By Patrick Holford

What makes us humans so different to other apes is our larger brain, especially the cortex. It is three times larger than a chimpanzee. How did this happen? How did Homo Sapiens evolve our level of intelligence despite sharing almost the same genes? 

The brain’s origin, for all species, is from the ocean. It had to be as that is where life began. Millions of years ago the rudimentary eye cell, dinoflagellate, which is a type or marine phytoplankton, used a specific fat – the omega-3 fat docosahexanoic acid (DHA) – to convert solar photon energy into the first nerve impulse or twitch – a twitch towards food. That is the origin of the nervous system and brain.

Back in the ‘80’s, when zoologist Professor Michael Crawford analysed the types of fat in different animal’s organs and muscles they varied according to their dietary environment, except the brain. He discovered that the brain is always rich in DHA. The more DHA the brighter the animal, with the sea mammals and us humans having exceptionally high levels.

Recently it has been proven that DHA (docosahexanoic acid) has a unique structure involving six double bonds, arranged in a horseshoe shape, which actually makes it a semi-conductor with unique electrical properties. Its close cousins, ALA (alpha linolenic acid) in chia or flax, and EPA (eicosapentanoic acid) don’t have this potential. It’s all about DHA. While some EPA converts into DHA less than 1 per cent of ALA in plant-based sources of omega-3 such as chia seeds converts to DHA, the richest source of which is marine-based food from rivers and the sea.

Over 6 million years ago our hominid ancestors split from other apes (chimps, gorillas and bonobos), culminating in Homo Sapiens around 100,000 years ago. It clearly wasn’t genes that made us different. We share 98.5% of the same genome. It had to be the environment our ancestors exploited. During this time brain size steadily increased up to 1.45kg 10,000 years ago, roughly three times the size of a chimpanzee, at 384g.

Homo Aquaticus

We have over twenty profound anatomical, physiological and biochemical differences apart from our vastly different psychological advancement as in intelligence and language. More than anything, it is this, illustrated by our brain size, that makes us different. But, before looking closely at the circumstances, and diet, that almost certainly drove our gain in brain size and intelligence, let’s take a look at the fundamental differences we have. These have been so clearly delineated in an excellent book, The Waterside Ape, by Peter Rhys-Evans, and ear, nose and throat surgeon. He explores why we:

Stand upright
Have (virtually) no body hair
Have a layer of sub-cutaneous fat
A waxy, waterproof layer, the vernix, at birth
A diving reflex at birth, meaning we are able to swim before we can walk, and hold our breath underwater
A descended larynx, a precursor of being able to have complex language/speaking
Enlarged sinus cavities
A nose shape that is good for keeping the water out while swimming
Ears that actually form a protective boney protusion in those who spend a lot of time diving
Different kidneys, in how they filter salt and water 
Manual dexterity
Crinkly fingers when in water for a few minutes

Of course, the story we’ve all been told is that we came out of the trees, into the savannah and stood upright for better hunting. Anyone who has been on safari will know that a) you don’t stand a chance catching anything by standing upright – you crawl; and b) all the good hunters can sprint much faster than man (lion 80kph, leopard 60kph, cheetah 100kph, man under 30kph) precisely because four legs are better than two. But, can you explain any one of these other changes, let alone our increase in intelligence, by moving from the trees into the savannah for hunting? If so, how did we suddenly develop manual dexterity, tools and spears overnight to even survive? Also, why do certain ‘sea nomad’ tribes exist, such as the Moken and Bajou, who can hold their breath for up to 10 minutes under water, spending up to five hours a day in the sea, giving birth in the sea? Their spleen is adapted to oxygenate tissue, as it is in dolphins, to enable long dives. Where did that evolutionary adaptation come from?

The only logical explanation that I have encountered, which eloquently fits all these adaptations, in that our hominid ancestors exploited the waterside – wetlands, swamplands, rivers, estuaries and coasts. In the process of so doing, became upright, and started to eat a diet high in marine foods, providing the essential nutrients for brain development, that is omega-3 DHA, phospholipids, plus vitamin B12, iodine, and all those other essential elements from magnesium to selenium. From this perspective let’s briefly examine all the changes listed above, between us and other apes:

Stand upright – better for wading in water, so gradually our anatomy adapts but, even so, we are prone to the problems of uprightness, eg hips and knees because it is  anatomically inferior to walk on all fours, with better weight distribution.
Have (virtually) no body hair and a layer of sub-cutaneous fat – consistent with semi-aquatic mammals better for floating and insulation
A waxy, waterproof layer, the vernix, at birth – found in no land mammals, only other semi-aquatic mammals such as seals and chemically identical
A diving reflex at birth, meaning we are able to swim before we can walk, and hold our breath underwater
A descended larynx, a precursor of being able to have complex language/speaking – being upright, and diving, could have led to this vital adaptation. This, by the way, only occurs after a year or so, before which a baby’s language cannot develop the complexity of sounds and voice control only we have
Enlarged sinus cavities, which help to keep the head above water, but still have drainage holes in the ‘wrong’ place, eg good if on all fours but bad if upright, which is why we are prone to sinus problems.
A nose shape that is good for keeping the water out while swimming
Ears that actually form a protective boney protusion in those who spend a lot of time diving
Manual dexterity – if we were wading, and swimming, not walking on all fours, we have ‘free’ hands. Opening shells would develop manual dexterity.
Crinkly fingers when in water for a few minutes – perfect for catching fish.

