From 13 December 2026, a profound but unheralded change is taking place in the diet of 71 million UK citizens. From that date, 99 per cent of the non-wholemeal flour sold in the UK — and incorporated into innumerable food products — will contain a synthetic chemical, folic acid, that is not present in natural foods. This unprecedented addition of a novel, synthetic chemical to the national diet has occurred without thorough public debate and has been enacted via secondary legislation, an amendment in 2024 to the Bread and Flour Regulations. The impetus for this change to the UK diet originates not from within the nation, but from international bodies such as the World Health Organization. They laud the change as a nutrition action that will help to achieve the United Nations 2030 Sustainable Development Goals and thank the Bill and Melinda Gates Foundation for financial support in promoting this change.
The addition of synthetic folic acid to the national diet has been sold to the public as a compassionate public health strategy. The stated objective is to prevent 200 UK pregnancies each year being affected with neural tube defects (NTDs) such as spina bifida. What has not been brought to the public’s attention is that folic acid has been shown to adversely affect health in a wide diversity of research studies. Despite this, the UK Government has excluded from its economic cost-benefit analysis the potential health implications of continuously exposing 71 million UK citizens to novel, synthetic folic acid. Furthermore, the UK Government’s analysis fails to acknowledge the moral and ethical boundaries that have been breached by the enforced addition of a synthetic chemical to the national diet. Given the ubiquity of non-wholemeal flour in processed food items, it will in future be virtually impossible to avoid ingestion of folic acid. The legislation therefore breaches the rights of citizens to bodily autonomy.
In this article, I will first take a detailed look at the evidence supporting the contention that mandating folic acid will reduce the rate of NTDs. I will argue that the blanket mandating of folic acid in non-wholemeal flour is not a rational policy; a more focused intervention is required. I will then explore research that has uncovered harmful effects of folic acid on health. Where it is possible, I will provide explanations of why these harmful effects are to be expected. I will conclude by arguing that a policy that potentially puts the health of 71 million citizens at risk for the sake of preventing 200 NTDs per year is neither rational, proportional, nor ethical.
NTDs are one of the commonest developmental abnormalities affecting babies in the UK (12.2 per 10,000 live births). They occur when, between the 17th and 30th day of foetal development, the neural tube fails to close. As a consequence, babies are born with debilitating conditions such as spina bifida that have lifetime consequences for their health. The incidence of neural tube defects is affected by numerous factors. There is a strong element of genetic predisposition; mothers who have had a child affected by an NTD are much more likely than the average to have another. Lifestyle affects the incidence of NTDs, which increases with maternal obesity and drug use. Environmental factors such as exposure to high temperature, passive smoking, and chemical toxins have also been found to increase the likelihood of NTDs.
In order to identify mothers predisposed to risk of NTDs, multiple studies have been undertaken to find biological markers associated with the occurrence of NTDs. This research has shown that, though there is much variation, mothers whose pregnancies result in NTDs have higher levels of homocysteine (116 per cent) and lower levels of both vitamin B12 (91 per cent) and blood folate (92 per cent) than mothers enjoying normal pregnancies. This suggests that NTDs are associated with a defect in so-called one-carbon metabolism in which homocysteine, vitamin B12, and folate are all involved. One-carbon metabolism is fundamentally important to growth and development because it supplies the building blocks used in nucleic acid synthesis and gene regulation.
Taking account of these results, trials have been conducted to determine whether artificially raising maternal blood folate levels can reduce the risk of NTDs. However, the medication that has been chosen for raising maternal blood folate levels is not the natural form of folate found in the blood, 5-methyltetrahydrofolate (5-MTHF), but folic acid. Folic acid is a synthetic, oxidised form of 5-MTHF, and it is not present in nature. The advantages of prescribing folic acid rather than 5-MTHF are that it is cheap to manufacture, is more stable than 5-MTHF, and, like other allopathic medicines, can be prescribed in strictly controlled quantities. However, there is an obvious problem with prescribing folic acid rather than 5-MTHF for raising maternal blood folate levels; folic acid must be converted into 5-MTHF before it can enhance maternal folate levels.
