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How To Break Free From Food Addiction

How To Break Free From Food Addiction

woman eating cake

Do you ever promise yourself you’ll stop eating sugar or junk food – only to find yourself back at the biscuit tin a few hours later? You’re not alone. Food addiction is real. In fact, it can be as powerful and pervasive as alcohol addiction.

The first step is awareness. According to clinical psychologist Dr Jen Unwin, there are six warning signs. If you recognise yourself in two or more, it may be time to take this seriously.

Read on to see if any apply to you.

Six Signs You May Be Addicted to Food

1. Certain foods feel impossible to resist

 “You’re craving a certain food so badly that you feel compelled to eat it, even when you know you shouldn’t,” Dr Unwin explains. At the height of her own addiction, she would secretly make a bowl of cake mixture – just butter, sugar and flour -and eat the entire thing raw. “It sounds ridiculous now, but I had such intense cravings for sweet, soft, sugary foods,” she explains.

2. You always need more

Like alcohol tolerance, food addiction builds over time. “One slice of cake may have been enough in the beginning, but soon you need two, three – or half the cake – to get the same dopamine hit,” says Dr Unwin. She recalls eating slice after slice at her daughter’s wedding, unable to stop until she felt sick.

3. Food takes priority over everything else

A common factor in addiction is that you begin to ignore what you once valued and prioritise food above socialising, hobbies, family time and even work. Often, Dr Unwin would leave the house and her family in secret to drive for 20 minutes to a cinema complex where she would order a large tub of Ben & Jerry’s Cookie Dough ice cream with chocolate sauce. She would then return to her car and eat the entire portion, feeling ashamed and elated at the same time, before returning home an hour later as if nothing had happened.

4. You lose control once you start

You might buy biscuits for your grandchildren, planning to have just one with your tea. Before you know it, the whole packet has disappeared.

5. Withdrawal symptoms kick in

If you try to cut down on sugary snacks and carbohydrates, do you experience withdrawal symptoms? “These include headaches, migraines, gastrointestinal symptoms, low mood, anxiety, fatigue and brain fog,” Dr Unwin says. “As people experience sugar withdrawal, they feel so bad that they just go back to eating it.” When Dr Unwin completely abstained from sugar, she experienced many of these symptoms for eight days. But after pushing through that difficult period, she began feeling better than ever.

6. You know it’s harming you – and carry on anyway

According to Dr Unwin, this is the defining sign: eating damaging foods despite knowing the consequences. She references a patient with Type 2 diabetes who kept bingeing on cake and sugar knowing how bad it is for their blood sugar. People in this situation often know the food is harmful, but they feel trapped in a cycle.

Why Processed Foods Hijack Your Brain

Breaking free from any addiction is not purely a matter of willpower. Addictive foods and drinks hijack your brain’s chemistry, making you crave them. This effect is purposely done so that you keep buying more.

Understanding how certain food ingredients and combinations work in the brain unlocks the secret to undoing food addiction. The most powerful trigger is the combination of fat and sugar – the two key components of most junk foods. Think cakes, biscuits, ice cream, chocolate bars and pastries. This pairing presses the brain’s dopamine “reward” switch, creating intense pleasure in the moment but diminishing feelings of satisfaction over time. Just like drugs, it fuels cravings and loss of control.
This hijacking of the dopamine-based reward system doesn’t just drive overeating – it also increases the risk of cognitive decline and brain shrinkage. Additionally, it disrupts glucose control and drives insulin resistance, a well-known promoter of cognitive decline.  (Read more –  ‘Is Sugar Killing Your Brain?)

Nutritional Tools That Reset Your Brain

In Patrick Holford’s book How to Quit without Feeling S**t  he recommends strategies that help restore balance to your brain chemistry:

  • Omega-3 fats – vital for healthy cell membranes and for receiving neurotransmitter messages.
  • B vitamins and methylationcheck homocysteine levels; if they are high, it may indicate poor methylation and raised risk of cognitive decline.
  • Tyrosine – dopamine is made from this amino acid. A supplement of 500mg twice daily can help support dopamine production.

Protein + slow carbs – pairing protein (such as nuts or Greek yogurt) with fruit like berries slows sugar release and provides fibre and nutrients.

If you feel like you are struggling to break free from food addiction, then join  Dr Jen Unwin’s live webinar on Wednesday, 24th September – find out more here.

 A clinical Psychologist’s Practical Tips on How to break free; 

  • Visualise how life will improve once you manage to quit your “drug foods”. These are typically ultra-processed and sugary foods with which you’re unlikely to have a healthy relationship.
  • Have an honest conversation with friends and family about the foods you struggle with, and ask for their support in resisting them..
  • Removing the “drug foods” from your home and diet is key. Replace them with natural, whole foods.
  • Give it time. Every day you resist, it gets easier. “Those foods are no longer in my thoughts at all,” says Dr Unwin.
  • If you take medication for diabetes or high blood pressure, consult your GPbefore reducing sugar and carbohydrates in your diet, as your dosage may need adjusting.
  • If you’re concerned about food addiction or would like to learn more, Dr Unwin recommends joining a Public Health Collaboration (PHC) support group in the UK, or Sweet Sobriety in the US. The PHC also runs a virtual lifestyle support group every Monday at 6pm, where you can learn more about overcoming food addiction and maintaining good metabolic health.

The Bigger Picture

Food addiction is more than a personal struggle and it impacts more people than you realise. It’s part of a wider public health crisis, fuelling obesity, diabetes and dementia – but no matter where you are at right now, change is possible!

Ways to get support:

Food or drink addiction? Discover how to beat cravings and food addiction in Dr Jen Unwin’s live webinar, 24 Sept.

Join the live webinar on food addiction with clinical psychologist Dr Jen Unwin on Wednesday, 24th September – find out more here.

International Food Addiction & Comorbidities Conference logo

ttend the International Food Addiction & Comorbidities Conference – IFACC 2025. Use discount code FFB to get 40% off:

  • Two-day in-person ticket: £150 (full price £250)
  • Two-day livestream ticket: £54 (full price £90)
Cognition Programme logo

Get ongoing support with the COGNITION™ programme. Receive monthly coaching when you become a. FRIEND of Food for the Brain.

Fork in a road logo

Read Dr Jen Unwin’s book, Fork in the Road a hopeful guide for identifying if you have a food addiction and learning what to do about it.

frontiers logo

Read this journal article in Frontiers in Psychiatry to support and join the movement to have food addiction classified as a real disease, thus enabling more research and support, and helping to make the dangers of ultra-processed foods more visible.

Further info

New Study: Is Red Meat Bad for Your Brain?

New Study: Is Red Meat Bad for Your Brain?

New Study: Is Red Meat Bad for Your Brain?

In a culture where the average plate still leans heavily towards meat – often processed, often excessive – it’s time to reassess the impact of our protein choices not just on our waistlines, but on our brains. A recent study in Neurology (2025) has added fresh weight to decades of evidence linking red and processed meat consumption to an increased risk of dementia and cognitive decline (1). Meanwhile, fish – particularly oily fish – continues to top the charts as the most protective food for your brain (2,3).

So, what does this mean practically for those of us trying to upgrade our brains and reduce our risk of cognitive decline? The answer may be as simple as this: eat more fish and fewer sausages.

Red Meat, Processed Meat and the Rising Risk to Brain Health

A new US cohort study, which followed over 77,000 adults across 30 years, found that:

  • Processed red meats (bacon, hot dogs, sausages, salami, bologna and other processed meat products) were clearly problematic. Consuming just 0.25 servings per day or more was associated with a 13% higher risk of developing dementia compared with those eating less than 0.1 serving (1).
  • Unprocessed red meat (e.g. beef or lamb) was linked to a 16% increased risk of subjective cognitive decline – that is people reporting that their memory or mental sharpness was worsening – when consuming more than one serving daily compared to less than half a serving per day. However, the researchers noted that this link did not reach statistical significance for diagnosed dementia overall (1).
  • More encouragingly, replacing one daily serving of processed red meat with a serving of nuts, lentils, or beans was associated with a 19% lower risk of dementia (1).

These findings are consistent with a large UK Biobank analysis of almost half a million adults, which found that each additional 25 g/day of processed meat (bacon, ham, sausages, meat pies, kebabs, burgers, chicken nuggets) was associated with a 44% higher risk of all-cause dementia and a 52% higher risk of Alzheimer’s disease. In contrast, each 50 g/day of unprocessed red meat was linked to a 19% lower risk of all-cause dementia and a 30% lower risk of Alzheimer’s disease (4).  This reinforces the idea that it is the processing – not necessarily the meat itself – that may be most harmful.

These associations were observed regardless of whether participants carried the APOE ε4 gene variant – further evidence that dietary choices have a significant impact and that Alzheimer’s is ‘not in the genes’. (4).

The Global Pattern

The irrelevance of genetics in these findings is further supported by global evidence. An ecological analysis across 204 countries found that higher national per-capita total meat supply – including both red and white meats – was significantly associated with higher dementia incidence, even after adjusting for ageing, economic development and genetic risk, including APOE ε4 prevalence where available (5). In other words, the meat-dementia link is not confined to particular genetic subgroups but is observable across populations worldwide, suggesting that the way we produce and consume meat may be influencing brain health trends on a global scale. 

