After the festive period, many will be feeling the negative impact of alcohol and food indulgence. In an effort to allow the body to recalibrate and shake-off the resulting low energy, brain fog and low mood, taking up Dry January is often a key strategy to start the year off on a good foot. 

However, those susceptible to alcohol cravings may find that a month off the booze is harder than expected. Symptoms such as poor sleep, sugar cravings and a long-winded hangover, are just some of the experiences that people have reported. One of the most common symptoms is an increase in anxiety, perhaps due to the reduction of a very important neurotransmitter called GABA, which is stimulated by alcohol. 

What is GABA?

GABA is the body’s main inhibitory neurotransmitter, meaning that it helps the body and brain to relax and promotes feelings/sensations of calm and tiredness. It does this by preventing excitatory neurotransmitters like dopamine and noradrenaline from over-stimulating the brain and helps to slow down the heart rate and breathing, as well as relaxing muscles. 

In those who are deficient in GABA, feelings of anxiety, stress and worry can be common symptoms, leading to alcohol cravings. Alcohol targets GABA receptors and mimics the effect of this neurotransmitter, helping to relax the mind and body. 

Have you ever craved alcohol after a stressful day and used a glass of wine to help calm the nerves and decompress the mind? This is your body’s way of telling you that GABA needs to be switched on! Whilst alcohol facilitates this, unfortunately the negative side effects of chronic alcohol use far outweigh the temporary feelings of calm and relax. 

The Relationship Between GABA and Alcohol 

Alcohol can cross  the blood brain barrier incredibly quickly – the brain’s very own protective mechanism that prevents things like toxins, bacteria and unwanted hormones from entering the brain and causing damage. This is why after drinking alcohol, its effects can be felt almost instantly. 

The brain has a very intelligent way of preventing overstimulation of neurotransmitters, so that balance is maintained. For example, when alcohol intake is high, in an effort to avoid an excessive accumulation of GABA (as well as other neurotransmitters), receptor response is dampened. Meaning  that over time, you’ll need more of the substance to provide the same effect, which may lead to potential addiction and alcohol dependency . This can make Dry January almost impossible to achieve, if other ways of increasing GABA aren’t employed. 

Below is a list of safe and natural ways you can help activate GABA, which will also enhance overall health and mental wellbeing. 

4 Ways to Increase GABA Naturally… 

1. Magnesium – nature’s relaxant

Magnesium has been shown to modulate GABA activity in the brain. It does this by acting on GABA receptors to help facilitate GABA neurotransmission and its consequent effects of relaxation. 

Magnesium also helps to relax the central nervous system, as well as the body’s muscles. It does this by helping to activate the parasympathetic nervous system – the branch of our autonomic nervous system that is responsible for helping us to relax, down-regulating cortisol output and for regenerating cells and tissues. 

We can find magnesium in foods such as avocado, nuts and seeds, legumes and some wholegrains. However, some studies have shown that supplementing with magnesium (around 300mg a day), can be very effective in reducing symptoms of anxiety. 

2. Consider a B6 Supplement 

GABA is produced via the activity of an enzyme called glutamic acid decarboxylase (GAD) and GABA transaminase, which require vitamin B6 as a cofactor. Studies show that the B6 status of an individual has significant effects on the central production of both GABA and serotonin, neurotransmitters that control pain perception, and for preventing symptoms of depression and anxiety. Whilst B6 is found abundantly in the diet, studies show that common deficiencies of B12 and B9 (Folate), can also indicate B6 deficiency, so it’s important to take into consideration if you have a history of anemia. In addition, those who have chronic alcohol intake are also at risk of B6 deficiency. 

B6 can be found in all animal products, as well as grains, pulses, eggs and dairy. However, you may want to consider a supplement that contains all the B vitamins to help boost B6 levels temporarily.