Part of the idea of the ‘savannah’ theory is that food became scarce with climate changes so we switched to hunting. But the water’s edge was, until recently, abundant with easily accessible food. Even 200 years ago, in 1706, Daniel Dafoe wrote this regarding the Firth of Forth. “Off the Pentland Firth the sea was one third water and two thirds fish; the operation of taking them could hardly be call’d fishing, for they did little more than dip for them into the water and take them up.” Our estuaries were packed with mussels, oysters and crabs.

Historically, wherever early man is found so too is evidence of seafood consumption, with remains of shells, fish bones etc. from Pinnacle Point in South Africa, where early remains are found together with sea shells, to Wales. When a 40,000 year old Homo sapiens was found in the Gower peninsular DNA evidence showed that a quarter of their diet was seafood.

A marine food diet high in critical brain building nutrients, especially DHA, phospholipids and B12, is the best explanation for our cerebral expansion. “Docosahexaenoic acid (DHA), the omega-3 fatty acid that is found in large amounts in seafood, boosts brain growth in mammals. That is why a dolphin has a much bigger brain than a zebra, though they have roughly the same body sizes. The dolphin has a diet rich in DHA. The crucial point is that without a high DHA diet from seafood we could not have developed our big brains. We got smart from eating fish and living in water.” says Crawford.

The dry weight of the brain in 60 per cent fat and DHA makes up over 90 per cent of the structural fat of neurons (brain and nerve cells). The intelligent membrane that makes up all neurons is composed of phosphorylated DHA – that is DHA attached to phospholipids. The most abundant phospholipid is phosphatidyl choline, found predominantly in fish, eggs and organ meats. These are bound together by a process called methylation, itself dependent on vitamins B12, folate and B6. While folate and B6 is found in both plant foods and seafood, B12 is only found in foods of animal origin, and is especially high in all marine foods.

The evidence that exists suggests we were eating a diet rich in marine food, as well as  plant foods along the water’s edge, enjoying the ‘fruité del mare’. We would have eaten much more than we do today – at least double the calories. Today’s convenience world has dramatically reduced the calories we need to expend hunting and gathering food, travelling and staying warm.

The idea that we were eating twice as much and at least a quarter from marine foods makes sense of what we know about the optimal intake of both omega-3 fats rich in DHA, phospholipids and vitamin B12, lack of which are the main drivers of today’s endemic dementia. This would be equivalent to at least half our diet today needing to be from marine foods rich in fats.

Optimal amounts of omega-3 from seafood is estimated at 2 grams a day by Joseph Hibbeln at the US National Institute’s of Health, while choline is estimated at 400mg to 800mg. An optimal intake of B12 is probably 10mcg. None of these can easily be achieved even by eating seven servings of oily fish a day. (Choline is rich in all fish, but DHA is only rich in oily fish, fish roe and liver.)

In the chart below the last column combines EPA and DHA and shows the amount provided in an 85g serving. None provide 2,000mg, although they do get close, suggesting that we would have needed to eat at least a serving of fish or seafood a day, if not more. 

Brain size remains reasonably constant from 100,000 to 10,000 years ago, then starts to shrink, perhaps coinciding with the birth of agriculture and diets based more on meat, milk and plants than marine foods. Today, average brain size is 1.35kg. 

The evolution of intelligence and self-awareness

Apart from brain size and, more pertinently, brain to body size ratio, what sets us apart from other animals is self-awareness. Animals have the equivalent of thoughts and feelings but humans are relatively unique in being able to witness one’s own thoughts and feelings, that is self- awareness. This is not an easy thing to measure, but some other mammals, notably dolphins, gorillas and chimpanzees, also have a degree of self-awareness. Other contenders for higher cognition include octopuses and elephants, all large brained creatures. However, it isn’t just size that counts. In essence, there are three evolutions of the brain. First, the reptilian brain located on the brain stem, which programmes basic survival needs. Then there’s the mammalian brain, with more cognitive and emotive functions (think dog), then the neo-cortex, associated with higher cognition. But, while elephants have larger brains they have smaller neo-cortexes. It’s the neo-cortex that starts to grow in our hominid ancestors.