What we put on our plate is powerful when it comes to reducing dementia risk – more so than any genetic variations that attract attention in the media.

Why Fish is Brain Food

The answer is not to go hungry, but to swap for something else – and when it comes to brain health, marine foods are your answer.

Unlike red meat, fish – especially oily varieties like salmon, sardines or mackerel – continue to show a strong protective effect.

A comprehensive 2024 meta-analysis found that:

  • Eating one to two servings of fish per day (roughly 150 g) is associated with a 20% reduced risk of Alzheimer’s disease and up to 30% slower cognitive decline (2).
  • Another study found that people who ate fish at least once a week had a one-third lower risk of Alzheimer’s compared with those eating fish less than weekly (3).

Why? Omega-3 fats, especially DHA, are critical for brain function and structure. They reduce inflammation, support synaptic plasticity and help clear beta-amyloid – a protein associated with Alzheimer’s disease.

As explained in the COGNITION™ 6-month programme, omega-3 fats from fish oil play a pivotal role in building and repairing the brain, particularly in mid-life, when early signs of cognitive decline can start to emerge.

That’s why we offer omega-3 at-home blood tests – so you can check whether you’re getting enough through your diet or if it’s time to add a supplement. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test where you can also check your homocysteine and glutathione status at the same time.

A Simple Swap with Profound Impact

From a cognitive health perspective, the data is now hard to ignore: if you’re regularly eating red or processed meat – especially more than once a day – your brain may be paying the price. But shifting even one of those servings towards fish, eggs or plant-based proteins could make a meaningful difference.

Interestingly, the main culprit in the latest studies was processed meat. This supports a key principle in brain-friendly eating: most natural whole foods – whether meat, fish, fruit, nuts, legumes, wholegrains or dairy – are not the problem. It’s when we distort them into ultra-processed, factory-made food that health is undermined.

This isn’t about becoming vegan or pescatarian. It’s simply more evidence to reduce processed foods and ensure optimal omega-3 intake. 

So next time you’re at the supermarket make a cow happy and buy a fish.

Resources:

Order your omega-3 test today to find out if you are eating enough of these essential fatty acids. You can test omega-3 on its own here, or as part of our 5-in-1 DRIfT test. Available globally.

References:

You J, Zhang L, Zhou Y, et al. Total meat supply and incidence of dementia: an ecological study of 204 countries. Front Public Health. 2025;13:1589936. doi:10.3389/fpubh.2025.1589936.

Li Y, Li Y, Gu X, Liu Y, Dong D, Kang JH, Wang M, Eliassen H, Willett WC, Stampfer MJ, Wang D. Long-Term Intake of Red Meat in Relation to Dementia Risk and Cognitive Function in US Adults. Neurology. 2025;104(3):e210286. doi:10.1212/WNL.0000000000210286.

Godos J, Micek A, Currenti W, Franchi C, Poli A, Battino M, Dolci A, Ricci C, Ungvari Z, Grosso G. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;36(1):171-182. doi:10.1007/s40520-024-02823-6.

Beydoun MA, Beydoun HA, Gamaldo AA, Teel A, Zonderman AB, Wang Y. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643. doi:10.1186/1471-2458-14-643.

Zhang Z, He P, Liu M, et al. Meat consumption and risk of incident dementia: cohort study of UK Biobank participants. Am J Clin Nutr. 2021;113(5):1228-1236. doi:10.1093/ajcn/nqaa343.

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The Truth about Alcohol and Your Brain

Alcohol section in suppermarket with wine bottles

If coffee is the worker’s fuel for the fast and frenetic pace of modern life in the digital age, alcohol is the opiate of the masses. 

Most people use coffee or tea to wake up the brain and alcohol to switch off daily feelings of stress and anxiety. But what are these habits doing to brain health? How much is too much, or too little? Are there other ways to unwind after a hectic day that can benefit the brain?

Alcohol – The Friendly Neurotoxin?

Alcohol is a neurotoxin that impairs cognition. That is the simple fact we often forget. Once the liver’s capacity to detoxify is exceeded, it is precisely this neurotoxic effect that creates the ‘drunk’ feeling – starting with reduced inhibitions, the onset of memory loss, (which some may consider useful after a stressful day), and slurred speech. These effects are due to cognitive impairment, rather than relaxation – hence the warning: ‘not safe to drive’.

Stress Relief – at a Cost

The short-term upside of alcohol is its ability to suppress adrenal stress hormones – key accelerators of brain ageing, particularly when the stress switch is stuck in the ‘on’ position. That background hum of stress and anxiety, pending doom or checking for problems, is a hallmark of life in the 2020s, with hourly news cycles cranking up reasons for gloom and fear. In this context, a drink may feel like a welcome antidote, offering temporary relief by dampening stress.

Alcohol also boosts GABA, a calming neurotransmitter which temporarily switches off adrenaline. This is why one drink can feel like relief – but the effect fades quickly and excessive drinking leads to GABA receptor downregulation, increasing anxiety the next day and impairing sleep quality – especially during the deep and REM phases. These two phases are vital for full brain recovery. As a result, one wakes up less cognitively alert, less energised and more likely to feel anxious or to react stressfully.

Alcohol – like all toxic drugs – is what Oscar Ichazo called a ‘door of compensation:  temporary escape we reach for when psychic tension runs too high. While it offers short-term reprieve, it ultimately drains vital energy.
(Do you need more guidance and support to help you make healthier choices and habits? Then become a FRIEND of Food for the Brain today to get access to monthly group coaching and COGNITION ™ for 6 months. Find out more here)

More on GABA

GABA is made from two amino acids – taurine and glutamine – and is promoted by theanine. These three amino acids are often included in supplemental ‘chill’ formulas. There are also herbs, which in combination, help to promote GABA. This effect is harnessed in some non-alcoholic drinks like SENTIA drinks called ‘GABA spirits’. These are non-alcoholic yet potentially calming and de-stressing, offering a viable alternative to alcohol.  

However, alcohol is not just ‘alcohol’ and its appeal isn’t only due to GABA promotion. Red wine, for example, is rich in polyphenols, which have real benefits for the brain. However, unless it is organic, it often contains sulphites and other chemicals added. Additionally, some individuals – particularly those who drink often – can develop sensitivity to alcohol or to a component such as yeast, triggering further inflammation in both the gut and the brain.

How Much Alcohol is Too Much?

Alcohol is, of course, addictive –  and it can become so very quickly, even in small amounts. There are two ends to this spectrum. At the extreme, more than 10,000 people under the age of 35 die each year from alcohol poisoning – literally from a single binge. It can be compared to a heroin addict who quits and then relapses, taking the same dose they had previously built tolerance to. Tragically, this was the case for Amy Winehouse, who died after one evening of excess following a period of sobriety.

But what about the other end of the spectrum – modest drinking? And does the type of drink make a difference? Let’s look at the evidence. 

Since Alzheimer’s dementia, which accounts for two-thirds of dementia, is diagnosed through both brain shrinkage and cognitive decline, let’s look at the effects of alcohol at various doses on both brain shrinkage and cognitive decline, the most severe consequence being an increased risk of a dementia diagnosis later in life.

A study of 36,678 MRI scans from UK Biobank found that consuming more than one unit of alcohol per day is associated with steadily decreasing white and grey matter in the brain. (5)  A unit is a small glass of wine, half a pint of beer or a single shot of spirits. 


A comprehensive study in the British Medical Journal in 2018, which followed more than  9,000 people over 23 years, found that both abstinence and drinking more than 14 units of alcohol a week, which is equivalent to a medium glass of wine (2.3 units) every day,  increased risk by 40%. (6) This is illustrated in the graph below.

Volume of gray matter relation to alcohol consumption chart

You will notice that the brain shrinking effect is more pronounced in women than men, and those drinking 3 to 4 units, the equivalent of a large 250 ml of wine, show four times as much brain shrinkage as those drinking one small glass. Half a bottle a night, which is more than 4 units,  is associated with nearly eight times the loss of brain volume (7). That’s a high price to pay. 


Two other large studies last year showed something similar. A Chinese analysis of UK Biobank data involving 314,000 drinkers found that the more a person drank, the higher their risk. Once again, the effect was more pronounced in women than in men. or women, the lowest risk was observed  at around 8 units a week (roughly the equivalent of a bottle of wine), with risk actually lower than in those who drank less. Overall, the lowest risk was in those consuming 11.9 units a week, or about 1.7 units a day. (8)

Red Wine – Poison or Polyphenol Powerhouse?

On the positive side, research shows that a 125 ml glass of red wine a day may actually reduce dementia risk more than abstinence.. Another study reported that the lowest risk for dementia was among those consuming about 2 units a day – the equivalent of  a small to medium glass of wine. (9)

Red wine in particular may be beneficial because of its higher levels of polyphenols. Red wine, chocolate, and tea are all rich in a polyphenol called epicatechin. 

Jeremy Spencer, a scientific advisor to Food for the Brain and Professor of Nutritional Biochemistry and Medicine at the University of Reading, has shown that polyphenol-rich plants improve blood flow in specific regions of the brain that are associated with attention, decision-making, impulse control, and emotion, improving overall ‘executive’ function. (10) What’s more, the level of flavanols in your bloodstream predicts your memory performance. 