3. Increase Exercise

Researchers have found that vigorous bouts of exercise can increase GABA. In addition, exercise helps to switch on a regenerative substance in the brain called Brain-Derived Neurotrophic Factor (BDNF) – helping create new and healthy brain cells and increases neuroplasticity, which prevents anxiety and depression. Engaging in just a small amount of exercise on a daily basis, as well as remembering to take ‘walking’ breaks away from the desk or the sofa is enough to switch on this ‘brain-protective’ mechanism.

4. Engage in a Mind-Body Movement 

There is a significant body of evidence that demonstrates how practices such as yoga, can help increase levels of GABA in the brain. For example, in a study comparing the effects of walking and yoga in two separate groups, MRIs that were taken following these activities demonstrated significant differences. Participants in the two control groups did these activities for one hour, three times a week, over a period of 12 weeks. The MRIs revealed a larger increase in GABA levels in a part of the brain called the thalamus amongst yoga practitioners. The yoga practitioners also reported improved mood and anxiety compared to the waking control group.  

A final word… 

These findings give us clues as to what our bodies need in order to maintain health and mental wellbeing. These simple, practical steps are easy to implement and can help reduce alcohol cravings and increase GABA in the brain. In addition, eating a balanced diet that helps to stabilise blood sugar levels, is also essential for preventing cravings. 

To help provide a sustainable source of energy, eating three meals a day which contain protein-rich foods such as poultry, fish, eggs and pulses, as well as complex carbohydrates, such as sweet potatoes, butternut squash, other root vegetables and brown rice, and a wide variety of vegetables, is essential. This helps to prevent anxiety caused by blood sugar lows and highs, which can also leave you vulnerable to craving alcohol and other substances. 

SAD, which stands for Seasonal Affective Disorder, isn’t just a case of the winter blues. It is a form of major depression and can be seriously debilitating, causing symptoms such as chronic low mood, excessive sleeping, carbohydrate cravings, irritability, poor concentration, low libido and lethargy. SAD occurs most typically throughout the winter months and currently affects around 6% of the UK population, and between 2-8% of people in other countries of higher latitude such as Sweden, Canada and Denmark. 

Curiously, around 80% of sufferers are women, mostly those in their early adulthood. Scientists such as Dr Robert Levitan, professor at the University of Toronto, have speculated that this may be due to evolutionary purposes, which encourages women of reproductive age to slow down during the winter months to help preserve energy, leading to healthier pregnancies. 

Research has yet to come to a definitive conclusion as to what causes SAD, however, there are a number of underlying biochemical triggers that have been identified. 

A leading theory looks at serotonin production and how levels of this neurotransmitter in the body are significantly affected by the amount of available sunshine. Research shows that exposure to sunshine has an impact on the binding-capacity of serotonin to receptor sites in the brain, which essentially allows serotonin to work its magic, leading to feelings of contentment and happiness. 

Other research also indicates how those suffering with SAD tend to have a dysregulated production of melatonin, the hormone produced in the pineal gland in response to darkness, which induces sleep. Instead of being produced in the evening, helping the body settle for the night, studies in those that suffer with SAD show melatonin being secreted during the day, hence feeling the need to sleep all the time and lack of energy. 

There are a few other biochemical underpinnings in the pathogenesis of SAD, however, there are some key nutrition and lifestyle strategies based on these initial findings, which can help support mood throughout the winter months.  

1. Get your body clock in check 

Our body’s hormones and biological processes are majorly governed by a natural, internal circadian rhythm, which regulates our sleep-wake cycle and is programmed by daylight and night. A disrupted circadian rhythm can be caused by shift work, not enough exposure to daylight, stress, insomnia and too much exposure to blue light in the evening, which can lead to an imbalance in neurotransmitters such as serotonin and melatonin. 

This is why it is incredibly important to try and attune the body to these cycles as much as possible, by doing things like avoiding electronic screens at night and doing relaxing activities to encourage melatonin production, as well as exposing the face to daylight first thing in the morning, or if it’s dark, buying a light therapy lamp. Putting these strategies into place, can help the body recalibrate and realign to a healthy sleep-wake cycle. 