An indication of an advancing intelligence could be supposed from the earliest evidence of ancient rock art, as well as use of complex tools and adornments.  The earliest rock art is found in South Africa, dating back 77,000 years ago, and in Western Europe about 37,000 years ago, and possibly in Australasia (Sulawesi) around that time.

The richest concentration of ancient rock art over 6,000 years ago, however, is found in sub-Saharan Africa, the Nile Valley and Red Sea hills, then a green belt with vast lakes, rivers and wetlands, hence abundant marine foods, which lasted until about 3,500 years ago when much of Egypt is becoming a desert. Whether the drying up of the Sahara was linked to the Younger Dryas (see below), a change in the Earth’s tilt or over grazing is a subject of debate.^[i]

Meanwhile, groups of our early ancestors who had left Africa, living in Europe as far west as Ireland, north as Scandinavia, East as China and Australia, were also struck by cataclysmic weather changes. In Europe the Magdalenian culture, with advanced stonework, exists from 17,000 years ago, coinciding with the end of the Ice Age, until 12,000 years ago, coinciding with the Younger Dryas, a period of extreme cooling which lasted for circa 1,000 years, possibly triggered by a meteor shower^[i]. One theory has ancestors migrating south, towards warmer climates with available water, possibly carrying with them the sticky grains they had previously gathered, and may have planted them in moist soil as a means to survive, thus giving birth to the agricultural age whereby mankind moves away from a hunter gatherer lifestyle towards an agricultural lifestyle. This also makes sense as these two pockets of humanity, in Mesopotamia (now Iraq), between the Tigris and Euphrates river, and Egypt, becoming more densely populated with the need for stored food, supplied by grains and domesticating animals. This stable food supply would have allowed expansion of these populations. (There is another evolutionary hotspot in Asia and China^[i].)

Early Enlightenment

The likely existence of an ‘enlightened’ culture, Atlantis, is eluded to in the writings of Plato, possibly existing around the fertile region of the then much smaller Black Sea, which is thought to have flooded across the Bosphorus peninsular when the Mediterranean sea levels rose to a critical mass, dated back to around 7,000 years ago. This may also be the origin of the Flood myth, which occurs in ancient Sumerian lore dating back 5,000 years and later Hebrew lore.

Thus we have this triangle between the Black Sea to the North, Egypt to the South, and Mesopotamia to the East, all with evidence of evolved culture, including monotheism. The Sumerian culture appears over 6,000 years ago in the fertile crescent of Mesopotamia. Later, circa 2,500 years ago, we have the enlightened Zoroastra in Mesopotamia forming the Parsi culture in what is now Iran. Also,The Aryan-(Dru)Vedic culture, sometimes located east of the Black sea, migrated into the Indus valley in northern India as the main influence of the now Hindu culture, and the start of the Greek culture, considered to be the origin of our Western culture. The earliest hint of a Druidic culture dates back to this time. One stream of ancient druidic lore talks of a cataclysmic event, stones pouring from the sky, raising the possibility that early stone structures and barrows were built effectively as ‘bomb shelters’.^[i] While the meaning of the word ‘dru’ is associated with oak (those who meet by the oak) and truth, it also may also mean worshippers of the red Sun (du rua). Sun and fire worship is shared by the early Egyptians (Ra), (dru)vedic culture (Agni and Surya), Zoroastrian culture(Mithra) and even Sumerian culture (Utu). The use of fire started much earlier, with it’s discovery a million years ago, and widespread use from 500,000 years ago, which expanded humanity’s ability to derive energy from previously indigestible carbohydrates, as evidenced in the DNA with the emergence of multiple variations in carbohydrate- digesting amylase enzymes. This is also linked to an expansion in brain size.^[ii]

Is Homo Sapiens devolving?

Globally, there is an increase in mental illness which is fast becoming the biggest health threat, according to the World Health Organisation. There is also evidence that our brain size has reduced by 10 per cent, from 1.45kg 10,000 years ago^[1] to an average now of 1.35kg, coinciding with a more land-based food supply. According to Scandinavian research, our IQ is also falling by 7 per cent a generation. Global rates of depression and dementia, suicide and stress-related disorders of anxiety and insomnia are escalating. One in six children in the UK are classified with ‘special educational needs’ (SEN). Suicide, globally, has become the most cause of violent deaths, ahead of all wars and murders. In the UK 790 people a day, nine double decker buses worth, are diagnosed with dementia. Global incidence will top 100 million this decade, already costing over 1% of GDP.

On the assumption that our brains still require at least the same supply of nutrients that our semi-aquatic ancestors were able to eat during the period of maximum brain evolution – although one could argue that the digital age has put more stress on our brain function, hence we might even need more nutrients – and the fact that we are simply not achieving anything like the same intake of the brain’s essential fats, phospholipids and micronutrients, is it any wonder that mental health is in sharp decline? With a growing population and declining available seafood, coupled with contamination with heavy metals, PCBs and micro-plastic particles, matters are likely to get much worse.