In the COSMOS study, the greatest benefit from increased flavanol intake was observed in those with the lowest dietary intake. Improvements were particularly noted in aspects of memory linked to the hippocampus – the brain’s central memory hub and the region most affected in Alzheimer’s disease (11). More recent research into cocoa, a rich natural source of flavanols – has also shown cognitive improvements, likely due to enhanced circulation (12). These findings were reinforced in a follow-up COSMOS trial involving more than 20,000 participants, who took a flavanol-rich cacao extract or placebo daily for five years (13).

Mitigating the Damage: Supplements for Protection

  • Quercetin (found in red onions), glutamine and vitamin C, support liver detoxification, helping to prevent hangover symptoms. (14)
  • Curcumin (especially water soluble Theracumin), reduces acetaldehyde by about a third, compared with drinking mineral water, thus easing hangover headaches.(15)  It has also recently been shown to protect the liver and reduce the risk of fatty liver disease.(16)
  • Glutathione – Alcohol-induced liver damage, fatty liver disease and reduced cognitive function are associated with a lower level of glutathione – an ideal level is around 1,000, though levels should certainly be above 500. 

Not sure what your glutathione levels are? Test your antioxidant levels accurately from home with a single Glutathione test or as part of our DRIfT 5-in-1  blood test

The Final Pour…

Alcohol may quiet stress in the moment, but in the long term it dulls cognition, shrinks the brain, and disrupts sleep. 

The good news is that with the right habits and smarter choices, from regular exercise to alcohol-free days, you can unwind without trading clarity for comfort.

Our Advice: Smarter Drinking Hacks

  • Limit yourself to a maximum of one small glass of red wine daily (about 125 ml) – but ideally avoid drinking every day.
  • Stay under 14 units per week  to reduce cognitive risk.
  • Hydrate: drink one glass of water for every alcoholic beverage.
  • Exercise at the end of the day is a great way to de‑stress and promote sleep if you usually turn to alcohol for this purpose. 
  • Practise intermittent drinking: take longer alcohol-free breaks – weeks or months- to improve sleep, mood, and liver function
  • Avoid sugary drinks: they put extra strain on the liver. Choose dry wines, low-carb beers and skip sugary mixers like tonic and juice. Opt for ‘brut’ champagne. 
  • Eat polyphenols: pair wine with olives, blueberries, and dark chocolate for added brain protection..

 Want more insight into how healthy your brain is?

  1. Take the FREE Cognitive Function Test today to gain personal insights into into your brain health. 

Join our research and test your glutathione, homocysteine and other essential brain health biomarkers with our accurate at home test kits – find out more and order yours today

References:
1 The Stress Cure, Patrick Holford & Susannah Lawson, Piatkus 2014

2 Shell W, Bullias D, Charuvastra E, May LA, Silver DS. A randomized, placebo-controlled trial of an amino acid preparation on timing and quality of sleep. Am J Ther. 2010 Mar-Apr;17(2):133-9. doi: 10.1097/MJT.0b013e31819e9eab. PMID: 19417589.   https://pubmed.ncbi.nlm.nih.gov/19417589/

3 Dr Javier Sánchez-Betancourt et al., ‘Effect of 5-hydroxytryptophan and melatonin supplementation on mood, sleep and cognition in adult patients with depression’, Archivos Venezolanos de Farmacologia y Terapeutica, January 2022, DOI: https://doi.org/10.5281/zenodo.7512797

4 S. Saul, ‘Sleep drugs found only mildly effective but wildly popular’, New York Times, 23 October 2007

5 Daviet R, Aydogan G, Jagannathan K, Spilka N, Koellinger PD, Kranzler HR, Nave G, Wetherill RR. Associations between alcohol consumption and gray and white matter volumes in the UK Biobank. Nat Commun. 2022 Mar 4;13(1):1175. doi: 10.1038/s41467-022-28735-5. PMID: 35246521; PMCID: PMC8897479.

7 Nurk E, Refsum H, Drevon CA, Tell GS, Nygaard HA, Engedal K, Smith AD. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. J Nutr. 2009 Jan;139(1):120-7. doi: 10.3945/jn.108.095182. Epub 2008 Dec 3. PMID: 19056649

8 Zheng L, Liao W, Luo S, Li B, Liu D, Yun Q, Zhao Z, Zhao J, Rong J, Gong Z, Sha F, Tang J. Association between alcohol consumption and incidence of dementia in current drinkers: linear and non-linear mendelian randomization analysis. EClinicalMedicine. 2024 Sep 5;76:102810. doi: 10.1016/j.eclinm.2024.102810. PMID: 39290634; PMCID: PMC11405827. https://pubmed.ncbi.nlm.nih.gov/39290634/

9 Zarezadeh M, Mahmoudinezhad M, Faghfouri AH, Mohammadzadeh Honarvar N, Regestein QR, Papatheodorou SI, Mekary RA, Willett WC. Alcohol consumption in relation to cognitive dysfunction and dementia: A systematic review and dose-response meta-analysis of comparative longitudinal studies. Ageing Res Rev. 2024 Sep;100:102419. doi: 10.1016/j.arr.2024.102419. Epub 2024 Jul 20. PMID: 39038743

10 Spencer JP. The impact of fruit flavonoids on memory and cognition. Br J Nutr. 2010 Oct;104 Suppl 3:S40-7. doi: 10.1017/S0007114510003934. PMID: 20955649. See also Professor Jeremy Spencer’s presentation at the Alzheimer’s is preventable masterclass (2022) – foodforthebrain.org/aipmasterclass;

11 Brickman AM, Yeung LK, Alschuler DM, Ottaviani JI, Kuhnle GGC, Sloan RP, Luttmann-Gibson H, Copeland T, Schroeter H, Sesso HD, Manson JE, Wall M, Small SA. Dietary flavanols restore hippocampal-dependent memory in older adults with lower diet quality and lower habitual flavanol consumption. Proc Natl Acad Sci U S A. 2023 Jun 6;120(23):e2216932120. doi: 10.1073/pnas.2216932120. Epub 2023 May 30. PMID: 37252983; PMCID: PMC10265949.

12127 Lamport DJ, Pal D, Moutsiana C, Field DT, Williams CM, Spencer JP, Butler LT. The effect of flavanol-rich cocoa on cerebral perfusion in healthy older adults during conscious resting state: a placebo controlled, crossover, acute trial. Psychopharmacology (Berl). 2015 Sep;232(17):3227-34. doi: 10.1007/s00213-015-3972-4. Epub 2015 Jun 7. PMID: 26047963; PMCID: PMC4534492.

13 Sesso HD, Manson JE, Aragaki AK, Rist PM, Johnson LG, Friedenberg G, Copeland T, Clar A, Mora S, Moorthy MV, Sarkissian A, Carrick WR, Anderson GL; COSMOS Research Group. Effect of cocoa flavanol supplementation for the prevention of cardiovascular disease events: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial. Am J Clin Nutr. 2022 Jun 7;115(6):1490-1500. doi: 10.1093/ajcn/nqac055. PMID: 35294962; PMCID: PMC9170467.

14 Markowska J, Kasprzak-Drozd K, Niziński P, Dragan M, Kondracka A, Gondek E, Oniszczuk T, Oniszczuk A. Quercetin: A Promising Candidate for the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). Molecules. 2024 Nov 6;29(22):5245. doi: 10.3390/molecules29225245. PMID: 39598636; PMCID: PMC11596905.

15Sasaki H, Sunagawa Y, Takahashi K, Imaizumi A, Fukuda H, Hashimoto T, Wada H, Katanasaka Y, Kakeya H, Fujita M, Hasegawa K, Morimoto T. Innovative preparation of curcumin for improved oral bioavailability. Biol Pharm Bull. 2011;34(5):660-5. doi: 10.1248/bpb.34.660. PMID: 21532153.

16Panahi Y, Kianpour P, Mohtashami R, Jafari R, Simental-Mendía LE, Sahebkar A. Efficacy and Safety of Phytosomal Curcumin in Non-Alcoholic Fatty Liver Disease: A Randomized Controlled Trial. Drug Res (Stuttg). 2017 Apr;67(4):244-251. doi: 10.1055/s-0043-100019. Epub 2017 Feb 3. PMID: 28158893.

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Snacks: Brain Boost or Brain Drain?

Colourful selection of snacks displayed on a flat surface

When that mid-morning dip or afternoon slump hits, it’s tempting to reach for a quick fix – something sweet, something carby, something to perk you up. But most conventional snacks don’t fuel your brain – they drain it.

In fact, snacking is one of the easiest ways to sabotage your long-term brain health and memory. Most people wouldn’t eat a plate of sugar at mealtimes (unless they start the day with shop-bought cereal or sweetened yoghurt), yet it’s common to reach for a bar, a biscuit, or something from a petrol station or coffee shop without a second thought.

These everyday choices are a silent driver of brain fog, low mood, memory problems – even dementia. It’s time to upgrade your brain by upgrading your snacks. Below, we share a free Brain Boost Bites recipe and some other smart snack ideas – perfect for long drives, picnics, or busy days on the go.

The Problem with Typical Snacks

The modern snack aisle is a minefield of ultra-processed foods: cereal bars, crisps, flavoured yoghurts, granola bites, and biscuits – many of them marketed as “healthy”. But beneath the surface, they’re often:

  • High in sugar or refined carbs – causing a rapid blood glucose spike followed by a crash. Many so-called healthy bars contain over 15g of sugar with little fibre, protein, or healthy fat to balance them.
  • Low in brain-essential nutrients – such as omega-3s, magnesium, or phospholipids.
  • Full of artificial additives – emulsifiers, preservatives, and even excitotoxins like MSG.
  • Designed for instant gratification – often with addictive properties rather than sustained energy.

