the same way that we crave food when we’re hungry.
Connection to others is just as much of a necessity to survive as it is to eat, and it’s not the first time that science is showing this. For example, we know that loneliness is a significant risk factor for poorer cognitive health, as well as depression and mortality. So, in light of this, and with the added pressures of the pandemic, how can we nurture our connection with
others to help us thrive throughout the festive season? Here are a few tips that can help to boost our sense of connectedness:
Review which kinds of social interactions energise you the most
This may be a time to reflect on which relationships/social circles you value the most and which ones may be leaving you a little drained. It is possible to feel lonely or disconnected, even when you’re with friends or family. Once you’ve determined those that you value the most, find time to nurture those connections away from distractions, such as phones or TV. Getting out in nature by finding a new park or green space you’ve never been to before and arranging a walk with a friend, or cooking a new recipe with your loved one and having a romantic dinner. The list is endless, but the most important thing is that it works for you.
Find a volunteering opportunity
Science shows that altruistic behaviour, kindness and compassion, increase levels of endorphins and oxytocin, as well as creating new neural connections. Find a local food bank distribution venue or another cause that you resonate with where you can meet new people and help support others.
Get creative
Getting involved in creative expression of any kind, from drawing and cooking, to gardening or dancing, can help to increase a sense of connection to ourselves and others. For example, making something creative with a friend or giving something creative as a gift, can be very therapeutic and rewarding, and has the added bonus of not requiring technology.
Final words…
It’s worth reiterating that loneliness can be a subjective experience, meaning that we can still be lonely despite having many loved ones around us. This highlights the need to take time to reflect and identify what makes each of us as individuals feel connected.
The gut microbiome, defined as the bacteria that colonises our digestive tract, seems to be a buzz word at the moment within the health industry, as a growing body of research is showing just how important quantity and quality of protective gut bacteria are for our health. But the most interesting recent discoveries concerning gut bacteria are how they interact with our brain, in a system that has been labelled the gut-brain axis. This axis represents a two-way relationship between the gut and the brain, whereby our bacteria help communicate messages to our brain and neurochemicals communicate from our brain to our gut. Not only have researchers found that gut bacteria are important for gut motility and nutrient absorption, but they are also finding that these 100 trillion microorganisms, that represent around 1000 different species, can actually modulate brain development and activity, as well as playing a role in conditions such as autism.
Autism and IBS
In the UK, there are over 700,000 people who are on the autism spectrum, which is a lifelong condition that can greatly impact the lives of those living with autism and their relatives. Research has continuously shown that those on the spectrum commonly have comorbidities related to digestive function, such as IBS. In a study of 255 (184 males/71 females) children with autism between two and 3.5 years of age and 129 (75 males/54 females) typically developing children in the same age group, it was found that preschool-aged children with autism were 2.7 times more likely to experience GI symptoms than their typically developing peers. Almost 50% of children with autism reported frequent GI symptoms — compared to 18% of children with typical development. It is not yet understood why this is the case, however the research on how our gut microbiome can influence brain activity is providing the grounds for new therapeutic measures for conditions like autism.
The role of short chain fatty acids
The composition of our gut bacteria and its diversity is often dependent on the food that we eat. Insoluble fibre such as cellulose, xylans and inulin found in foods such as vegetables and whole grains, provide fuel for our gut bacteria to flourish and ferment to create short-chain fatty acids (SCFAs). These fatty acids, produced by protective bacteria, can reduce the production of proinflammatory molecules called cytokines and can enhance anti-inflammatory processes. SCFAs produced by certain strains of bacteria have also been found to be capable of producing neurotransmitters such as GABA, which is an inhibitory neurotransmitter that helps to regulate anxiety. Bacteria can also produce a set of neurotransmitters called monoamines such as dopamine, which helps control the brain’s reward and pleasure centres, serotonin, our mood stabilizer, and noradrenaline, a neurotransmitter that’s involved in our fight or flight stress response. The vagus nerve, which travels from the intestine to the brain, enables neurochemicals produced by the gut bacteria to be signalled to the brain.
