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Letters to the Editor Issue 291

by Letters(more info)

listed in letters to the editor, originally published in issue 291 - January 2024

Over Half of Brits may have High Cholesterol. Will Ending ‘Bad’ Cholesterol Testing Add to the Problem?

The most comprehensive research into cholesterol ever conducted in the UK has found 54% of Brits could have high total cholesterol levels. Now a medical expert says the recent switch from measuring LDL ‘bad’ cholesterol levels to a new ‘non-HDL’ test could be causing many Brits confusion.

October is Cholesterol Awareness Month, and a leading medical expert says increased awareness of this condition can’t come too soon. A quarter of a million volunteers have taken part in a huge testing programme for blood pressure and cholesterol levels, and the results are very concerning.

Dr Avinash Hari Narayanan (MBChB), Clinical Lead at London Medical Laboratory, says: 

“27% of people taking part in Our Future Health’s new research programme were found to have high blood pressure and a huge 54% were found to have high total cholesterol levels.

“High cholesterol is a major underlying risk factor for cardiovascular disease (CVD), which is the leading cause of death worldwide, often leading to heart attacks and strokes. In England, high cholesterol leads to over 7% of all deaths and affects up to 60% of adults, according to NHS figures. Further research has revealed that, if 90% of people with CVD were identified and treated, almost 14,000 heart attacks, strokes and deaths would be prevented in three years.

“With cholesterol levels having such a critical long-term impact on our overall health and 54% of us likely to have the condition, absolute clarity is needed in test results and interpretation. However, the UK has recently switched from the well-known and understood measurement of LDL (low-density lipoprotein), traditionally known as “bad” cholesterol, to a new measure. It’s vital that this change doesn’t confuse anyone receiving a test.

“Previously, the focus of a cholesterol test was on our LDL (“bad”) cholesterol levels. That’s because not all cholesterol is a problem. It’s a natural fatty substance in our blood, produced in the liver and in some of the foods we eat, which helps to keep the cells in our bodies healthy. However, high LDL levels, uncontrolled, can increase our risk of heart attack and stroke. 

“Our LDL “bad” cholesterol levels used to be compared alongside our HDL (high-density lipoprotein) “good” cholesterol levels, as well as the total cholesterol level. Many people who are carefully watching their diet have become used to measuring their LDL levels over time as a key indicator of their potential health risks.

“However, some researchers believe that measuring your “non-HDL” cholesterol levels gives a better assessment of the risk for heart disease than measuring only “bad” LDL levels. Because of this change, your “non-HDL” level is the measurement patients will probably be given now by their GPs.

“Many people with high blood pressure will have become knowledgeable about LDL cholesterol, which makes up most of the body’s cholesterol. LDL carries cholesterol to the cells that need it. If there’s too much cholesterol for the cells to use it can build up in the artery walls, leading to disease of the arteries. In general, the higher your total and LDL cholesterol levels, the higher your risk for coronary heart disease. The former NHS guidance (still given by NHS Scotland) said LDL levels should be 3mmol/L or less.

“However, the new non-HDL measure is very different. England’s NHS says, as a guide, your non-HDL cholesterol should be lower than 4mmol/L. That is potentially confusing, as a 4mmol/L reading of LDL would put you at a notably higher risk of cardiovascular disease.

“So why has this change been made and are patients always clear about what their new measurements should be?

“There are some good reasons for the change. Some heart attacks happen to people who don't have a high LDL level. Researchers found we also need to consider other parts of “bad” cholesterol, known as VLDL (Very low-density lipoproteins), IDL (Intermediate-density lipoproteins) and lipoprotein(a), a type of LDL with an added protein. Previous testing also ignored triglyceride, another type of blood fat.

“What do these new measurements tell us? VLDLs carry triglycerides and, to a lesser degree, cholesterol to our tissues. IDLs are created when VLDLs give up their fatty acids. They’re then either removed by our liver or converted into LDL. The added protein in lipoprotein(a) makes it stickier, narrowing arteries. It is thought to be largely caused by our genes rather than diet. Finally, triglycerides are another type of blood fat. If your triglycerides are high, it can mean you’re at risk of heart disease, liver disease and diabetes. 

“When you take the new test, as well as your new non-HDL reading, you will also be given an HDL (good cholesterol) and total cholesterol reading, which should be 5mmol/L or less. With cholesterol becoming something of a “silent epidemic”, impacting 1-in-2 people, the new, more accurate testing should be welcome. However, those used to checking their LDL “bad” cholesterols may feel confused or still wish to monitor this reading separately. Many people have monitored their LDL cholesterol levels for years, to see how diet and lifestyle are impacting their readings. Losing this continuity could potentially lead to complications.