High sugar intake, in animals, has been shown to lead to shrinking of the brain’s hippocampal region. This is where the nucleus accumbens, the seat of the brain’s dopamine-based ‘reward’ system, stimulated by sugar, caffeine and tech addiction, (especially that based on variable rewards such as the ‘like’ button) resides. Marketeers have learnt how to create addiction to their products by stimulating the reward system, selling short-term pleasure, the dopamine-based feeling, in the guise of happiness. The happy hour, the happy meal, happiness in a bottle etc. Over-stimulation of the reward system ultimately leads to dopamine depletion and brain cell death, coupled with a decline in serotonin, the tryptamine associated with happiness, connection, love, empathy and other essential qualities of a harmonious society – and the very qualities that make us human.

We are therefore witnessing the devolution of the brain, the decline and fall of mental health and harmonious society, a situation that is likely to get worse as population expands, unless we rapidly find a way to optimally nourish the brain.

Building Healthy Brains

The emphasis in human nutrition has, for too long, been on the body. With more protein, meat and dairy products, we have grown taller, but not smarter. As director of the Institute of Brain Chemistry at the Chelsea and Westminster Hospital, Professor Michael Crawford has been able to accurate predict which pregnant women are most likely to have pre-term babies, with an increased risk of cognitive delay or impairment. This is based on determining the supply, by analysing the pregnant woman’s blood, of DHA. In its absence levels of a surrogate fat, oleic acid, rises to fulfil the requirement of the neonatal brain, when DHA is in short supply. It is, however, an inadequate substitute and thus cognitive development is impaired. Babies born of mothers with low blood DHA levels, compared to those supplementing DHA, have smaller brains.^[2]

According to Crawford, with a growing population and shrinking fish supply, we must develop marine agriculture on a massive scale to survive and protect the brain. In the same way that man moved from hunter gatherer on the land to peasant farmer, we too must move from hunter gatherer in the oceans to marine farmer. In Japan he has been instrumental to the creation of artificial reefs in the estuaries to attract back the marine food web, from mussels to crustaceans, and fish, as well as farming seaweed on a massive scale. By processing seaweed it is possible to create DHA, the critical brain fat that is crucially lacking in a plant-based diet. As Crawford says “We now face a world in which sources of DHA – our fish stocks – are threatened. That has crucial consequences for our species. Without plentiful DHA, we face a future of increased mental illness and intellectual deterioration. We need to face up to that urgently.”

At the other end of the lifecycle, more and more older people are slipping into dementia, which is a preventable but not reversible condition. At the University of Oxford, Professor David Smith has shown that inadequate omega-3 fats (DHA and EPA) and B vitamins, especially vitamin B12, are the principle drivers of cognitive decline. Yet, by providing these nutrients to those with pre-dementia, further memory decline and brain shrinkage can be arrested. B12 is only found in animal foods and is especially rich in seafood. A plant-based diet alone does not provide sufficient DHA, B12 or phospholipids require for optimal brain development.

Therefore, it is vital that the needs for optimal brain function are put at the top of the health agenda to prevent the decline of our mental health and potentially the fall of Homo Sapiens. Without our fully functioning brains humanity will neither have the insight nor cooperation to face and resolve the challenges we face with a growing population, reducing food supply, increasing pollution, climate changes and ever-increasing energy demands.

Food for the Brain is a non-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.

References

^[1] https://www.astrobio.net/news-exclusive/how-earths-orbital-shift-shaped-the-sahara/; see also https://phys.org/news/2019-01-sahara-swung-lush-conditions-years.html; see also https://www.ncdc.noaa.gov/abrupt-climate-change/End%20of%20the%20African%20Humid%20Period

^[2] https://en.wikipedia.org/wiki/Younger_Dryas_impact_hypothesis

^[3] https://www.nature.com/news/how-china-is-rewriting-the-book-on-human-origins-1.20231

^[4] https://www.youtube.com/watch?v=t9Zjd0TIHsY

^[5] K. Hardy et al., ‘The importance of dietary carbohydrate in human evolution’, Quarterly Review of Biology(2015), vol 90(3):251–268.

^[6] https://www.discovermagazine.com/planet-earth/the-human-brain-has-been-getting-smaller-since-the-stone-age

^[7] Randomized controlled trial of brain specific fatty acid supplementation in pregnant women increases brain volumes on MRI scans of their newborn infants.

Ogundipe E, Tusor N, Wang Y, Johnson MR, Edwards AD, Crawford MA.

Prostaglandins Leukot Essent Fatty Acids. 2018 Nov;138:6-13. doi: 10.1016/j.plefa.2018.09.001. Epub 2018 Sep 21.