SCFAs produced by pathogenic bacteria, such as the Clostridial species, have on the other hand, been shown to be elevated in those with autism. Disrupted gut bacteria has been frequently associated to autism in studies showing unfavourable amounts of pathogenic bacteria in stool samples and in biopsies of children on the autism spectrum. A variety of drivers such as early weaning from breast milk to infant formula, which was related to increased fecal concentrations of SCFAs produced by pathogenic bacteria, and genetic alterations that can negatively impact how food is digested, have been shown to play a role in symptoms associated to autism.
Stress and the gut
Research has also shown how psychosocial stress can negatively impact our gut, by altering the composition of gut bacteria and thereby increasing inflammation. This is further evidence for the two-way relationship that exists between the brain and the gut, whereby externally-perceived stress can have a direct influence on the health of our digestive tract. A study measuring lactic acid bacteria (protective bacteria) in college students undergoing the stress of final examinations, found a significant decrease in this type of bacteria after the examination. In addition, studies observing the behaviour of bacteria-free mice, showed a wide range of deficits in brain and gut biochemistry, social behaviour and stress responses compared to mice inoculated with gut bacteria, again giving strong evidence for the role of gut bacteria in modulating brain activity.
Periodontitis is another word for gum disease, caused by a specific bacteria called Porphyromonas gingivalis, that leads to infection of the tissue holding the teeth in place, and as a consequence, symptoms such as bleeding gums and loose teeth.
The association between chronic gum disease and cognitive impairment has long been established, with several studies showing a strong correlation between periodontitis and Alzheimer’s disease. In 2009, a cross sectional observational study on participants of 60 years and over, tested 2355 people for IgG antibodies to P. gingivalis. Those who had the highest levels of IgG antibodies, were more likely to have poor delayed verbal recall and impaired subtraction, compared to those with the lowest. This is significant, as we know that the presence of IgG antibodies demonstrates that the body has created an inflammatory response to the bacterium, which is strongly associated with the pathogenesis of Alzheimer’s disease.
We already know that patients with Alzheimer’s disease exhibit neuroinflammation that is akin to a reaction to an infectious agent, like bacteria, leading to the activation of the brain’s immune cells called the microglia, as well as a cascade of cytokine production – another hallmark of inflammation. For this reason, infectious agents have been robustly studied as a key contributing factor to the development of Alzheimer’s. However, a direct causal role is yet to be established.
“People who have suffered from gum disease for 10 years or longer are 70% more likely to develop Alzheimer’s disease…”
Despite the lack of evidence for a causative role, associations between cognitive decline and bacterial infection have continued to be established. In another more recent study, published in Alzheimer’s Research & Therapy in August 2017, where more than 25,000 people aged 50 or older participated, researchers found that people who have suffered from gum disease for 10 years or longer are 70% more likely to develop Alzheimer’s disease. This study also highlighted that in those with chronic gum disease, there was a higher prevalence of depression, traumatic brain injury and hyperlipidaemia, which may all be contributors in the development of dementia. This research suggests that there may be various factors at play, rather than just gum disease on its own.
Gingipains destroy brain cells
The bacteria responsible for the infection is not only found in those with gum disease, but has also been found at low levels in 25% of healthy individuals with no presence of oral disease. However, what more recent studies are showing is that it is the proteins called gingipains, that are released by the bacteria that are responsible for damage to nerve cells in the brain, rather than just the bacteria on its own. During experiments carried out in mice that were infected orally by P.gingivalis, scientists discovered that they later demonstrated signs of brain deterioration and infection, which are concurrent with humans showing symptoms of early-stage dementia.
In this same study, carried out by researchers from a variety of universities, brain tissue samples from approximately 100 people with and without Alzheimer’s were analysed and tested for two different types of gingipain proteins. They also tested for the presence of gingipain DNA in both the cerebrospinal fluid and the saliva of people that had been diagnosed with Alzheimer’s. What they found was that the level of gingipains in brain tissue of those with Alzheimer’s was between 91% and 96% (for the two different proteins), in comparison to 39% and 52% in those without Alzheimer’s. Furthermore, they found gingipain DNA in 7 out of 10 cerebrospinal fluid samples in those with Alzheimer’s and 10 out of 10 for the saliva samples.