“Fortunately, there are some up-to-date tests that, while offering the new non-HDL measure, also continue to identify LDL “bad” cholesterol levels. For example, London Medical Laboratory’s Cholesterol Profile test is a revolutionary and convenient home-finger prick test. It measures total cholesterol, LDL, HDL, non-HDL, triglycerides and two other key markers.

‘London Medical Laboratory’s finger prick Cholesterol Profile test is considered the gold standard in regular testing. It is used to measure seven key biomarkers enabling people to make the positive lifestyle and dietary changes needed to improve their chances of a long and healthy life.  It can be taken at home through the post, or at one of the many drop-in clinics that offer these tests across London and nationwide in over 95 selected pharmacies and health stores.” For full details, see:

Further Information

London Medical Laboratory’s Clinical Lead, Dr Avinash Hari Narayanan, is available to supply exclusive written comment or for interview. To contact Dr Hari Narayanan, or for more information, please email London Medical Laboratory’s Head of Public Relations, David Jinks M.I.L.T., at



Aberdeen University Cancels Vitamin C Study in Care Homes

It’s well known that conditions in care homes are such that the patients are often deficient in Vitamin C, along with other vitamins and minerals. The most recent study found that 40% of residents had a level of vitamin C consistent with scurvy. Early signs of this horrible condition include weakness, unexplained exhaustion, loss of appetite, irritability and aching legs.

Within three months their condition can become a lot worse. Symptoms include anaemia, bleeding gums, areas of bruising on legs and feet, tooth decay, tender and swollen joints, mood swings, gastrointestinal bleeding and a high risk of infection. Finally, vitamin C deficiency leads to death from pneumonia. Medical texts describe

( untreated scurvy as, “a life threatening condition and cause of death”.

Surprisingly there is no official figure for the amount needed to preserve normal immunity to infections such as Covid. Since scurvy is a condition well worth banishing from care homes, we – being the not-for-profit VitaminC4Covid, a community interest company supported by over 1,000 scientists, doctors, nutritionists and frontline workers – teamed up with vitamin C expert, Associate Professor Anitra Carr (University of Otago, NZ), to devise a cheap and simple way to find out how much vitamin C a person in a care home actually needs, using vitamin C urine sticks. Each day the vitamin C dose would be increased until a change in the colour of the urine stick showed there was enough in the system.

It seemed like the best sort of science, lifesaving, not expensive and likely to win plaudits for the university that supported it. We have just discovered that although it ticked all the grant and organisational boxes, the crowd funded study by VitaC4Care, was cancelled at the last minute by Aberdeen University for reasons they won’t reveal.

We had earlier approached another top vitamin C researcher Professor Phyo Myint, at the University of Aberdeen, to run the study in Scotland. He also enrolled representatives of NHS Grampian and the Rowett Institute to make a robust research team to run this world-first study. It  was first approved by the University’s internal processes, then applied for and got ethical approval, and was registered on in June 2022 which is viewable by all.

The university then requested funding of £21,820, plus various study materials. We raised all of this from people like you, and a US charity, whom the University invited to be listed as a university supporter and benefactor. We sent the money at the end of last year into their designated bank account. Materials required for the study were purchased. After two years hard work by the team the study was ready to roll early this year. Everyone at the University involved in the study, and its funding, were positive and excited to get it underway.

Then, on 9th June 2023, we receive a letter effectively cancelling the study. It said:

"following internal due diligence, the University of Aberdeen is not in a position to accept these donations. We have discovered the name of the University of Aberdeen, the Rowett Institute and those of Professor Myint and Dr Sneddon have been used on the  page: Vit C deficiency driving COVID care home deaths? The University of Aberdeen has not given permission for the use of the University and Rowett names and of our staff to be used in this material and we request that the VitaminC4Covid and Crowdfunder organisations are asked to remove this information immediately".

We were perplexed. How could the University authorities claim to not know about their own registered study, their own requests for funding and then complain, one year later, that the university’s name had been referred to ‘without permission’ in an agreed and accurate Crowdfunder campaign. We asked to see their ‘due diligence’ report. They provided nothing. We put in an official appeal.

They replied:

“It is correct that for most university processes there will be an appeal process, ensuring that the University is accountable for the education it provides and the efficacy of its business processes. However, the right to accept funding is at the discretion of the institution. This ensures that the University is not required to undertake projects which are not a strategic priority. There is, therefore, no appeal process".

So, despite being really keen last year, it appears it is no longer in the ‘strategic interest’ of the University to find a simple and effective way to reduce the awful suffering that scurvy can cause in hundreds of care homes. The reasons given for their decision make no sense.

What was the ‘due diligence’? A Freedom of Information request provided internal emails saying: “Was the conversation and the reasons why we did not accept the donations recorded in any way? It may be that if we do not hold the information, then we can apply the exemption of “Information Not Held”...” The response was:  “There is no due diligence report, it was a conversation with Bhatty and Liz Rattray”.