PMID:

30392581

Today, the US FDA has licenced aducanumab, an amyloid protein drug developed for dementia treatment. It has already failed in clinical trials, adding to the 300 studies that have failed. In a normal world, if you test a theory 300 times and it fails 300 times you discard the theory – that amyloid plaques in the brain are what causes Alzheimer’s.

While aducanumab has been demonstrated to reduce brain amyloid, it hasn’t been shown to deliver any meaningful improvement in cognition. A recent meta-analysis of 14 anti-amyloid drug trials found no significant slowing of cognitive decline despite lowering of amyloid. Nor has it been shown to reduce the rate of brain shrinkage.

In contrast, the combination of B vitamins and sufficient omega-3 has been shown to reduce brain shrinkage by 68% over the period of one year in research by Professor David Smith and colleagues at Oxford University. No drugs have shown such a positive effect on brain shrinkage. What’s more, memory loss was not observed to decline further and 70% of participants were classified with a Clinical Dementia Rating of zero.

In many cases dementia may be preventable – not with drugs but with nutrition and lifestyle changes.

Omega-3 and B vitamins are a Dynamic Duo

B vitamins and omega-3 are so important for mental health because the membrane through which brain signals are passed is made out of an omega-3 fat called DHA, which attaches to a phospholipid. DHA is 98% of the structural fat of the brain. Seafood is a rich source of DHA and phospholipids, and phospholipids can also be found in eggs.

These two vital components of brain cells are actively bound together by a process called methylation. Methylation is dependent on B vitamins, especially B12, folate and B6. Zinc also has a vital role to play. If these nutrients are low a toxic amino acid called homocysteine starts to accumulate in the blood stream. More often than not the critical deficiency is vitamin B12, found in fish, eggs, milk and meat. The ‘deficiency’ may be due to dietary deficiency, but also may be due to malabsorption triggered by a lack of stomach acid, potentially exacerbated by certain drugs.

Putting Prevention into Action

Scientific research shows that the following factors are key in the prevention of dementia:

·     Sufficient intake and absorption of B vitamins
·     Sufficient intake of omega-3
·     Sufficient intake of antioxidants including Vitamin C
·     A low sugar diet
·     Good digestion
·     Having an active mind and social life
·     Regular physical activity
·     Good sleep and reducing stress

These are all areas in which you can make simple changes to support your brain health. Take our popular Cognitive Function Test today to discover the actions you can take that will make the biggest difference. We encourage everyone over 40 to take this test.

Like our Cognitive Function Test? Help us Upgrade It

Food for the Brain is crowdfunding to support the upgrade of its Cognitive Function Test, already taken by 360,000 people around the world.

COG-NITION® is a personalised and interactive ‘brain upgrade’ programme designed to help people make positive changes step by step, with the support of an engaging and encouraging community. It has been created in collaboration with leading dementia experts including Professors David Smith and Jin-Tai Yu.

By supporting our crowdfunding campaign, you can help us launch COG-NITION® this autumn. The ultimate goal is to save a third of people from getting dementia, which means a 100,000 fewer cases a year in the UK alone.

As a charitable foundation, we rely on donations to continue our vital work in this area. Please give whatever you can – every £1 you give helps someone somewhere make the changes to prevent dementia.

Thank you for your support.

Estimated reading time: 9 mins

Chronic fatigue syndrome (CFS) is a debilitating condition that is otherwise known as myalgic encephalomyelitis (ME). Due to the diverse set of seemingly unrelated symptoms that people with this condition present with, it is commonly misdiagnosed and can often be confused with other conditions such as depression. 

Typical symptoms of CFS can be: 

Sleep problems
Muscle and joint pain
Headaches
Memory and concentration problems
Flu-like symptoms
Feeling dizzy or nauseous
Low mood

A mysterious illness 

CFS has long been stigmatised and ignored by many doctors due to its mysterious aetiology, often leaving many physicians baffled. This has commonly led to doctors concluding that it is purely a psychiatric illness, rather than a disease of some kind. Sadly, this means that many patients go through years of seeing various doctors before they get a proper diagnosis. 

According to the National Institutes of Health, CFS impacts 15 million to 30 million people worldwide, and leaves 75% of those affected unable to work and 25% homebound or bedridden. Although the aetiology of CFS is unclear, the condition commonly arises following a viral illness, in particular Epstein-Barr virus, herpes and mononucleosis. Since the coronavirus outbreak, there has been a large number of reports of people suffering with long-term symptoms that are akin to those of CFS. This has led to a new line of research opening, to examine the biochemical mechanisms that are leading to symptoms, such as debilitating fatigue, low mood and brain fog, headaches and more in those who have been infected with COVID-19.

A new angle to understanding COVID-19?