P.gingivalis has, in addition, been shown to be extremely virulent – unlike other bacteria, studies demonstrate that broad-spectrum antibiotics rarely eradicate itand may lead to resistance to it. In addition, P.gingivalis depends on the secretion of gingipains to maintain its survival. They do this by supporting the bacteria’s colonization and the inactivation of the host’s immune defences. Whilst drugs have been developed to block the neuroinflammatory action of gingipains, trials have yet to be completed on humans to assess the efficacy of them.
“We are working on the theory that when the brain is repeatedly exposed to bacteria and/or their debris from our gums, subsequent immune responses may lead to nerve cell death and possibly memory loss.”
Researchers from the University of Central Lancashire in the UK, report that bacteria like P.gingivalis can enter from oral cavities into the bloodstream through a variety of daily activities, such as eating, brushing teeth and chewing. However, they mention in a study published in the Journal of Alzheimer’s Disease, that the bacteria is more likely to enter the circulatory system after invasive dental treatment, which then goes on to trigger inflammation. Dr. Sim K. Singhrao, Senior Research Fellow at UCLan said: “we are working on the theory that when the brain is repeatedly exposed to bacteria and/or their debris from our gums, subsequent immune responses may lead to nerve cell death and possibly memory loss.”
Whilst we know that having dementia can lead to difficulties maintaining daily habits like brushing teeth properly, the findings of many studies suggest that gum infections precede the diagnosis of dementia. This means that, like other modifiable risk factors such as diet, smoking, obesity and diabetes, there are things that we can do to help reduce the chance of developing Alzheimer’s disease.
How to prevent periodontal disease
Besides from the obvious dental hygiene habits like brushing teeth and the tongue after every meal to remove food and plaque, flossing and using an antibacterial mouthwash, there are also dietary measures that can be put in place to offer extra support.
For example, research shows that there is a strong association between type 2 diabetes and periodontal disease. This may be due to the fact that increased levels of glucose in the blood, due to insulin resistance, can favour the growth of certain species of bacteria such as P.gingivalis. In addition, diabetes can lead to a malfunctioning of the immune system, which leads to a decrease in antibody function and therefore more opportunity for bacterial infection.
On that basis, it is therefore essential to avoid sugar, in all its forms, including the seemingly ‘natural’ alternatives to regular cane sugar, as well as focusing on a diet that helps to stabilise blood sugar levels.
Here are some practical dietary steps to help protect your teeth and gums from periodontal disease:
Avoid sugar and any products with added sugar in them. Beware of the different names for sugar – just because a product doesn’t contain sugar in the ingredient list, does not mean it hasn’t had an added sweetener to it. Here are some examples of sugar substitutes to be aware of and avoid:
Dextrose, Fructose, Galactose, Glucose, Lactose, Maltose, Sucrose, Beet sugar, Cane juice crystals, Coconut sugar, Corn syrup solids, Crystalline fructose, Date sugar, Dextrin, Diastatic malt, Ethyl maltol, Florida crystals, Glucose syrup solids, Grape concentrate, Maltodextrin, Agave Nectar/Syrup, Barley malt, Blackstrap molasses, Brown rice syrup, Buttered sugar/buttercream, Caramel, Carob syrup, Corn syrup, Evaporated cane juice, Fruit juice, Fruit juice concentrate, Golden syrup, High-Fructose Corn Syrup (HFCS), Honey, Invert sugar, Malt syrup, Maple syrup, Molasses, Rice syrup, Refiner’s syrup, Sorghum syrup, Treacle.
2. Avoid fruit juices and in particular shop-bought fruit juices, which often contain fruit concentrates. Whilst fruit is a natural form of sugar, fruit juices often contain the juice of the fruit without its pulp or fibre. This means that it is very quickly converted into glucose (sugar) in the body, which leads to blood sugar imbalances and eventually insulin resistance, if consumed too frequently.
3. Eat a diet that mainly consists of foods in their natural form, paying attention to meals that prioritise protein such as in pulses, eggs, poultry, meat and fish, along with a wide variety of vegetables and healthy fats found in nuts and seeds, avocado and extra virgin olive oil.
4. Switch refined carbohydrates for complex carbohydrates – these are foods that are naturally high in fibre such as whole grains like brown rice, wholemeal bread, quinoa and oats, as well as starchy vegetables like beetroot, sweet potatoes, carrots, pumpkin and butternut squash.
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