So, the claim that the decision was taken following a due diligence process was untrue. This supposedly rigorous process was just an unrecorded conversation that was used to wipe out a humanitarian study and two years’ work of the research team.

Despite the claim of ‘due diligence’ being demonstrably false the documents show that Batty and Rattray approve this statement: “the conclusion of our internal due diligence... is the University is not in a position to accept this donation.” Something which the University had requested, received, accepted and left in their bank account for over six months.

Who are Bhatty and Rattray?

Bhatty is Dr Siladitya Bhattacharya –  head of medicine at the University while Rattray is Dr Liz Rattray , head of ‘research and innovation’. Two medics who apparently have no interest in alleviating suffering and improving health, but have casually blocked funding for a study that could help to achieve those goals. We have asked for a letter of explanation and apology to share with all the donors who gave money in good faith. None has been provided.

Politics over Science

Professor Jeanne Drisko , Professor of Orthomolecular Medicine at the University of Kansas, who had helped raise a substantial part of the funds from a US charity, aptly replied: “politics over science”. Professor Phyo Myint  said, “It was equally disappointing for me". But, having pursued every means possible to have the study continue we have to conclude it is not going to happen and have, regretfully, had to accept back the funds. It’s another case of important vitamin research being blocked while the NHS spends £160 million on vastly expensive new immunotherapy drugs that are unlikely to be better than vitamin C, but can be guaranteed to produce undesirable adverse effects. Wouldn’t preventing vitamin C deficiency be an obvious first step? This study could have established how much vitamin C is actually needed for those in care homes.

Further Information

Copyright © Alliance for Natural Health International

[Insert YouTube Video: ]

Watch (/news/help-crowdfund-a-no-brainer-vitamin-c-study-that-could-save-lives/) – Rob Verkerk PhD’s interview with Patrick Holford on the vitamin C study.  

Go to our Vitamin C campaign (/campaigns/vitamin-c-for-covid/)



Estimating Gastric Cancer Risk Using DNA Methylation and Lifestyle Data

Aberrant DNA methylation in the gastric mucosa is an important biomarker for gastric cancer. While exposure to pathogens like Helicobacter pylori can exacerbate such aberrant DNA methylation, it is unknown whether these are a direct indication of future tumour development or gastric neoplasia. Scientists from Japan and Singapore have found that integrating DNA methylation data with patients’ lifestyle and clinical data improves risk stratification for predicting gastric neoplasia.

Gastric cancer is the fourth leading cause of cancer-related mortalities worldwide. Various environmental and lifestyle-related factors, like tobacco and alcohol consumption, are known to contribute to the risk of gastric cancer. Further, infection by Helicobacter pylori – a bacterium found in the stomach–is another leading risk factor for the onset of the disease. H. pylori infection can cause inflammation and exacerbated aberrant DNA methylation in the stomach mucosa. Aberrant DNA methylation due to H. pylori infection can accumulate in the gastric mucosa years before the onset of gastric cancer. DNA methylation in the promoter region of tumour-suppressing genes is known to cause silencing of these genes and eventual carcinogenesis in the tissue. However, it remains to be confirmed whether DNA methylation caused by H. pylori infection can be used as a marker for future gastric cancer. Further, there are no reports on how the interaction between DNA methylation and lifestyle factors influences the development of gastric cancer.

An international team of researchers, led by Prof. Atsushi Kaneda from Chiba University, Japan, with Prof. Patrick Tan, Senior Vice-Dean for Research & Professor, Cancer & Stem Cell Biology Signature Research Programme, Duke-NUS Medical School and Prof. Khay Guan Yeoh, Kishore Mahbubani Professor in Medicine and Health Policy from the Department of Medicine at the Yong Loo Lin School of Medicine, National University of Singapore, has recently demonstrated how DNA methylation and lifestyle factors interact and influence the risk of gastric tumour development, also known as gastric neoplasia (GN). The study also involved Dr Genki Usui and other researchers from the following institutions in Japan and Singapore: Chiba University, The University of Tokyo, NTT Medical Center Tokyo, Tokyo University of Science (all in Japan); and Duke-NUS Medical School, the Yong Loo Lin School of Medicine, National University of Singapore, National University Hospital, Tan Tock Seng Hospital, Singapore General Hospital, and Changi General Hospital (all in Singapore). They collaborated on co-authoring the manuscript published in eBioMedicine on October 26, 2023 [1]. Discussing his motivation to pursue the research, Dr. Kaneda, who was formerly a gastrointestinal surgeon, says,

“It is, of course, very important to cure patients who have already developed cancer, but I believe it would be more helpful if we can manage cancer risk before cancer development.”