Folic acid is metabolised to 5-MTHF via a two-step process with tetrahydrofolate (THF) as the intermediate. The conversion of folic acid to THF is inefficient in all individuals. This means that for all recipients, folic acid may remain in the bloodstream for many hours after ingestion. The rate of conversion of THF to 5-MTHF varies according to individual genotype, with rates being very low in some individuals. In these cases, high levels of THF derived from folic acid may accumulate, interfering with both conversion of folic acid to THF and the dynamics of one-carbon metabolism. Thus, administration of folic acid, while ultimately achieving greater levels of folate in blood, is likely to be accompanied by side effects arising from prolonged presence of folic acid in the bloodstream and altered one-carbon metabolism. This should be borne in mind as we consider the results of experiments to determine the effects of folic acid treatment on the rate of NTDs.
The initial trials of the effects of folic acid treatment on NTDs were conducted on populations of women who had already borne a child with an NTD and were therefore at high risk of another such birth (recurrence trials). In a randomised double-blind recurrence trial, organised across seven countries, the recurrence of NTDs was reduced from 349 cases per 10,000 to 101 cases per 10,000. In a further trial held in five centres in India, recurrence of NTDs was reduced from 704 per 10,000 to 292 per 10,000. Folic acid treatment in this high-risk group is clearly effective in reducing the incidence of NTDs by as much as 70 per cent. However, the treatment does not eliminate the problem since the rate of NTDs after treatment is still 10 to 30 times higher than in the general population.
Following the success of the recurrence trials, a single large trial was conducted that involved not a high-risk group, but a random sample of over 5,000 women, approximately half of whom were prescribed folic acid before and during pregnancy, with the remainder acting as controls. In the folic acid treatment group, there were no cases of NTDs, whereas in the controls, six children were born with NTDs. Folic acid treatment had apparently prevented NTDs. However, a careful analysis of pregnancy outcomes revealed that pregnancy losses were significantly greater in the folic acid treatment group than in the control group. For every NTD prevented, nine babies were lost. Indeed, it was speculated that increased pregnancy loss might be sufficient to account for the reduction of NTDs in the folic acid treatment.
Further evidence that folic acid ingestion in pregnancy can have undesirable side effects comes from studies on the incidence of gestational diabetes in pregnant women. In Australia, a dramatic rise in gestational diabetes from 6 per cent to 18 per cent took place in the ten years after folic acid was mandated in flour in 2009. This rise cannot be completely accounted for by changes in lifestyle factors and appears to be in part a consequence of excessive folic acid intake due to a combination of folic acid supplements and folic acid present in flour. A causal link is supported by a positive relationship between folic acid intake and incidence of gestational diabetes. Thus, excessive folic acid ingestion in pregnancy increases risk not only to the unborn child, but also to the mother.
The overall conclusions that can be drawn from these trials are that folic acid treatment is effective for reducing the occurrence of NTDs in that subset of women who are at elevated risk. Folic acid acts as a medication to reduce this risk. However, medication of women who are not at high risk is likely to increase the probability that they will lose their unborn child and increase the chances that they will develop gestational diabetes. These considerations argue for a targeted rather than a blanket approach to raising folate levels in pregnancy, focusing on treating only those at high risk who may be identified through the screening of maternal markers. They also point to the need to switch away from folic acid as the medication used to increase folate levels. Some form of natural folate that requires minimal conversion before being utilised by the body is an obvious and safe alternative. One such natural folate is [6S]-5-methyltetrahydrofolate, which has been shown to be more efficient than folic acid in raising blood folate in women of childbearing age.
The discovery of negative side effects of folic acid treatments in pregnancy begs the question of whether folic acid treatment poses wider health problems. This is particularly pertinent given that the mandatory addition of folic acid in non-wholemeal flour will effectively expose 71 million UK citizens to folic acid medication. One of the anticipated side effects of mandated folic acid in flour is that it will lead to the prolonged presence of unmetabolised folic acid (UMFA) in the blood. This is because the rate of conversion of folic acid to folate is so inefficient. This is not just a theoretical possibility. After mandating added folic acid in flour in the US, 95 per cent of all children, adolescents, and adults were found to have UMFA circulating in their blood. The same or even higher prevalence of UMFA is to be expected in the UK population given that the rate of addition of folic acid to flour is 40 per cent greater than in the US. What are the likely health implications of this circulating UMFA?