According to a report¹ published by the Centers of Disease Control and Prevention, more than a third of those who have tested positive for COVID-19 and have symptoms don’t feel like they’re fully recovered, even weeks and months later. Why might this be occurring at such alarming rates? Some researchers, such as Mady Hornig, Immunologist at Colombia University, have proposed that this may be due to inflammation levels going haywire in the body. COVID-19 patients exhibit abnormally high levels of inflammatory molecules², such as certain cytokines like interferon gamma, which are coincidentally the same inflammation driving molecules that are chronically present in CFS patients. This overactivation of the immune system, which has frequently been labelled the ‘cytokine storm’ in the acute phase of COVID-19, may be what is leading to long-term problems.  

Neurovirologists such as Avindra Nath, at the National Institute of Neurological Disorders and Stroke, believe that there should be more attention placed on the long term risks of COVID-19. Nath purported, in an article published in The Scientist, that viruses can seek long-term refuge in organs to hide from the immune system, which can essentially cause a constant trickling of virus particles to escape into the bloodstream leading to a chronic trigger of inflammation. However, the most obvious mechanism by which viruses can cause symptoms related to CFS is autoimmunity. Nath explains how during the acute phase of a viral infection, the body’s immune system can mistake its own proteins with viral proteins, due to an overactivation of inflammation. This, over time, can lead to mitochondrial dysfunction

A defect in the batteries of our cells?

The mitochondria are the battery-like organelles of our cells, which play an important role in a wide range of physiological processes, such as creating APT (the energy currency of our body), as well as neurotransmitter synthesis, production of insulin, iron metabolism, heat production and many more. Damage to the mitochondria can therefore have a global effect on the body, and many chronic diseases such as diabetes, psychiatric conditions and heart disease, are related to poor mitochondrial function. A key example is in the lack of ATP production that can occur in mitochondrial dysfunction – without enough ATP, we begin to experience symptoms of overall malaise, exhaustion, muscle pain, brain fog and low mood. A chronic inflammatory response that can be triggered by acute viral infections, can literally wear down the mitochondria, altering the metabolism and functioning of cells. This can have a far-reaching impact on our body and even lead to problems in normal bodily functions such as sleep. 

An example of this was seen in a case-controlled study³ carried out in 2011 and published in BMC Neurology, which looked at 22 healthcare workers who had been infected in 2003 with SARS-CoV-1 and were left with chronic exhaustion, musculoskeletal pain and sleep disturbances. After performing EEGs (electroencephalogram) on the study participants, they found elevated levels of alpha EEG anomaly and apnea. The alpha-EEG anomaly has been found to interrupt normal restorative aspects of sleep and many studies⁴ have identified this anomaly as a consistent feature in patients with fibromyalgia, a condition that leads to similar symptoms to CFS. 

The best offence is a good defence 

As the well-known adage goes, ‘the best offence is a good defence’ – the most important thing we can do to protect ourselves from the negative impact of viral infections like COVID-19, as well as prevent potential long term effects, is to optimise our health via nutrition and lifestyle approaches. A key trigger for mitochondrial impairment is oxidative stress⁵, caused by the following factors:

High blood sugar levels/insulin resistance
Consumption of inflammatory foods 
Chronic stress 
Alcohol
Cigarette smoking 

Oxidative stress is a term used to describe the impact that reactive oxygen species (ROS) can have on our health, which are chemically reactive unstable molecules that contain oxygen. These molecules scavenge electrons from other molecules, leaving a trail of disruption called free radical damage.  It is well known that under normal conditions, our bodies maintain a healthy balance between ROS and antioxidants, which are molecules that can donate electrons without becoming ‘unstable’ themselves and are therefore able to halt free radical damage. 

Having chronically high blood sugar levels, drinking too much alcohol, smoking, eating too many processed foods and chronic stress, are a recipe for free radical damage and therefore mitochondrial dysfunction. Here are some simple dietary changes to prevent this from happening:

Avoid sugar, in all its forms

Sugar can come in many forms, which is why it’s important to read ingredient labels. Food manufacturers often try to sneak sugar in by using other types of sweeteners such as dextrose, maltodextrin, syrups, fructose, sucrose, high-fructose corn syrup, agave, fruit concentrates and honey. Avoid products that contain any added sugars in them, as well as using sugar at home in foods and drinks.

Prioritise protein, fibre and healthy fats

To help avoid chronically high blood sugar levels, it’s important to base your diet on wholefoods rich in proteins, fibre and healthy fats. Protein can be found in meats, poultry, fish, eggs and pulses and healthy fats in oily fishes, nuts and seeds, coconut (and its oil), extra virgin olive oil and avocado (and its oil). Aiming for 50g of fibre a day is also incredibly important to help balance blood sugar levels. This means eating various types of vegetables throughout the day in your main meals. You can do this by aiming to dedicate half of your plate to a variety of vegetables at lunch and dinner.