As explained in our Four Horsemen of the Mental Health Apocalypse series (read Part 1 here and Part 2 here), poor glucose control is a key driver of accelerated brain ageing and cognitive decline. A high-sugar snack spikes blood sugar, then causes a crash that reduces brain energy and impairs mental performance. Over time, this rollercoaster leads to insulin resistance, which is strongly linked to cognitive decline and Alzheimer’s disease.

The Smart Snacking Solution

The answer isn’t to stop snacking altogether – it’s to snack smart.

Our in-house chef and lecturer in culinary nutrition and functional health, Kim Close, shares a free recipe below from the Upgrade Your Brain Cook App. It’s packed with brain-supportive nutrients and perfect for keeping your energy and focus steady.

And if you’re not sure what to eat for better brain health, the Cook App includes 120+ recipes (and growing) to guide you meal by meal.

Brain Boost Bites

Refined sugar-free | Fibre-rich | Brain-fat fuelled | Brain Boosting

Brain Boosting snacks - bite balls in a plate

Ingredients:

  • 100g (3½ oz) almonds
  • 30g (1 oz) walnuts
  • 50g (1¾ oz) goji berries
  • 2 tbsp ground flaxseed
  • 2 tbsp almond butter
  • 1 tbsp raw cacao powder
  • 1 tbsp water (if needed for blending)

Method:

  1. Blend all ingredients in a food processor until the mixture becomes sticky and holds together.
  2. Roll into small balls.
  3. Chill in the fridge for at least 30 minutes.

Servings: Makes 10-12 balls

Cook’s Tips: Store in an airtight container in the fridge for up to a week. Add orange zest or vanilla extract for flavour variation.

Other Smart Snack Ideas:

  • Oatcakes with almond butter or smoked mackerel pâté
  • Olives 
  • Square of Dark Chocolate Bar (Recipe in Cook App)
  • Hummus or nut butter with raw veggie sticks
  • A boiled egg with cherry tomatoes
  • A handful of walnuts or pumpkin seeds
  • A small cup of full-fat Greek yoghurt with blueberries
  • Chia pudding made with coconut milk (recipe in the app)
  • 2 squares of 85%+ dark chocolate

Snacking wisely is one of the easiest daily upgrades you can make for your brain. And with the right ingredients, it can be delicious too.

Further info

Homocysteine and Dementia: The Evidence They Don’t Want You to See

Imagine if a simple, well-researched nutrient protocol could prevent cognitive decline in millions of people worldwide. Imagine further that this protocol has been known for years, supported by multiple clinical trials and global experts, yet systematically ignored by the very institutions meant to protect public health. That is precisely the case when it comes to homocysteine, B vitamins, and dementia.

Last year, the UK-based Lancet Commission on Dementia Prevention, Intervention and Care released its third major report, once again omitting any mention of homocysteine as a modifiable risk factor. This was despite direct submissions of evidence and letters from leading scientists demonstrating that lowering homocysteine with B vitamins can slow brain shrinkage and cognitive decline.

Now, in response to this silence, six of the leading dementia researchers, Professors Joshua Miller (Rutgers), David Smith (Oxford), Helga Refsum (Oslo), Jin-Tai Yu (Fudan), Babak Hooshmand (Karolinska), and Andrew McCaddon (Wrexham), have published a powerful rebuttal in the Journal of Alzheimer’s Disease. Many of these experts serve in the Alzheimer’s Prevention Expert Group (APEG) at Food for the Brain.

They wrote:

“In 2018, we published an ‘International Consensus Statement on Homocysteine and Dementia’ in this journal, in which we concluded that elevated plasma total homocysteine is a modifiable risk factor for the development of cognitive decline, dementia, and Alzheimer’s disease (AD) in older persons. (1)

We further stated that intervention trials in elderly people with cognitive impairment show that homocysteine-lowering treatment with B vitamins markedly slows the rate of both wholeand regional brain atrophy, and also slows cognitive decline. We were therefore puzzled as to why the Lancet Commission on Dementia Prevention, Intervention and Care, failed to discuss the possible role of homocysteine and B vitamins in any of their three reports, including the most recent one.” (2)

A Systematic Omission

The UK-based Lancet Commission on Dementia Prevention is meant to objectively consider the evidence on dementia prevention. Yet each edition, despite being sent the relevant papers, has ignored the evidence concerning homocysteine.

Furthermore, it’s expected to uphold the standards for critical debate which allows for experts to question Published findings. That is exactly what these experts did – yet it declined to publish their letter, instead printing a rebuttal from its own Commission while refusing to let readers see the original letter. (3, 4)

The experts wrote to The Lancet again to respond to the Commission’s letter, but their second letter was also rejected. 

Thatetter has now been published in the leading Alzheimer’s journal where the authors finally have their rightful say. It includes the following:

We wish to reply to the Commission and continue the debate with the aim of reaching a common view on homocysteine, B vitamins and dementia. This is an important matter of public health.”

In other words, The Lancet published the ‘case for the defence’ for the exclusion of homocysteine without allowing readers to even read the ‘case for the prosecution’. (5)

So, what was The Lancet’s case against B vitamins? It rested on three criticisms – each of which these leading dementia researchers refute with scientific precision in their recent journal paper.

Criticism 1: Misunderstanding Who Benefited in the VITACOG Trial

The Lancet Commission questioned the relevance of the VITACOG trial, arguing that the results “do not show benefits in populations already consuming B vitamins in their food or through supplements.” But this fundamentally misrepresents the study population.

In the VITACOG trial, participants with mild cognitive impairment were given high doses of B6, B12, and folic acid for two years. The result was a 31% reduction in whole brain shrinkage and significantly slower rate of cognitive decline in those with raised homocysteine (6). In participants with levels above 11.3 μmol/L – the median – both cognitive and clinical improvements were observed. Importantly, key Alzheimer’s-related brain regions shrank seven times more slowly in these individuals (7, 8).

The Lancet Commission implied that participants were already supplementing, but that is incorrect. The study excluded anyone taking more than 300 mcg of folic acid, 3 mg of vitamin B6, or 1.5 mcg of vitamin B12 – doses lower  than those found in many common multivitamins. Only 16 to 20 percent were taking low-dose supplements, while the majority were not.. No one was excluded based on their dietary intake of B vitamins.

The experts respond:“The Commission authors’ comment is analogous to expecting additional drug treatment to provide benefits over and above the benefits being obtained in people already taking a high dose of the drug, which is why it puzzles us.”

Criticism 2: No Benefit in the Hong Kong Trial?

The Commission’s response also cited a Hong Kong trial that reported no benefit of B vitamins over two years in people with mild cognitive impairment (MCI) (9). However, this overlooks several important confounders.

Firstly, 22% of participants were taking aspirin, which the study authors themselves found to impair the effect of B vitamins. This interference has since been confirmed in further research (10).

Secondly, the authors of The Lancet response failed to consider another critical factor: omega-3 status. Numerous studies show that B vitamins only deliver cognitive benefits when omega-3 fatty acid levels are sufficient. The Hong Kong study did not measure or control for omega-3 status, which likely explains the lack of consistent benefit over the two-year period.

Thus, the absence of effect in this trial does not disprove the role of B vitamins.  The experts go on to demonstrate in their article the overwhelming body of evidence –  reported by us – that homocysteine-lowering B vitamins do not work optimally in individuals with low omega-3 status.

Criticism 3: No Benefit in the VITAL Trial in Alzheimer’s Patients?

The Lancet authors also referenced the VITAL trial, which reported no overall cognitive benefit from B vitamins in patients already diagnosed with Alzheimer’s disease (11). But again, this conclusion overlooks key details.

In a subgroup analysis, those in the early stages of Alzheimer’s disease did show significant benefit (12). The authors of the VITAL trial themselves highlighted this in their paper, suggesting that earlier intervention is more effective. This finding aligns with multiple other studies showing that B vitamin treatment is most effective in the pre-dementia stages (13).

Furthermore, participants in the VITAL trial began with an average homocysteine level of 9 μmol/L, which is below the threshold (>10–11 μmol/L) associated with brain atrophy.  It is extremely rare to find a group of people with Alzheimer’s disease that start with such a low homocysteine level.  While the B vitamins did reduce homocysteine further to 7μmol/L, there was no overall cognitive benefit observed. But this is akin to giving painkillers to people who are not in pain and then reporting no change in pain levels. At Food for the Brain, we consider a homocysteine level above 10μmol/L as in need of correction with B vitamins.

There are also concerns about conflicts of interest. The lead author, Paul Aisen, is described as “a consultant to the following pharmaceutical companies involved in the development of potential treatments for Alzheimer’s disease”. with more than a dozen firms listed. These companies would certainly favour a trial designed to fail – especially if it were widely publicised.

Additionally, when an anti-amyloid drug trial for lecanemab was published – now licensed in the US and UK – the names of Paul Aisen and Christopher Van Dyck appeared once again as lead authors. In other words, the paid pharmaceutical consultants, responsible for running the drug trial were also tasked with overseeing a trial – designed to fail – on a competing approach: lowering homocysteine with B vitamins. The conflict of interest here is both clear and concerning.