When present in the blood, folic acid interacts with and blocks the receptors normally used by natural folate to cross the blood/brain barrier. Folic acid acts as a competitive inhibitor of natural folate. The presence of UMFA in blood after folic acid treatment is therefore likely to compromise the supply of folate to the brain, which could lead to both neurological and developmental impairment. In support of this contention, clinical evidence has recently been obtained for a reduction in folate supply to the brain following folic acid treatment.
The presence of UMFA in the blood has also been shown to affect the potency of natural killer (NK) cells that are responsible for destroying tumours. In postmenopausal women, the ability of NK cells to destroy tumour cells (their cytotoxicity) was 23 per cent lower when UMFA was present in the blood (17). Furthermore, cytotoxicity of NK cells declined with increasing UMFA concentration, supporting a causal link. The consequence of reduced NK cytotoxicity is anticipated to be an increase in the incidence of cancer. Accordingly, numerous studies have been conducted to determine whether folic acid treatment is associated with increased cancer risk. A combined analysis of these trials showed that folic acid treatment was responsible for a marginally significant increase of 7 per cent in any form of cancer, but a highly significant increase of 24 per cent in prostate cancer.
Additional risks posed by folic acid medication are well recognised by the NHS, which identifies certain groups for whom folic acid is contraindicated. These include those suffering from cancer and anyone who has had a heart stent fitted. These groups constitute a significant proportion of the UK population. Approximately 5.5 per cent of the UK population is estimated to be living with cancer. Every year, heart stents are fitted to 100,000 patients in the UK, 75 per cent of whom are alive 10 years later. In this group, folic acid treatment led to a 50 per cent increase in the need to repeat the stent treatment. With the mandating the addition of folic acid in non-wholemeal flour, it will be very difficult, if not impossible, for these groups to avoid the ingestion of folic acid in their diet.
One final group for whom supplementation of flour with folic acid is likely to be problematic is those suffering from vitamin B12 deficiency, which is more common in the elderly. A readily diagnosed symptom of vitamin B12 deficiency is anaemia associated with low levels of blood folate. Addition of folate to the diet in the form of mandated folic acid may cure this symptom without resolving the underlying problem. This may result in chronic undiagnosed vitamin B12 deficiency, which causes permanent nerve damage and irreversible neurological impairment.
Evidence that these effects of folic acid supplementation occur in patients with vitamin B12 deficiency comes from a recent study using data from the UK Biobank. In the absence of vitamin B12 supplementation, folic acid medication is significantly associated with a higher risk of Alzheimer’s disease and vascular dementia as well as adverse alterations in brain structure. However, these associations are not found when vitamin B12 supplements are provided in addition to folic acid medication. The NHS advises that folic acid medication should be avoided by those with vitamin B12 deficiency. This advice cannot be followed if the entire UK population, including those with vitamin B12 deficiency, is medicated with folic acid by mandating this chemical in their diet.
As a father and grandfather, I know that the greatest gift I have ever been given is a healthy child, and any steps that we can take to ensure that babies are born without neural tube defects are to be wholeheartedly welcomed. As I have indicated already, a rational policy for reducing neural tube defects would be an education campaign with a focus on leafy greens for women of child bearing age, and, if prudent, the prescribing of natural folate. Instead, the policy that has been chosen by the government is to medicate the whole of the UK population with the synthetic chemical folic acid. As evidenced above, this policy will bring with it adverse effects that will lead to human suffering and impose a further economic burden on health services. The policy adopted, despite the availability of a benign alternative, is both blatantly irrational and morally indefensible. The evidence of this is so clear that we have a duty to resist and overturn this measure with every legitimate means at our disposal.
I would like to finish by paying tribute to the vast amount of work on the issue of folic acid in flour that has been undertaken by Dr Clare Craig and is published on the HART Substack. Clare has almost single-handedly brought this issue to the attention of a wider public and successfully attracted more than 130,000 signatures to a parliamentary petition calling for an end to the ‘fortification’ of flour with synthetic folic acid. This will be debated in Parliament on 14 December based on science and not on emotion. In parallel, we are planning a crowdfunder to support a judicial review of the relevant secondary legislation that is being used to implement the folic acid mandate. The importance of resisting this legislation should not be underestimated. This represents the thin end of a wedge. The UK Government is attempting to legitimise the mass medication of the public without their informed consent and in contravention of their right to bodily autonomy. Food is being weaponised, and the target is the UK public.