Avoid processed foods

Processed, ready-made meals, often contain ingredients that can be detrimental to our health if eaten too often. Hydrogenated oils, sugars and additives feature frequently in packaged foods, which can trigger oxidative stress and can have a negative impact on mitochondrial health. Focus on whole foods and cooking from scratch as much as possible, so that you have control over what’s going into your meals. 

Eat a rainbow

The pigments in plants that cause them to have vibrant colours, such as the red in tomatoes, orange in carrots and sweet potatoes and greens in spinach and kale, are rich in antioxidants like polyphenols and flavonoids. These molecules scavenge free radicals from the body’s cells and help mop up any damage left by them. Try to vary your vegetable intake so that you make sure you’re benefitting from a wide variety of antioxidants. 

Nutrients and enzymes to support mitochondrial health

Aside from the above dietary changes, there are a few nutrients and enzymes that have been well researched in the context of supporting mitochondrial function.

Enzyme CoQ10

CoQ10 is an important endogenous antioxidant and enzyme that is produced by the body, which plays an important role in something called the electron transport chain, an important process that occurs in the mitochondria, which triggers the production of ATP or energy in simpler terms. CoQ10 is something that is created inside the body, however, we can get small amounts directly from external sources such as our diet. Foods such as organ meats and oily fish have been shown to contain some CoQ10. In addition, deficiencies in cofactor nutrients such as B2, B3 and vitamin E have been shown to play a role in CoQ10 deficiency, as well as the use of statin medication⁶. 

L-carnitine

Carnitine is an amino acid that’s synthesised from dietary sources of lysine and methionine, also amino acids. It is responsible for the transport of long-chain fatty acids into the mitochondria to be oxidised and used to create ATP. In previous studies, patients with CFS have displayed significantly lower levels of acetyl-L-carnitine, total carnitine, and free carnitine; and those with the lowest levels have shown the worst functional capacity ⁷. Whilst carnitine deficiency is rare, those on long term restrictive diets, as well as those with poor liver function may have issues synthesising carnitine. Lysine and methionine are widely found in many foods such as meats, poultry, eggs, fish, as well as in nuts and seeds, wholegrains such as oats, brown rice, and finally, in pulses.  

Alpha lipoic acid

Alpha lipoic is an important antioxidant that plays an essential role in supporting mitochondrial enzymes involved in glucose metabolism and energy production. In particular, Alpha lipoic acid has been shown to prevent damage caused to the mitochondria by increased levels of a substance called nitrous oxide (NO) in the body. Whilst NO is essential for blood vessel health, too much of it can be detrimental to our cells. This often occurs in acute inflammation, such as during the initial stages of an infection. Alpha lipoic acid has been shown to effectively restore mitochondrial enzyme activities inhibited by excess NO, which has a consequent positive impact on ATP production⁸. 

Supplementation with these nutrients has been explored in some studies⁹. However, it is important to work with a nutritional therapist or a nutritionist to make sure you’re taking the right dose and to investigate potential drug-nutrient interactions, for those taking medication. In the meantime, following the above dietary and lifestyle guidelines can have a profound impact on health and mitochondrial function. 

References

1.  Tenforde MW, Kim SS, Lindsell CJ, et al. Symptom Duration and Risk Factors for Delayed Return to Usual Health Among Outpatients with COVID-19 in a Multistate Health Care Systems Network — United States, March–June 2020. MMWR Morb Mortal Wkly Rep 2020;69:993-998. DOI: http://dx.doi.org/10.15585/mmwr.mm6930e1external icon  

2.  Distinct plasma immune signatures in me/cfs are present early in the course of illness

3.  Moldofsky, H., Patcai, J. Chronic widespread musculoskeletal pain, fatigue, depression and disordered sleep in chronic post-SARS syndrome; a case-controlled study. BMC Neurol 11, 37 (2011). https://doi.org/10.1186/1471-2377-11-37 

4.  A. M. Drewes, Pain and sleep disturbances with special reference to fibromyalgia and rheumatoid arthritis, Rheumatology, Volume 38, Issue 11, November 1999, Pages 1035–1038, https://doi.org/10.1093/rheumatology/38.11.1035

5.  Guo, Chunyan et al. “Oxidative stress, mitochondrial damage and neurodegenerative diseases.” Neural regeneration research vol. 8,21 (2013): 2003-14. doi:10.3969/j.issn.1673-5374.2013.21.009. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145906/ 

6.  Kristin Filler, Debra Lyon, James Bennett et al, ‘Association of mitochondrial dysfunction and fatigue: A review of the literature’, BBA Clinical, Volume 1, June 2014, Pages 12-23. https://doi.org/10.1016/j.bbacli.2014.04.001

7.  Sanford H. Levy MD, FACP, ABIHM, in Integrative Medicine (Fourth Edition), 2018. https://www.sciencedirect.com/topics/medicine-and-dentistry/carnitine 