The team studied the association between clinical factors and GN development. They examined gastric mucosal biopsy samples collected from asymptomatic subjects who developed GN later or didn’t develop GN during a health check-up. Methylation analyses were performed on DNA extracted from these biopsy samples and also from GN tissue, and the mucosae in its vicinity taken from patients who developed GN later. The data revealed that DNA methylation that highly accumulated in the gastric mucosa many years prior to GN formation was associated with higher GN risk and a shorter period for the onset of disease. Interestingly, the data also showed that methylation levels in the patients’ DNAs were linked to H. pylori infection and a lifestyle that involved tobacco and alcohol consumption.

While DNA methylation was determined to be an independent GN risk factor, drinking and smoking were found to amplify the pro-carcinogenic DNA methylation alterations caused by H. pylori.

“The combination of unfavorable lifestyle factors and DNA methylation resulted in a much higher risk of GN development,” says Prof Tan. “Most importantly, when integrated into our analyses, this information accurately reflected the risk of GN and offers the possibility of tailoring management according to the risk of the patient,” adds Prof Yeoh.  

The study’s findings could go a long way in securing a future with lower healthcare costs. Dr. Kaneda is quick to note that stratifying the GN risk across a population opens the door to implementing appropriate cancer prevention strategies at an early stage. Additionally, he is hopeful the findings emphasize how lifestyle choices like tobacco and alcohol consumption impact long-term health.

“We foresee a scenario where high-risk individuals get an early start on gastric cancer interventions. This could be achieved by developing an examination kit that identifies the diagnostic DNA methylation markers and provides a precise GN risk assessment,” conclude Drs. Usui and Kaneda.

About Professor Atsushi Kaneda

Atsushi Kaneda is Professor of the Department of Molecular Oncology and Director of the Health and Disease Omics Center, Chiba University, Japan. Prof. Kaneda earned his PhD in 2004 from the Graduate School of Medicine at the University of Tokyo, and his research explores epigenetics and cancer. Through his research, he wants to investigate how epigenetic aberrations accumulate in normal cells under environmental stresses and influence tumor evolution, and apply this information to the development of more effective cancer therapies. He has published around 130 peer-reviewed articles since 1993.


  1. Genki Usui1,2,3, Keisuke Matsusaka1,4, Kie Kyon Huang5, Feng Zhu6, Tomohiro Shinozaki7, Masaki Fukuyo1, Bahityar Rahmutulla1, Norikazu Yogi1,8, Tomoka Okada1, Mizuki Minami1,4, Motoaki Seki1,9, Eiji Sakai10,11, Kazutoshi Fujibayashi12,13, Stephen Kin Kwok Tsao14, Christopher Khor15, Tiing Leong Ang16, Hiroyuki Abe2, Hisahiro Matsubara17, Masashi Fukayama2, Toshiaki Gunji12, Nobuyuki Matsuhashi10, Teppei Morikawa3, Tetsuo Ushiku2, Khay Guan Yeoh6,18*, Patrick Tan5,19,20*, Atsushi Kaneda1,21*. Integrated Environmental, Lifestyle, and Epigenetic Risk Prediction of Primary Gastric Neoplasia Using the Longitudinally Monitored Cohorts.   eBioMedicine  DOI:    October 26, 2023.

Affiliations :

1 Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Japan
2 Department of Pathology, Graduate School of Medicine, The University of Tokyo, Japan
3 Department of Diagnostic Pathology, NTT Medical Center Tokyo, Japan
4 Department of Pathology, Chiba University Hospital, Japan
5 Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore
6 Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore
7 Department of Information and Computer Technology, Faculty of Engineering, Tokyo University of Science, Japan
8 Department of General Surgery, Graduate School of Medicine, Chiba University, Japan
9 Cancer Genomics Center, Chiba University Hospital, Japan
10 Department of Gastroenterology, NTT Medical Center Tokyo, Japan
11 Division of Gastroenterology, Yokohama Sakae Kyosai Hospital, Japan
12 Center for Preventive Medicine, NTT Medical Center Tokyo, Japan
13 Department of General Medicine, Juntendo University Hospital, Japan
14 Department of Gastroenterology and Hepatology, Tan Tock Seng Hospital, Singapore
15 Department of Gastroenterology and Hepatology, Singapore General Hospital, Singapore
16 Department of Gastroenterology and Hepatology, Changi General Hospital, Singapore
17 Department of Frontier Surgery, Graduate School of Medicine, Chiba University, Japan
18 Department of Gastroenterology and Hepatology, National University Health System
19 Genome Institute of Singapore
20 Cancer Science Institute of Singapore
21 Health and Disease Omics Center, Chiba University, Japan

 Contacts and Further Information

Atsushi KANEDA Graduate School of Medicine, Chiba University

Public Relations Office, Chiba University, 1-33 Yayoi, Inage, Chiba 263-8522 JAPAN  Tel: +81-43-290-2018; 