2. Check your vitamin D levels

Research shows that having sub-optimal levels of vitamin D3 can interfere with proper serotonin production. Whilst scientists don’t understand exactly how, there is a significant body of research that demonstrates a strong link between vitamin D3 levels and depression.In one particular study, scientists found that vitamin D3 helps to convert the amino acid, tryptophan, into serotonin. 

Check your vitamin D3 levels and make sure that they are above 75 nmol/L, for optimal serotonin production. 

3. Balance your blood sugar levels 

More than any other organ in the body, the brain is dependent on a constant supply of energy, which very much related to our diet. Eating foods that are high in sugar and simple carbohydrates leads to rapid fluctuations in blood sugar levels, which can have a significant impact on the brain and its neurotransmitters. Typical symptoms of imbalanced blood sugar levels are low mood, anxiety, brain fog and fatigue. 

This is why it is important to eat foods that provide the body and brain with a consistent and sustainable source of energy. This means making sure you’re eating complex carbohydrates that contain ample amounts of fibre, such as brown rice, starchy vegetables and tubers like sweet potato, butternut squash and beets, as well as eating protein-rich foods with every meal and snack. Avoiding refined grains like white bread, pastries, cakes, biscuits and white rice, as well as foods with added sugar like in processed foods, sweet yoghurts, fruit juices and cereals, is absolutely key to avoiding blood sugar imbalances. 
4. Get moving! 

According to a recent study published by JAMA Psychiatry, people are 26% less likely to become depressed with regular physical activity. It is well established that exercise can stimulate the release of endorphins such as serotonin, dopamine and norepinephrine – all of which regulate mood and prevent symptoms of depression. 

We also know that exercise stimulates the release of protective molecules such as Brain-Derived Neurotrophic Factor, which helps to trigger the growth of new brain cells. 

The key takeaway is to include some form of movement into your everyday life to help encourage the brain to produce its ‘feel-good chemicals’. Whether it’s fast paced walking or a more intensive exercise like HIIT, it is vital to be moving. 

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.

In the UK, at any one time about 220,000 people are being treated for schizophrenia by the NHS. Whilst it is a less common mental health condition, statistics show that there is a higher risk associated to suicide and greater vulnerability to physical conditions like diabetes, perhaps due to medications such as antipsychotics. Due to this, statistics show that people with schizophrenia die on average 10 – 20 years earlier than the general population.

Schizophrenia is characterised by two different groups of symptoms, which are classified as ‘positive’ and ‘negative’. Positive symptoms are the changes in behaviour and thoughts described as hallucinations (hearing voices or seeing things that others don’t), delusions and paranoia. The negative symptoms include feeling disconnected from other people, less interested in life, emotionless and sometimes disorganised thought and speech. 

The exact cause of schizophrenia is still misunderstood, with various theories pointing to a number of different biochemical imbalances, including genetic mutations that can provide the foundations for the disorder to develop. 

What causes schizophrenia?

One of the most popular theories on the cause of schizophrenia, which is widely accepted by the scientific and medical community, is the dopamine excess hypothesis, that is, too much dopamine in the brain that can cause the positive symptoms of psychosis to occur. Antipsychotics are the most commonly prescribed medications to target positive symptoms and prevent psychosis. Whilst they have proven to be critical in targeting excessive dopamine signalling in the brain, antipsychotics can also lead to health complications such as metabolic syndrome, the worsening of negative symptoms and nutrient depletion, which overall can be detrimental to a patients’ health over a long period of time. Studies show that common antipsychotics such as clozapine can lead to the depletion of selenium and l-tryptophan. Both nutrients are incredibly important to maintain health – selenium is an essential mineral, which is a precursor to glutathione, the body’s most important antioxidant and l-tryptophan is an amino acid precursor to serotonin, which is known to prevent depression and enhance mental wellbeing.