8.  Sylvia Hiller, Robert De Kroon, Eric D.Hamlett et al, ‘Alpha-lipoic acid supplementation protects enzymes from damage by nitrosative and oxidative stress’,  Biochimica et Biophysica Acta (BBA) – General Subjects, Volume 1860, Issue 1, Part A, January 2016, Pages 36-45. https://doi.org/10.1016/j.bbagen.2015.09.001 9.  Kristin Filler, Debra Lyon, James Bennett et al, ‘Association of mitochondrial dysfunction and fatigue: A review of the literature’, BBA Clinical, Volume 1, June 2014, Pages 12-23. https://doi.org/10.1016/j.bbacli.2014.04.001

Worldwide 46.8 million people have dementia. In the UK, 1 in 14 people over 65 have Alzheimer’s, the most prevalent form of dementia; and increasingly dementia sufferers are also struggling with other chronic conditions, such as diabetes and depression. Research on new strategies for earlier diagnosis is among the most active areas in Alzheimer’s science. This is as the majority of cases are diagnosed when irreversible brain damage or mental decline has already occurred. 

The amyloid protein test used for earlier diagnosis

Amyloid beta is a protein found in the brain that is involved in the pathophysiology of Alzheimer’s and cognitive decline. This 2019 study found that a blood test to measure amyloid, is 94% accurate in earlier diagnosis of Alzheimer’s disease. This is specifically when in combination with age and genetics (testing positive for the APOE4 gene) as risk factors. Whilst this is a positive development for future considerations in treating Alzheimer’s, there has been no successful amyloid-lowering drug trial to date.

In addition, it is well-known that the damaging clumps of amyloid protein can begin to develop and lead to brain atrophy decades before an individual even begins to experience symptoms of memory loss and cognitive function, so unless testing is given earlier on in life as a preventative measure, an amyloid-lowering drug when the damage has already been caused may not be very effective. 

Amyloid, a protective mechanism?

To date, the majority of research into the treatment of Alzheimer’s has been focused on the “amyloid hypothesis”. In 2018 alone, the US National Institutes of Health spent $1.9 billion on Alzheimer’s research. However, according to this study, there has been a 99% failure rate in the development of drugs that target this disease. Questions about the reliability of the amyloid protein hypothesis are being posed by scientists, after various studies discovering how amyloid plaques actually function as a type of sticky defence against bacterial invasion, lead to a different hypothesis. In one significant study, where mice that were genetically engineered to make Alzheimer’s proteins had bacteria injected into their brains, researchers found that amyloid plaques engulfed bacterial cells overnight, suggesting a protective mechanism.  

Why we cannot ignore the link between high homocysteine levels and Alzheimer’s 

According to a Consensus Statement released by an international panel of experts on dementia: Research has shown, time and time again, that having high homocysteine (Hcy) levels, and low folic acid and B12 levels in the blood correlate with an increased risk for Alzheimer’s disease.

An earlier review written by Professor David Smith in 2008, highlighted that there are a total of ‘seventy-seven cross-sectional studies on more than 34,000 subjects and 33 prospective studies on more than 12,000 subjects’…that…‘have shown associations between cognitive deficit or dementia and homocysteine and/or B vitamins.’ 

In a meta-analysis published in 2014 by BMC Public Health, raised homocysteine was considered to be one of the three strongest risk factors, along with low education and decreased physical activity.

Two further trials have clearly shown that lowering homocysteine, through the supplementation of B vitamins, reduced age-related cognitive decline in normal ageing and also slowed down both brain atrophy and cognitive decline in people with Mild Cognitive Impairment.

The efficacy of B vitamins to prevent the progression of Alzheimer’s.

In one study, 270 people over 70 with Mild Cognitive Impairment were recruited to trial the efficacy of B vitamins to prevent the progression of Alzheimer’s. MRI scans were done at recruitment and half the participants were given high doses of three B vitamins (B6, B9 and B12), half took a placebo tablet.

After 2 years, participants were scanned again and scientists found that the rate of brain atrophy in those treated with the B vitamins was on average 30% slower than those taking placebo. In addition, in those that had the highest homocysteine levels at baseline, the effect of B vitamin treatment was even more potent, helping to slow down brain atrophy by 53%. This result fits all the criteria for a disease-modifying treatment and so is especially important. There is, therefore, ample evidence to propose that lowering homocysteine by giving appropriate supplemental levels of homocysteine lowering nutrients, including B6, B12 and folic acid, would reduce risk.

In a commission published by the Lancet, 9 modifiable risk factors were outlined, clearly excluding homocysteine:  

Ignoring homocysteine is surprising, since a meta-analysis from the National Institute of Aging estimated that about 22% of Alzheimer’s disease may be caused by raised levels of homocysteine.

Integrating homocysteine testing and inexpensive B vitamin-based treatment into the heart of mainstream health strategies on Alzheimer’s could potentially play a vital role in the prevention of dementia, if caught early enough.