Contact from NUS Medicine: Gladys SIM, Senior Assistant Manager, Communications, Yong Loo Lin School of Medicine, National University of Singapore Tel: +65 9007 1322;

Contact from Duke-NUS Medical School: Federico GRACIANO Senior Media & Content Specialist / Media Lead Duke-NUS Medical School,  Tel: + 65 6601 3272;



Schizophrenia Is Chronic Encephalitis...and Niacin Cures It

by Thomas E. Levy, MD

Originally Published at


Orthomolecular medicine is based on the concept that most chronic diseases are ultimately initiated, and then sustained, by the chronic deficiency of one or more vitamins, minerals, nutrients, or other natural agents. When the deficiency can be lessened, the disease improves. Conversely, the worse the deficiency and the longer it persists in the body, the more advanced and entrenched the disease becomes. What often is unclear for both the public as well as many healthcare providers is that the clinical benefits of some nutrient supplements continue to increase as the doses are increased. These doses can vastly exceed the Recommended Dietary [or Daily] Allowance (RDA) disseminated by the Food and Nutrition Board, a committee established by the United States National Academy of Sciences. Since 1997, the term Dietary Reference Intake (DRI) has been in use to describe much the same information as the RDA. The DRI recommendations have not significantly deviated from the earlier RDA recommendations. [1]

While a few nutrients can rapidly become toxic with minimally excessive intake (calcium, copper, and iron), many nutrients have little toxicity at almost any dose. [2] In general, the doses of vitamins are difficult to push to the point of clinical toxicity. However, nearly all the nutrient minerals can readily be taken to excess and result in various presentations of toxicity. Toxicity in this context refers to definable physiological damage to the supplement taker, not occasional side effects such as nausea in a sensitive stomach (niacin) or osmotic diarrhoea (vitamin C or magnesium) when too much is not efficiently absorbed but accumulates in the colon instead.

However, the concern about potential toxicity keeps supplements like niacin, vitamin C, and magnesium severely underdosed, resulting in a loss of the incredible benefits they offer when optimally dosed.

Vitamin C and Magnesium Supplementation

Vitamin C is the safest of all known nutrient supplements. In fact, there has never been established any dose of vitamin C above which toxicity will reliably ensue. This is consistent with the fact that vitamin C is the molecule on which the physiology of all cells runs, and the healthy function of the body relies on having large amounts of it both inside the cells as well as outside of them. Arguably, vitamin C is the safest consumable agent in existence. Rare individuals can experience minimal side effects, but this should not be confused with any degree of cell-damaging toxicity. By contrast, too much water intake is toxic and can even result in death. [3-5]

The vitamin C RDA for older children and adults ranges from 45 to 90 mg per day. However, many people maintain a much higher level of general health when multigram supplementation is taken regularly, on the order of 100 times the RDA. Furthermore, the administration of vitamin C in doses 1,000 times the RDA are frequently given intravenously around the world for the treatment of a wide range of infections and medical conditions, with excellent effect and unrivaled safety. [6-8]

Magnesium, like all minerals, can be pushed to toxic levels of intake. However, it is almost impossible to induce toxicity with ORAL magnesium intake, as the highest levels of intake will reliably induce an osmotic diarrhea from unabsorbed magnesium reaching the colon. But when given intravenously, enough magnesium will reliably lower even the most elevated of blood pressures to hypotensive levels. In some surgeries, sufficient magnesium is infused to deliberately keep blood pressure below normal levels to help achieve hemostasis and keep the surgical field from bleeding excessively. [9-11]

Such highly-dosed infusions should only be administered in a hospitalized setting. However, the addition of a few grams of magnesium can always be added to a therapeutic vitamin/mineral IV bag and be safely infused over an hour or so in the clinic setting. In fact, the appropriate administration of magnesium by IV infusion is the best way to help restore low body levels of magnesium, especially in patients who cannot take very much orally. [12,13] Some caution and dosage adjustments need to be made by the clinician when there is decreased kidney function.

Just like vitamin C, but much less dramatically so, oral magnesium supplementation of several grams daily can be taken as long as the osmotic diarrhea is not induced. With a magnesium RDA of roughly 300 to 400 mg daily, the amounts of supplementation to keep most adults out of a significant deficiency of magnesium will be in the range of 5-fold or more of this RDA. Furthermore, very few people can reach an optimal magnesium status with oral supplementation. Rather, the practical goal is to minimize the degree of magnesium deficiency. Nevertheless, as a significant magnesium deficiency causes some diseases and makes all diseases worse, taking as much magnesium supplementation as can be readily tolerated is always a good idea. [14]

Of the 13 essential vitamins (A, C, D, E, K, B1, B2, B3, B5, B6, B7, B9, B12), increased intake and/or increased blood levels have been associated with decreased all-cause mortality for 11 of them. [15-23] Studies clearly establishing the same associations with biotin (vitamin B7) and pantothenic acid (vitamin B5) were not found. For the most part, these studies only examined vitamin intakes in the range of the RDA or DRI values, further supporting their critical support of good health even when ingested in relatively small amounts. While toxic effects can be seen with vigorous dosing of vitamin A, vitamin D, or vitamin E, the rest have RDA or DRI values that can be greatly exceeded, resulting in only improved health and blood chemistries.