What Does the Evidence Really Say?

You can read the full expert response published in the Journal of Alzheimer’s Disease here. 

Their conclusion is clear:

“We hope that the Lancet Commission will consider the substantial existing evidence of raised homocysteine as an important risk factor for dementia and the possibility of modifying its harm by supplementation with B vitamins.”

They emphasise that the evidence for B vitamin intervention is as strong – or stronger than –  many of the risk factors the Commission did include in its 2024 report. To continue ignoring the proven impact of homocysteine, and the benefits of lowering it through B vitamins is not merely a scientific oversight –  it is a missed opportunity with major implications for medicine and public health.

Remember, prevention is better than cure, and there is so much you can do to protect your brain health

The perfect time to start? Today.

What Can You Do?

  1. Test your homocysteine (and omega-3 status) TODAY –  especially if you’re over 50 or at risk of cognitive decline. At Food for the Brain, we offer an accurate at-home test kit that reliably measures plasma homocysteine reliably. 

    You can order your single Homocysteine test here or save money and test both omega-3 index and homocysteine (plus other markers) as part of our DRIfT tests here. International shipping available.
  2. Act on your results –  if your level is above 10 μmol/L, supplementation with vitamin B6 (20 mg), methylfolate (400 µg), and vitamin B12 (500 µg) is recommended.
    Read more on supplements and homocysteine here.
  3. Support our mission – become a FRIEND of Food for the Brain! Your donation helps us advance prevention-focused brain health research and education.

    As a Friend, you’ll also gain access to:
    • Monthly group coaching
    • Your personalised brain upgrade programme: COGNITION™
  4. Share the knowledge – public awareness can change public health.
    We need a paradigm shift, and it starts with us.

References

1. Smith AD, Refsum H, Bottiglieri T, et al. Homocysteine and dementia: an international consensus statement. J Alzheimers Dis 2018; 62: 561–570.

2.Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet 2024; 404: 572–628.

3.Miller JW, McCaddon A, Hooshmand B, et al. The Lancet ‘Omission’: Why are  homocysteine and B vitamins missing from the Lancet Commission’s Report on Dementia Prevention, Intervention and Care? https://foodforthebrainorg/lancet-commission-letters/ (2024).

4.Livingston G, Costafreda SG, Kivimaki M, et al. B vitamins and the 2024 Lancet Commission on dementia. Lancet 2025; 405: 623.

5. Miller JW, McCaddon A, Yu J-T, Hooshmand B, Refsum H, Smith AD. Concerning the debate about homocysteine, B vitamins, and dementia. Journal of Alzheimer’s Disease. 2025;0(0). doi:10.1177/13872877251350297

6. Smith AD, Smith SM, de Jager CA, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brainatrophy in mild cognitive impairment. A randomized controlled trial. PLoS One 2010; 5: e12244.

7. de Jager CA, Oulhaj A, Jacoby R, et al. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. Int J Geriatr Psychiatry 2012; 27: 592–600.

8. Douaud G, Refsum H, de Jager CA, et al. Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. Proc Natl Acad Sci U S A 2013; 110: 9523–9528.

9. Kwok T, Wu Y, Lee J, et al. A randomized placebo- controlled trial of using B vitamins to prevent cognitive decline in older mild cognitive impairment patients. ClinNutr 2020; 39: 2399–2405.

10. Wu Y, Smith AD, Refsum H, et al. Effectiveness of B vitamins and their interactions with aspirin in improving cognitive functioning in older people with mild cognitive impairment: pooled post-hoc analyses of two randomized trials. J Nutr Health Aging 2021; 25: 1154–1160.

11. Aisen PS, Schneider LS, Sano M, et al. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial. JAMA 2008; 300: 1774–1783.

12. Smith AD and Homocysteine RH. B vitamins, and cognitive impairment. Ann Rev Nutr 2016; 36: 211–239.

13. Chen H, Liu S, Ge B, et al. Effects of folic acid and vitamin B12 supplementation on cognitive impairment and inflammation in patients with Alzheimer’s disease: a randomized, single-blinded, placebo-controlled trial. J Prev Alzheimers Dis 2021; 8: 249–256.

Further info

Smart Eating for Sharper Thinking: Wild Salmon Salad + 24 New Brain-Boosting Recipes

When it comes to eating for brain health, flavour and fun are often the first casualties. But what if you could have it all – taste, ease of preparation, and science-backed nutrition – in one delicious dish? That’s exactly the idea behind our Wild Salmon and Chickpea Salad with Rocket and Pesto, a featured free recipe from the Upgrade Your Brain Cook App.

This isn’t just lunch or dinner. It’s brain fuel – loaded with the nutrients your brain craves, without the blood sugar spikes that leave you foggy and fatigued.

Why This Recipe is Brain-Optimised

Your brain is made mostly of fat and thrives on nutrient-rich, anti-inflammatory foods. This recipe is a nutritional powerhouse tailored to support cognitive function, memory, and mood – all key pillars of the COGNITION® brain upgrade programme.

Here’s how it delivers:

  • Omega-3 fats from wild salmon support the structural integrity of your neurons. DHA, in particular, is vital for sharp thinking and memory retention.
  • B Vitamins, especially B12 (from salmon), B6 and folate (from chickpeas and rocket), are key players in methylation – the process that powers your brain’s biochemistry and detoxification pathways.
  • Protein + Fibre Combo (salmon and chickpeas) keeps your blood sugar stable, sustaining energy and focus throughout the day.
  • Antioxidants in rocket, lemon, garlic, and optional red pepper help neutralise brain-ageing free radicals.
    Low Glycaemic Load supports stable mood and mental clarity by avoiding sugar crashes.

Eating for brain health doesn’t mean boring. This salad is fresh, zingy, and ready in minutes – ideal for picnics, packed lunches, or a light dinner.

Prep tip: Double the pesto and keep it in the fridge – you’ll have a brain-friendly dressing ready to jazz up any salad or veggie dish. No boring meals required.

Wild Salmon and Chickpea Salad with Rocket and Pesto Recipe

Ingredients

  • 100g cooked wild salmon (3½ oz) 
  • 80g cooked chickpeas (2¾ oz) 
  • 1 handful rocket 
  • 1 tbsp olive oil 
  • 1 tbsp lemon juice 
  • 1 tbsp pumpkin seeds 
  • ½ garlic clove 
  • 1 tsp nutritional yeast optional 

Instructions:

1. Blend rocket olive oil lemon juice garlic and pumpkin seeds to make pesto 

2. Toss salmon and chickpeas with the pesto 

3. Serve on a bed of leafy greens

Cooks notes: 

  • Use frozen wild salmon for ease 
  • Add red pepper slices for extra brain-friendly antioxidants
  • Double up the pesto recipe and keep in a sealed jar in the fridge to dress a different salad.

Add red pepper slices for extra brain-friendly antioxidants

Why Now’s the Perfect Time to Join the Cook App

Right now, subscribing to the Upgrade Your Brain Cook App doesn’t just give you access to over 100 delicious, nutritionist-designed recipes – it also unlocks our Summer Recipe Bonus Bundle: 12 new recipes, each one optimised for brain health and bursting with flavour.

Here’s a taste of what you’ll get:

  • Brain Boost Balls – a perfect mid-afternoon focus snack
  • Stuffed Portobello Mushrooms with Walnut Lentil Pâté – hearty and satisfying
  • Blueberry Chia Pudding – low GL and ideal for a nourishing wind-down
  • Turmeric and Cauliflower Soup – warming, silky, and anti-inflammatory
  • Mackerel and Broccoli Stir-Fry with Ginger Tamari Glaze – a 10-minute omega-3 hero

And that’s just the beginning.

Join the Brain Food Revolution

Every dish in the app is scored for omega-3s, B vitamins, GLs, and antioxidants – making it easier than ever to eat smart. With new features like the “Goes Well With” section, meal planning becomes seamless. Whether you’re following low GL, keto, or simply want to feel sharper, calmer, and more energised – this is your toolkit.

Let your fork do the upgrading. Try the salmon and chickpea salad now, and discover how good brain food can really be.

Want the Ultimate Recipe for Brain Health?

Here’s your 3-step action plan:

  1. Take the FREE Cognitive Function Test. Get personalised insights into your brain health and identify any key risk areas.
  2. Subscribe to the Upgrade Your Brain Cook App. Discover exactly what to eat to improve your scores and support long-term cognitive health – all in one delicious, easy-to-use tool.
  3. Order the At-Home Pin-Prick Blood Test here
    Available internationally, this test gives you deeper insight into the critical biomarkers affecting your memory, mood, and mental energy – so you can take action with precision.

Further info

Telomeres and the Ageing Brain: How to Protect Your Mind at a Cellular Level

Your body is continually renewing itself by producing new cells. When it comes to protecting and enhancing your brain health, especially as you age, the quality of these new cells becomes increasingly important. A key factor in this cellular renewal process is the health of your telomeres – the protective caps at the ends of your chromosomes. A recent report has reinforced the strong link between telomere length and brain health, with shorter telomeres now recognised as early indicators of cognitive decline and increased dementia risk.