Another key theory, founded by the late Dr Abraham Hoffer and his colleagues Humphrey Osmand and John Smythies in 1954, is the adrenochrome theory. This theory initially came about after studying the symptoms caused by hallucinogenic drugs such as LSD, mescaline and amphetamines. The researchers noted these symptoms were similar to those experienced by schizophrenics including euphoria, derealisation and hallucinations, accompanied by paranoia and depression. They then discovered that the chemical structure of adrenaline was also similar to mescaline and LSD, which lead them into researching the effect of adrenochromes on the brain. 

What are adrenochromes? 

Adrenochromes are metabolites of adrenaline, the hormone and neurotransmitter that is responsible for our body’s ‘fight or flight’ response. It is believed that derivatives of adrenaline and other similar compounds such as dopaminochrome and noradrenochrome, can be neurotoxic in large quantities and cause mood-altering effects. 

The adrenochrome theory is further supported by studies that have shown how in those with schizophrenia, the enzyme glutathione s-transferase, (responsible for clearing the brain from neurotoxic compounds such as adrenochrome, dopaminochrome and noradrenochrome) is commonly defective, thus leading to an accumulation of these substances in the brain. 

What is niacin’s (B3) role in preventing symptoms of schizophrenia? 

Abraham Hoffer and his team theorised that in order to reduce the production of adrenochromes, a methyl acceptor such as B3 would be needed. Methyl acceptor is the name for nutrients, mainly in the B vitamin family, which each play an important role in a biochemical process known as methylation. This process is needed for a variety of biochemical reactions, such as building and breaking down neurotransmitters, supporting liver detox pathways and DNA repair, to name a few.  

Upon studying the pathway for adrenaline production in the brain and the cofactor nutrients supporting and inhibiting this pathway, Hoffer deduced that by giving large doses of vitamin B3, which is a methyl acceptor, this would effectively prevent the conversion of noradrenaline to adrenaline, and by limiting the amount of adrenaline, this would then prevent the build up of adrenochromes. 

In addition, B3 is also a precursor to nicotinamide adenine dinucleotide (NAD), a compound that is involved in redox reactions, which prevents oxidative stress caused by free radicals. These are unstable molecules that scavenge electrons from other molecules, causing a chain reaction that can eventually damage tissues in the body. NAD prevents the oxidation of adrenaline, which is what turns adrenaline into adrenochromes, therefore preventing the production of these neurotoxins that over time can damage the brain.


How reliable is the adrenochrome theory? 

Between the years 1953 to 1960, Hoffer researched and studied patients with schizophrenia, publishing a total of six double-blindclinical trials. In one study, conducted in 1962, 82 patients (39 in the niacin group and 43 in the placebo group) were involved and were given niacin throughout a period of 33 days. The results showed that 79.5% in the niacin group improved significantly in comparison to the placebo group, which was 41.9%. 

Despite the positive results that these 6 studies showed, other studies on patients with chronic schizophrenia who had been suffering for longer periods of time, demonstrated how B3 was not as effective. In one particular study using 32 patients, after two years of niacin use no positive effect was registered. However, Hoffer realised after performing initial studies that niacin treatment needed to be carried out for longer periods of time in those with chronic schizophrenia. 

A recent meta-analysis of the effects of vitamins and minerals on schizophrenia identified 18 clinical trials in which 832 patients on antipsychotics were involved. The analysis found that high dose B vitamins (including B3, B6 B9 and B12) were consistently effective for reducing psychiatric symptoms, in comparison to studies where low dose B vitamins were used. 

How safe is niacin treatment? 

Doses of niacin for schizophrenia are recommended between 3,000mg – 18,000mg a day in order to have a substantial effect. It should be noted, however, that niacin treatment must be monitored by a qualified health professional or doctor and should not be self-prescribed. Due to niacin’s side-effects, which are characterised by hot flushes and red skin rashes, many may choose to opt for a ‘no-flush’ version of the niacin supplement. However, studies have shown the risk of liver toxicity with high doses of the timed release and no-flush version of niacin, so this should be avoided. 

In addition, niacin on its own is rarely enough to address symptoms of schizophrenia. Each person is unique, and therefore there are many other factors which should be taken into consideration, such as digestion and inflammation.