Niacin: Nomenclature and Physiology

Confusion can easily arise in sorting through the literature on niacin and its derivatives. Niacin is vitamin B3. It is also known as nicotinic acid. These are all synonyms for the chemically identical substance. Niacin, vitamin B3, and nicotinic acid are completely interchangeable terms. For completeness, niacin is also rarely referred to in the literature as "vitamin PP," with the PP meaning "pellagra-preventive." Pellagra is the clinical condition that results from a severe deficiency of niacin in the body. [24]

Niacin has several vitamers. Vitamers are derivatives or related chemical substances that fulfil the same specific vitamin functions despite not being chemically identical. Niacin derivatives that qualify as vitamers include niacinamide (also known as nicotinamide or nicotinic acid amide), nicotinamide riboside, and nicotinamide mononucleotide. Referring to nicotinamide as niacinamide decreases the possibility of niacin and its vitamers as being perceived by the public as having nicotine-like properties, which it does not. All these substances promote the biosynthesis of NAD (nicotinamide adenine dinucleotide) throughout the body, and they are the primary sources of NAD. [25,26]

Large amounts of NAD are essential for optimizing the electron supply in the first of the four steps of the electron transport chain (ETC). Located along the membranes of the mitochondria inside every cell, the ETC is responsible for the production of all the ATP (adenosine triphosphate) in the body. ATP is the most important energy-providing molecule in the body. Any compromises in its production results in a decline in the healthy function of all affected tissues and organs. When there is not enough NAD present at the beginning of the ETC, sufficient ATP simply cannot be generated.

Optimizing the production of NAD for ATP synthesis in the cells is the most important function of niacin and its vitamers.

Furthermore, greater deficiencies in available NAD results in even more pronounced declines in cellular function throughout the body. Nothing is more important for optimal health than maximal amounts of intracellular ATP. [27] Low NAD levels have been recognized as a sign of aging in not only humans, but in all living cells, including those in animals and insects. [28-34]

Niacin Supplementation

Names of forms of niacin supplementation that directly fuel NAD production in the body:

  • Niacin
  • Niacinamide
  • Nicotinamide
  • Nicotinamide riboside
  • Nicotinamide mononucleotide
  • Inositol hexaniacinate
  • Inositol hexanicotinate

Of note, niacin has an additional important property that its vitamers do not have. Reported as early as 1955, niacin has been documented to lessen the abnormal lipid metabolism that promotes atherosclerosis. [35-37] It reduces triglycerides and the lipoproteins VLDL and LDL while raising HDL, the "good" lipoprotein. [38]

If well-tolerated, niacin is the best of the supplement forms itemized above to take, as it has both the positive impact on the lipids as well as on the NAD levels in the body. It also costs less. However, niacin causes a warm to hot flushing effect in many people who supplement it. While for many people this flushing effect is either minimal or even disappears after several doses, for some people it is not tolerable. The other supplement forms noted above are largely "flush-free," and can be easily taken by nearly everyone. The downside is that the non-flushing forms do not have the positive lipid impact of unmodified niacin.

Niacin and all its vitamers profoundly impact ATP generation throughout the body, as noted above. However, like so many other powerful orthomolecular therapies, the niacin RDA and DRI is amazingly tiny, completely misleading the health seeker as to its importance and impact of much higher doses. The optimal energy-supporting doses of niacin can be 200- to 1,000-fold higher than these officially-advised doses. And other than nausea in a few individuals, side effects are decidedly uncommon. [39] Very high doses have been linked to liver toxicity, as reflected in significant liver enzyme elevation. However, minor enzyme elevation that typically resolves without discontinuation of the supplementation is not uncommon. Such enzyme increases are felt to represent a temporary increased metabolic activity in the liver cells and not inflammatory damage. [40]

In the toxin-laden, pro-oxidant environment in which we now all live, virtually everyone is deficient in the antioxidant impact provided by niacin supplementation and the NAD levels it supports. Everybody should take at least some niacin supplementation. There really does not exist a dietary regimen that can provide the NAD-producing benefits of even a minimal supplementation of niacin.