The process of making a new cell in your body starts by copying the map of how to build that cell, which is contained in a package of DNA strands, called a chromosome. The chromosome divides in two, giving a new set of instructions to the new cell. At the end of the chromosome is something called a telomere, which is a bit like the hard tip at the end of a shoelace. This becomes shorter with each cell division, until it is too short and the DNA is no longer protected. This triggers rapid ageing because cells stop dividing and, therefore, stop being replaced. Meanwhile, there is an enzyme, called telomerase, which can lengthen the telomere. The more telomerase activity, the slower the ageing process. For example, there is one bacterium called Tetrahymena thermophila, that has superactive telomerase so its telomeres never shorten – and it can live indefinitely.

Telomeres and Brain Ageing: The New Frontier

A recent report highlighted that shortened telomeres are not just markers of biological ageing, but also significant predictors of neurodegenerative diseases such as Alzheimer’s and other forms of dementia. According to the report, individuals with the shortest telomeres were at greater risk of developing age-related brain diseases, underscoring the urgency of protecting telomere integrity as part of a comprehensive dementia prevention strategy.

This aligns perfectly with our 6-month COGNITION brain upgrade programme, which targets eight nutrition and lifestyle domains known to support brain health, including sleep, stress, diet, and nutrient status – each of which has been shown to influence telomere length. In fact, many of the nutrients and behaviours proven to protect telomeres, such as vitamin D, omega-3 fatty acids, anti-inflammatory diets, and methylation support through B vitamins, are key focus areas within our COGNITION framework.

So, what does the research say about how we can lengthen our telomeres and protect our future?

Reduce your stress

Chronic stress, such as caring for someone with dementia, has been shown to reduce telomerase activity and shorten telomeres. Childhood trauma, depression, and even cynicism (1) also have a negative impact. On the other hand, practices like meditation have been shown to support longer telomeres (2).

Prioritise sleep

Quality sleep is linked to longer telomeres (3). For healthy ageing and longevity around seven hours per night appears optimal.

Get moving

Physical activity is another powerful protector of telomeres. Even individuals with PTSD who engaged in regular exercise were found to avoid the usual telomere shortening. (4)

Avoid smoking and maintain a healthy weight

Both smoking and obesity are linked to shortened telomeres.

Increase omega-3 and vitamin D

Studies show that higher intakes of omega-3 fish oils are associated with longer telomeres. A 2013 study found that DHA and EPA reduced telomere shortening (5). Other research links higher vitamin D levels with longer telomeres ( 6, 7). Both nutrients are abundant in oily fish.

Lower homocysteine levels

Homocysteine is a neurotoxic amino acid. Higher levels of B12 and folate, and lower homocysteine levels, are associated with longer telomeres (8, 9). A Singaporean study confirmed that elevated homocysteine levels predicts shorter telomeres (10).

This would seem to indicate that testing your homocysteine level is one of the smartest things you can do for your long-term brain health. That’s why we include it in our DRIFT 5-in-1 blood test here. This accurate at-home test measures five crucial biomarkers for assessing dementia risk and cognitive resilience.

Eat anti-inflammatory foods

A 2015 study found that individuals who consumed more anti-inflammatory foods had longer telomeres (11). Another study showed that greater vegetable intake is associated with longer telomeres (12). Even multivitamin use, which typically includes B12 and folate, has been linked to longer telomeres (13). (Find out advice on supplementation here).

If you want more personalised guidance on how to protect your brain – and your future health – Become a FRIEND today and get access to your personalised 6-month brain upgrade programme COGNITION®.

Join us in building a future where cognitive decline is not inevitable but preventable.

4 https://pubmed.ncbi.nlm.nih.gov/20520771/

7 http://www.ncbi.nlm.nih.gov/pubmed/22417715

12 http://www.ncbi.nlm.nih.gov/pubmed/2656006413


Further info

Eight Ways to Lower Your Homocysteine

Homocysteine may not be a household word, but at Food for the Brain, we want it to become one!

It is arguably one of the most important blood biomarkers for your brain and overall health, predicting the risk of over 100 diseases, from cardiovascular issues to cognitive decline, depression, and developmental disorders in children (1,2,3). For many years it was difficult to obtain accurate testing privately or at home – which is why we developed a new, accurate at-home pin-prick test that is one of our most popular options.

The reason we think this is such a good biomarker to track and research is that whilst high homocysteine is linked to increased risk of over 100 diseases – it can be quick and easy to lower!

Learn more about homocysteine and why it matters in the video below:

What level should you be aiming for?

Based on Patrick Holford’s research in his book Upgrade Your Brain, the recommended homocysteine levels are:

  • Ideal/Optimal Level: Below 7.5 µmol/L –  This is especially important for women preparing for pregnancy, as higher levels are linked to increased risk of chromosomal damage and developmental problems in children.
  • Treatment Threshold: Above 10 µmol/L  – Anyone with a homocysteine level above this should be treated with B vitamins to reduce brain shrinkage and risk of dementia.
  • Warning Level: Above 11 µmol/L – Associated with increased brain shrinkage and elevated risk for Alzheimer’s and cardiovascular disease.

Ideally, with regular testing, you should maintain homocysteine levels well below 10 µmol/L to support optimal brain health and reduce the risk of neurodegenerative conditions.

Here are eight proven ways to bring your homocysteine levels into the optimal range and keep your brain firing on all cylinders:

1. Supplement Smart: The B Vitamin Trio (and Friends)

The fastest way to reduce homocysteine is through targeted supplementation. The ‘magic trio’ is vitamin B6 (20mg), B12 (500µg as methylcobalamin), and methylfolate (400µg). A major paper has shown that supplementing these B vitamins not only lowers homocysteine, but also slows brain shrinkage and cognitive decline in people with mild cognitive impairment. Add trimethylglycine (TMG), zinc, and N-acetyl cysteine (NAC) for additional support, particularly in older adults with memory concerns. These nutrients work synergistically to support methylation and brain function. (1) Get our supplement guidelines here.

2. Eat for B12: Fish, Eggs, Dairy and Meat

Vitamin B12 is primarily found in animal-derived foods. Aim to eat oily fish three times a week, eggs most days, and small amounts of organic meat or dairy (if tolerated). Pescatarians thrive here. For vegans, the focus should be on fortified foods and sources such as shiitake mushrooms. However, supplementation and regular testing are strongly recommended to ensure optimal levels. Poor B12 absorption – particularly in older adults or those taking proton pump inhibitors – is a common risk factor for elevated homocysteine and brain shrinkage (1,2).

3. Load Your Plate with Greens and Beans

Folate is critical for methylation. Aim for seven servings of fruit and vegetables ​​a day. Prioritise leafy greens, broccoli, lentils, chickpeas, and asparagus. These naturally support homocysteine metabolism and keep your methylation processes running smoothly (1).

4. Move Your Body

Regular physical activity helps lower homocysteine. Studies show that consistent aerobic or resistance exercise can reduce levels, improve circulation, and support metabolic health. Aim for at least 30 minutes of brisk walking, cycling, or swimming five times a week to complement your nutritional strategy (3).

5. Cut Back on Coffee – Especially Excessive Intake

Drinking more than two cups of coffee a day can raise homocysteine levels. While low to moderate coffee intake may  offer  some antioxidant benefits, high intake (six or more cups a day) has been linked to elevated homocysteine levels and an increased risk of dementia (4).

6. Mind Your Alcohol

Keep it light. Up to seven small glasses (125ml) of red wine or two pints of beer per week is the maximum. Excess alcohol increases homocysteine levels and impairs nutrient absorption – particularly of B vitamins (1).

7. Manage Stress and Prioritise Quality Sleep

Chronic stress may indirectly raise homocysteine by increasing inflammation and depleting vitamin B6 – both linked to higher mortality and accelerated cellular ageing (5).Make stress reduction a priority. Meditation, yoga, deep breathing, regular exercise, and talking therapies are all effective. Equally important is prioritising restorative sleep. The brain clears toxins and resets during deep sleep – both are vital for healthy methylation. Learn more about sleep and your brain here.

8. Test, Don’t Guess – Know Your Level

You can’t manage what you don’t measure. Have your homocysteine levels tested.. We now offer at-home pinprick tests, which also contribute to our ongoing research. Don’t be surprised if your levels are higher than expected. Forty per cent of people over 60 have homocysteine levels above 11 µmol/L. As we age, our ability to absorb vitamin B12 declines (3).

Homocysteine is a key indicator for cognitive and overall health. As we can see, with a few dietary tweaks, lifestyle upgrades, and targeted nutrients, you can lower your homocysteine, support methylation, and quite literally upgrade your brain!

Start today:

  1. Join our research and test your homocysteine level today. Purchase a single homocysteine test here or get it as part of the DRIfT 5 in 1 test, which also measures your antioxidant status (another world first in accurate home testing), omega-3, vitamin D and HbA1c.
  2. Read more in the Upgrade Your Brain book – This fully referenced guide offers practical strategies to improve your brain health – including how to lower homocysteine through diet, lifestyle, and supplementation.
  3. Support our charitable work by becoming a FRIEND. From just £5 a month, you can help fund vital research and public education. Become a FRIEND today

References:
1 Smith AD, Refsum H. Homocysteine – from disease biomarker to disease prevention. J Intern Med. 2021 Oct;290(4):826-854.

2 Vogiatzoglou A, Refsum H, Johnston C, et al. Vitamin B12 status and rate of brain volume loss. Neurology. 2008 Sep 9;71(11):826-32.