Niacin, Health, and Schizophrenia

Optimizing the production of ATP in the body is a very desirable goal. Many clinicians today regard chronic fatigue patients as having "mitochondrial dysfunction" or "mitochondrial fatigue." While decreased ATP production is uniformly present in such patients, different patients can have different reasons for that decline in production. [41] However, except for individuals with genetic deficiencies that typically cannot be completely resolved, increasing the production of ATP not only can resolve the fatigue and associated symptoms, it can also infuse the needed energy into the dysfunctional metabolic pathways to completely resolve the biochemical abnormalities that decreased the ATP production in the first place. Quite literally, this results in cellular healing. Niacin supplementation has been shown to restore healthy NAD levels (which then increase ATP production), greatly improving muscular strength in patients with mitochondrial dysfunction. [42]

Ultimately, all such dysfunction inside the cytoplasm as well as inside the mitochondria comes from increased numbers of inactivated, oxidized biomolecules relative to the numbers of normal, reduced biomolecules. This is traditionally referred to simply as increased oxidative stress. Improvements in all pathological states can be anticipated with increased ATP production, although certain conditions, such as muscle fatigue from low ATP levels, can be expected to respond even more dramatically. The heart muscle in heart failure is a classic example of a tissue severely depleted of ATP, no longer able to respond to significant exercise with a sufficiently increased production of ATP. [43]

Endomyocardial biopsies have documented that heart muscle in congestive and hypertrophic cardiomyopathies have significantly depressed levels of both ATP and NAD. [44] Normal heart muscle has the highest NAD levels in the body. [45] In both congestive and hypertrophic cardiomyopathy impaired energy metabolism has been identified. [46] Consistent with these findings, the elevation of NAD levels in different studies has been shown to improve atherosclerosis as well as different forms of heart failure, including ischemic, hypertrophic, and congestive cardiomyopathies. [47,48] In an animal study, niacin has also been shown to lessen damage in myocardial infarction. [49] Studies in both animals and humans have shown that niacinamide can lower elevated blood pressures and decrease cardiac mortality. [50,51] In a mouse model of cardiac arrest, niacinamide administration was able to normalize NAD levels and improve survival. [52]

Niacin vitamer supplementation in humans has been clearly shown to dramatically increase blood levels of NAD. [53] Not surprisingly, NAD-increasing agents, with their strong support of ATP production, are also being increasingly appreciated as being useful for both anti-aging and overall good health. [54-59] In an animal study of sepsis, probably the most advanced and dire of medical conditions, a niacin vitamer was shown to increase survival and prevent the lung and heart injury otherwise seen. [60]

Some studies indicate that lower NAD and ATP levels are the primary abnormalities that result in cancer. [61-63] In one human study, it was shown the niacinamide supplementation was effective in reducing the appearance of new skin cancers. [64] This is consistent with the pellagra-associated skin inflammation (dermatitis) seen when niacin levels are very low. [65] Higher niacin intake has been linked to decreased all-cause mortality, indicating its importance in every cell in the body. [66,67]

The clinical effectiveness of daily multigram niacinamide dosing depends on how severely the affected tissues or organs in a disease are depleted of the NAD needed to make ATP. Heart failure, while not always responsive to increased NAD production, will often respond dramatically to an improved NAD status. A significant number of patients with congestive cardiomyopathy and low cardiac output have been spared heart transplantation after adequately-dosed Coenzyme Q10 (CoQ10), another agent capable of increasing ATP production via the ETC in the mitochondria. In many of those patients, ejection fractions have increased dramatically, and all-cause mortality decreased along with an improved exercise capacity. [68-74] Also, like niacinamide, CoQ10 also improves heart failure patients with preserved ejection fractions (hypertrophic cardiomyopathy with diastolic dysfunction). [75,76]

Niacinamide has also been shown to enhance acetyl-CoA production, which in turn enhances the biosynthesis of CoQ10.

This means that niacinamide supplementation can provide the substrates needed for both NAD and CoQ10 production, directly powering two of the four steps of the ATP-producing ETC. [77,78]

Like heart muscle, the brain and central nervous system (CNS) require very high levels of ATP for normal function relative to the rest of the body. As such, having inadequate building blocks for ATP production in the body will be reflected more often and more prominently as nervous system and psychiatric disorders than other medical conditions. Many studies have indicated that niacinamide is essential for the development, growth, and maintenance of the CNS. [79-81] Furthermore, niacinamide has been shown to readily pass the blood-brain barrier in both directions, supporting its supplementation as a simple and effective approach to treating various CNS conditions. [82] Also, oral niacinamide supplementation has been shown to be very well-absorbed. [83]

Animal studies have shown that niacinamide will protect against ischemia-induced (decreased blood supply) damage in the brain and CNS. Neuronal death is reduced, and the recovery of affected sensory and motor function is improved as well. [84-87]