3 Vincze G, et al. Physical activity and plasma homocysteine in the elderly: the Rotterdam Study. Am J Clin Nutr. 2011;93(5):1025–31.

4 Grubben MJAL, et al. Unfiltered coffee increases plasma homocysteine concentrations in healthy volunteers: a randomized trial. Am J Clin Nutr. 2000;71(2):480–4.

5 Pusceddu I, et al. Subclinical inflammation, telomere shortening, homocysteine, vitamin B6, and mortality: the Ludwigshafen Risk and Cardiovascular Health Study. Eur J Nutr. 2020;59:1399–411.


Further info

Cognitive Decline Starts at 18 – and So Should Alzheimer’s Prevention

By Patrick Holford

Most people think forgetfulness and failing memory only begin in later life. But what if you found out that cognitive decline actually begins much earlier – around the age of 18 – and that what you do when you’re young can dementia-proof yourself for when you’re older?

This is the latest discovery from Food for the Brain’s research! Now that hundreds of thousands of participants have completed the Cognitive Function Test, we are starting to extract these world first findings.  Although the test was designed to identify those at risk for dementia later in life, the extraordinary finding is that cognitive function declines, on average, year by year from the age of 18.

The results involving 172,098 people who took the free test between 2011 and 2024 show that there is a steady decline, on average, with a sharp drop-off after the age of 80. 

In one alarming case that underscores the need to promote prevention as early as possible, researchers in South China recently diagnosed probable Alzheimer’s disease in a 19-year-old male – the youngest ever recorded – highlighting the fact that dementia, while rare in youth, is not exclusively a condition of old age (1).  This makes early prevention not only relevant but essential.

This isn’t a message of fear.  It’s one of hope and empowerment, emphasising that it’s never too early to start supporting your brain health. (This is why we created the Smart Kids & Teens COGNITION Programme.) Cognitive slippage doesn’t happen to everyone – it’s possible to maintain or even improve brain function with optimal nutrition and lifestyle habits. Food for the Brain’s research also found that those whose Dementia Risk Index is in the top quarter, in ‘the green’- are not expected to come close to the zone of cognitive decline before age 100. A person’s Dementia Risk Index is calculated from completing the COGNITION diet and lifestyle questionnaire that follows the free Cognitive Function Test.

The five most impactful prevention steps are: 

  1. Sufficient intake of B vitamins
  2. Omega-3 from seafood and supplements
  3. More vegetables and fruit, and less sugar and refined carbohydrates
  4. More exercise
  5. Less alcohol 

See the Alzheimer’s Modifiable Risk Factor chart below:

Understanding that decline can start early in life means you can take steps now – whether you’re 18 or 80 – to protect your brain. This is also where our Citizen Scientist FRIEND community plays a vital role! Whether you’re a parent, grandparent, teacher, coach, youth worker, mentor, or simply someone who cares about young people, you can help the next generation build lifelong resilience – by becoming a FRIEND of Food for the Brain, accessing your personalised six-month Brain Upgrade Programme and encouraging as many as possible to take the free Cognitive Function Test to become ‘dementia-proof’.

How to ‘Dementia-Proof’ Yourself

We describe someone as ‘dementia-proof’ when the projection of their Cognitive Function Test results suggest they will remain in the healthy ‘green zone’ (optimal cognitive health) beyond the age of 100, as shown in the graph above.

Food for the Brain is helping thousands  of people achieve this dementia-proof status through our COGNITION programme, which identifies a person’s ‘quick wins’ and supports behaviour change with personalised, interactive emails and live group health coaching. For some, this means going to bed earlier for more sleep. For others, it might mean avoiding foods with added sugar, cutting back on alcohol or getting outdoors to exercise. For many it means optimising intake of B vitamins, omega-3, vitamin D, and antioxidants.
(Do you know what your levels of these important brain-protecting nutrients are? If not, make sure you order our accurate  at-home pinprick DRIfT test, another way to support our research and upgrade your brain.)

Start Young to Prevent Cognitive Decline

Brain fog, poor concentration, low mood, or forgetfulness aren’t just part of “being busy” or “getting older.” These can be early signs that your brain isn’t getting what it needs.  Better sleep, nutrition, regular activity, and lower stress levels all help preserve cognitive function as you age.  

Investing in your brain health early means:

  • Sharper focus and concentration for study, work, and everyday life
  • Greater emotional resilience, reducing anxiety and improving your mood
  • Improved memory and creativity, helping you perform optimally in all areas of life
  • More energy and better sleep, to improve the way you feel and function every day

When you support your brain health, you support every other aspect of your health too!h. Be it that outer glow on the skin, more balanced hormones, or improved gut health, all of it starts with brain health. It’s never too late, and it’s never too early – it is only important to make a start!

Whether you’re a teenager, a student in your 20s, raising a family in your 40s, or retired in your 70s, your brain is changing every day – and the good news is that it can respond positively to lifestyle changes at any age.

Remember: there is so much you can do to help to prevent Alzheimer’s and optimise your brain health – whatever your age.

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Further reading: This idea is echoed in the work of Associate Professor Tommy Wood, Head of Research at Food for the Brain, in his article Use it or Lose it: Why an Active Lifestyle is a Brain Essential.

Reference:
1. Jia J, Zhang Y, Shi Y, Yin X, Wang S, Li Y, Zhao T, Liu W, Zhou A, Jia L.  A 19-Year-Old Adolescent with Probable Alzheimer’s Disease.  J Alzheimers Dis.  2023;91(3):915-922.  doi: 10.3233/JAD-221065.  Erratum in: J Alzheimers Dis.  2023;92(4):1501-1502.  doi: 10.3233/JAD-239001.  PMID: 36565128.


Further info

Psychiatric Drugs Are The Third Leading Cause Of Death

By Patrick Holford

The reason we advocate natural, nutritional, and lifestyle-based approaches to mental health is simple – because they work, and they’re safe.

Unspoken Risks of Psychiatric & Dementia Drugs

The next big challenge is to discover which combination of changes has the most impact. This is what our research is focused on.

From depression to dementia, the typical approach is still, all too often, medication While it’s valid to compare a nutrient or diet to a pharmaceutical – take omega-3s, for example, which have been shown to be as effective as antidepressants – the real concern is how rarely we hear about the risks of psychiatric drugs. For many, by the time those dangers become clear, it’s already too late.

A classic example of this is the well-known increased risk of suicide particularly in young people prescribed antidepressants. Not only did this take more than ten years to ‘come out’, even now, despite on-the-box warnings, many remain unaware of this well-established risk.

A similar situation is emerging with the new anti-amyloid antibody treatments being proposed for dementia sufferers. Reported deaths are often downplayed or not fully disclosed.. In trials of the two drugs Lecanemab and Donanemab, eight deaths were reported. Eight deaths were reported during the trials, which involved 1,785 participants – a rate of one in every 219 – though not all were officially attributed to the drug. That’s quite a risk. But it is also the nature of these deaths, caused by brain bleeding and swelling, that is even more concerning. 

Investigative journalist Charles Piller, in his book ‘Doctored’, interviewed the pathologist for the first Lecanemab death who said it was like “her brain exploded”. Another Lecanemab associated death was a 65 year-old woman, who had a blood clot induced stroke and was given a common, often lifesaving intervention (tPA) which went badly wrong. “As soon as they put it in her, it was like her body was on fire,” the woman’s husband told me, he said. “She was screaming, and it took, like, eight people to hold her down. It was horrific. Everybody’s running in and (asking) ‘What the hell is going on?’” His wife was sedated and recovered to intensive care, he said. Soon the woman suffered seizures and was placed on a ventilator. After a few days the family approved disconnecting the device and she died. In his book Piller also reports another case in which a participant ‘died after hideous brain swelling and bleeding, and violent seizures.’

The UK has licensed the use of Lecanemab. The EU has not. The UK has licensed Donanemab, but NICE hasn’t approved it for NHS use.

Safer, Evidence-Based Alternatives

Despite more effective and safer alternatives being available, Alzheimer’s charities continue to advocate for NHS access to these drugs. This raises an important question: why? The combination of homocysteine-lowering B vitamins and omega-3 already has stronger evidence of efficacy – with no adverse effects – and certainly no risk of death (Read Alzheimer’s: Prevention is the Cure for the evidence and the comparison).

We invited Dr Peter Gøtzsche – co-founder of the Cochrane Collaboration, originally established to evaluate health treatments without bias – to speak about the risks of psychiatric drugs and their link to mortality. When the Cochrane Collaboration became corrupted, which he later criticised for being influenced by commercial interests, he founded the Institute for Scientific Freedom.

 “Overtreatment with drugs kills many people, and the death rate is increasing. It is therefore strange that we have allowed this long-lasting drug pandemic to continue, and even more so because most of the drug deaths are easily preventable.” he says.

In 2013, I estimated that our prescription drugs are the third leading cause of death after heart disease and cancer,(1) and in 2015, that psychiatric drugs alone are also the third leading cause of death”.(2)

Read on to understand how he arrived at the conclusion that psychiatric drugs may be the third leading cause of death.

How many people are killed by psychiatric drugs?

If we want to estimate the death toll of psychiatric drugs, the most reliable source of data comes from placebo-controlled randomised trials. However, we need to consider their limitations.

First, these trials typically last just a few weeks, despite the fact that most patients take psychiatric medications for many years.(3, 4) 

Second, polypharmacy – the use of multiple medications –  is common in psychiatry, and this significantly increases the risk of mortality.. As an example, the Danish Health Authority has warned that adding a benzodiazepine to a neuroleptic increases mortality by 50-65% (5).

Third, up to half of all deaths go unreported in published clinical trial data.(6)  For dementia, published data shows that for every 100 people treated with a newer neuroleptic for ten weeks, one patient dies as a result. (7) This represents a high mortality rate for a pharmaceutical intervention, but FDA data on the same trials show it is double this number, equivalent to two deaths per 100 people over ten weeks. (8) And if we extend the observation period, the death toll becomes even higher.  A Finnish study of 70,718 community-dwellers newly diagnosed with Alzheimer’s disease reported that neuroleptics kill 4-5 people per 100 annually, compared to patients who were not treated.(9)

Fourth, the design of psychiatric drug trials is biased. In almost all cases, patients were already in treatment with psychiatric medication before they entered the trial, (1, 2), and some of those randomised to placebo will therefore experience withdrawal effects that will increase their risk of dying, due to withdrawal symptoms such as akathisia. Placebo-controlled trials in schizophrenia cannot be reliably used to assess the effect of neuroleptics on mortality because of the drug withdrawal design. The suicide rate in these unethical trials was 2-5 times higher than the norm. (10,11) Among those enrolled in trials of risperidone, olanzapine, quetiapine, and sertindole, one in every 145 patients died. However, none of these deaths were mentioned in the published scientific literature, and the FDA did not require their inclusion in trial reporting.

Fifth, events occurring after the trial period are often ignored. In Pfizer’s trials of sertraline in adults, the risk ratio for suicides and suicide attempts was 0.52 when follow-up lasted only 24 hours, but increased to 1.47 when follow-up was extended to 30 days — indicating a rise in suicidal events. (12) Furthermore, when researchers reanalysed the FDA trial data on depression drugs and included harms occurring during follow-up, they found that antidepressants were associated with twice the number of suicides in adults compared to placebo (13, 14)

Estimating the True Death Toll of Mental-Health Medications

In 2013, I estimated that, in people aged 65 and above, neuroleptics, benzodiazepines or similar, and antidepressants kill 209,000 people annually in the United States.(2) I used relatively conservative estimates, however, and usage data from Denmark, which is far lower than those in USA. I have therefore updated the analysis based on US usage data, again focusing on older age groups.

For neuroleptics, I used the estimate of 2% mortality from the FDA data.(8)

For benzodiazepines and similar drugs, a matched cohort study showed that the drugs doubled the death rate, although the average age of the patients was only 55.(15)  The excess death rate was about 1% per year. In another large, matched cohort study, the appendix to the study report shows that hypnotics quadrupled the death rate (hazard ratio 4.5). The study authors estimated that sleeping pills kill between 320,000 and 507,000 Americans every year. (16)  A reasonable estimate of the annual death rate would therefore be 2%.

For SSRIs, a UK cohort study of 60,746 depressed patients older than 65 showed that they led to falls and a 3.6% annual mortality rate among those treated.(17) The study was well-designed, in that the patients were their own control in one of the analyses, which helps control for confounding variables. Nonetheless, the reported death rate is notably high.

Another cohort study, of 136,293 American postmenopausal women (age 50-79) participating in the Women’s Health Initiative study, found that depression drugs were associated with a 32% increase in all-cause mortality after adjustment for confounding factors, which corresponding to an estimated 0.5% annual mortality rate among women treated with SSRIs.(18). The authors noted that the mortality rate was likely underestimated. The authors warned that their results should be interpreted with great caution due to a high risk of exposure misclassification, which would make it more difficult to find an increase in mortality. Further, the patients were much younger than in the UK study, and the death rate increased markedly with age and was 1.4% for those aged 70-79. Finally, the exposed and unexposed women were different for many important risk factors for early death, whereas the people in the UK cohort were their own control.

For these reasons, I decided to use the average of the two estimates, a 2% annual death rate.

These are my results for USA for these three drug groups for people at least 65 years of age (58.2 million; usage is in outpatients only): (19, 20, 21, 22)

A limitation in these estimates is that you can only die once, and many people receive polypharmacy. It is not clear how we should adjust for this. In the UK cohort study of depressed patients, 9% also took neuroleptics, and 24% took hypnotics/anxiolytics. (17)

On the other hand, the data on death rates come from studies where many patients were also on several psychiatric drugs in the comparison group, so this is not likely to be a major limitation considering also that polypharmacy increases mortality beyond what the individual drugs cause.

Statistics from the Centers for Disease Control and Prevention list these four top causes of death: (23) 

Heart disease: 695,547
Cancer: 605,213
COVID-19: 416,893
Accidents: 224,935

COVID-19 deaths are rapidly declining, and many of such deaths are not caused by the virus but merely occurred in people who tested positive for it because the WHO advised that all deaths in people who tested positive should be called COVID deaths.

Young people have a much smaller death risk than the elderly, as they rarely fall and break their hip, which is why I have focused on the elderly. I have tried to be conservative. My estimate misses many drug deaths in those younger than 65 years; it only included three classes of psychiatric drugs; and it did not include hospital deaths.

I therefore do not doubt that psychiatric drugs are the third leading cause of death after heart disease and cancer.

Learn more and begin your brain upgrade journey today:

  • Complete the free online brain assessment – the Cognitive Function Test – to get personalised feedback on your brain health
  • Order the Upgrade Your Brain book here
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  • Contribute to our research and order your accurate, at home, blood tests here.
  • If you are looking for personalised one to one support, visit the Brain Bio Centre here.

References:
1 Gøtzsche PC. Deadly medicines and organised crime: How big pharma has corrupted health care. London: Radcliffe Publishing; 2013.

2 Gøtzsche PC. Deadly psychiatry and organised denial. Copenhagen: People’s Press; 2015.. US News 2016; Sept 27. 

2. Gøtzsche PC. Mental health survival kit and withdrawal from psychiatric drugs. Ann Arbor: L H Press; 2022.

 3 Gøtzsche PC. Long-term use of antipsychotics and antidepressants is not evidence-based. Int J Risk Saf Med 2020;31:37-42. 

4 Gøtzsche PC. Long-term use of benzodiazepines, stimulants and lithium is not evidence-based. Clin Neuropsychiatry 2020;17:281-3.

5 Forbruget af antipsykotika blandt 18-64 årige patienter, med skizofreni, mani eller bipolar affektiv sindslidelse. København: Sundhedsstyrelsen; 2006.

6 Hughes S, Cohen D, Jaggi R. Differences in reporting serious adverse events in industry sponsored clinical trial registries and journal articles on antidepressant and antipsychotic drugs: a cross-sectional study. BMJ Open 2014;4:e005535. 

7 Schneider LS, Dagerman KS, Insel P. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294:1934–43.

8 FDA package insert for Risperdal (risperidone). Accessed 30 May 2022. 

9 Koponen M, Taipale H, Lavikainen P, et al. Risk of mortality associated with antipsychotic monotherapy and polypharmacy among community-dwelling persons with Alzheimer’s disease. J Alzheimers Dis 2017;56:107-18.

10 Whitaker R. Lure of riches fuels testing. Boston Globe 1998;Nov 17.

11 Whitaker R. Mad in America: bad science, bad medicine, and the enduring mistreatment of the mentally ill. Cambridge: Perseus Books Group; 2002:page 269.

12 Vanderburg DG, Batzar E, Fogel I, et al. A pooled analysis of suicidality in double-blind, placebo-controlled studies of sertraline in adults. J Clin Psychiatry 2009;70:674-83.

13 Hengartner MP, Plöderl M. Newer-generation antidepressants and suicide risk in randomized controlled trials: a re-analysis of the FDA database. Psychother Psychosom 2019;88:247-8.

14 Hengartner MP, Plöderl M. Reply to the Letter to the Editor: “Newer-Generation Antidepressants and Suicide Risk: Thoughts on Hengartner and Plöderl’s ReAnalysis.” Psychother Psychosom 2019;88:373-4.

15 Weich S, Pearce HL, Croft P, et al. Effect of anxiolytic and hypnotic drug prescriptions on mortality hazards: retrospective cohort study. BMJ 2014;348:g1996.

16 Kripke DF, Langer RD, Kline LE. Hypnotics’ association with mortality or cancer: a matched cohort study. BMJ Open 2012;2:e000850.

17 Coupland C, Dhiman P, Morriss R, et al. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ 2011;343:d4551.

18 Smoller JW, Allison M, Cochrane BB, et al. Antidepressant use and risk of incident cardiovascular morbidity and mortality among postmenopausal women in the Women’s Health Initiative study. Arch Intern Med 2009;169:2128-39.

19 O’Neill A. Age distribution in the United States from 2012 to 2022. Statista 2024;Jan 25.

20 Olfson M, King M, Schoenbaum M. Antipsychotic treatment of adults in the United States. Psychiatrist.com 2015;Oct 21.

21 Maust DT, Lin LA, Blow FC. Benzodiazepine use and misuse among adults in the United States. Psychiatr Serv 2019;70:97-106.

23 Centers for Disease Control and Prevention. Leading Causes of Death. 2024;Jan 17.

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