Significant infection protection and resolution can be seen when NAD production is optimized with niacin and several other NAD-producing agents. Sepsis recovery is supported by increased niacin levels. COVID has also been shown to resolve more rapidly with agents that help to optimize cellular ATP levels. [88-91] Improved outcomes in COVID-related acute kidney injury have been seen with niacinamide therapy. [92] Niacinamide has also been shown to lessen inflammation-induced renal failure in an animal model. [93] It has a protective effect against the pro-inflammatory toxicity of paraquat in rats. [94]

Severe niacin deficiency results in a disease known as pellagra. This syndrome has been characterized by a triad of symptoms: delirium, dermatitis, and diarrhea. More accurately, the triad should be referred to more broadly as neurocognitive, dermatological, and gastrointestinal symptoms. A substantial variation in this symptom pattern can be seen, as the circumstances resulting in a deficiency of niacin can result in a variety of other significant nutrient and micronutrient deficiencies in a given patient. [95-97] Nevertheless, the complete restoration of niacin levels in the body, along with the micronutrients supplied by a balanced diet, reliably resolves the symptoms of pellagra, including those involving the CNS.

The neurocognitive symptoms in patients with severe niacin deficiency are always present, and they can be very pronounced clinically. Both Alzheimer's disease and Parkinson's disease typically have depleted NAD levels in the affected tissue, and some of their symptoms can be lessened with increased niacin intake. [98] Other CNS symptoms, including disorientation, memory loss, confusion, dementia, poor sleep, and even frank psychosis can be seen in the severely niacin-deficient patient. [99] Of note, the statistical risk of Parkinson's disease is lessened in individuals having an increased consumption of niacin-containing foods. [100,101]

Schizophrenia is one of the most devastating of diseases, with enormous societal impact in addition to the symptoms endured along with the effective loss of a functional life in the patient. [102] Chronically increased oxidative stress defines a state of chronic inflammation in the brain (neuroinflammation). The presence of chronic inflammation in the brains of schizophrenic patients has been well-documented. [103,104] Studies have shown that schizophrenia in younger individuals can be initiated following exposure to the toxins, or pro-oxidants, encountered in prenatal exposures to infection. [105,106] Consistent with this, many cases of schizophrenia start early in life with toxin-induced abnormal neurodevelopment. [107,108]

The symptoms of schizophrenia are numerous and diverse, with some symptoms assuming a much more prominent role in one patient versus another. The bulk of the literature simply recounts the classical and well-known symptoms of schizophrenia that focus solely on brain dysfunction. Such symptoms include hallucinations, delusions with loss of contact with reality, difficulty thinking clearly, and social/emotional withdrawal, sometimes to the point of staying in a largely motionless, catatonic state. However, it has also been recognized that symptoms not directly referable to brain dysfunction are often present as well. These include the classical symptoms of pellagra, the potentially fatal condition secondary to severe niacin deficiency in the body.

The niacin deficiency in pellagra can result brain and CNS pathology manifesting as irritability, difficulty concentrating, some social withdrawal, depression and manic depression, insomnia, delirium, hallucinations, coma and even frank psychosis. Some authors have termed this "pellagroid encephalopathy." [109] Furthermore, the psychosis with associated delusions that sometimes occurs in pellagra is indistinguishable from some cases of schizophrenia. [110] These symptoms all typically resolve with adequate restoration, and maintenance, of niacin levels in the body. [111] The effective use of niacin for psychiatric symptoms has also spawned the concept of "reversible dementia," a remarkable term since dementia is generally considered to be progressive and non-resolving in nature, especially in older individuals. [112] Similarly, the close relationship between pellagra and brain dysfunction has spawned the term "niacin-respondent subset of schizophrenia." [113]

The niacin deficiency in pellagra always has symptoms of brain dysfunction, and niacin restoration treats them very effectively.

Pellagra causes significant gastrointestinal problems and symptoms. This is significant in understanding the contribution and worsening that a pellagra-related leaky gut with a pathogen-overgrown microbiome does to diseases of the CNS (and elsewhere in the body). Alzheimer's, Parkinson's, amyotrophic lateral sclerosis (ALS), and schizophrenia have all been clearly documented to either have pathogens and/or their toxic metabolites present in the affected nervous tissue. [114-125] The damage that niacin deficiency (pellagra) does to the microbiome is a major factor in the associated neuropsychiatric problems and schizophrenia-like symptoms seen with it as well. Niacin deficiency not only results in decreased energy production in the brains of schizophrenics, it also results in the continued exposure of pathogens and/or their toxic metabolites from an abnormal gut microbiome to the CNS of those patients.

Schizophrenia most commonly appears in late adolescence or early adulthood. [126] But it can occur later in life as well. Increased intracellular oxidative stress, left unchecked, results in premature death of the affected cells. Brain volume studies have established that schizophrenic patients progressively lose grey matter and the actual physical mass of the brain over time, well beyond the deterioration seen with aging. [127-130] Microglia, the scavenger white cells of the brain, become activated in the inflammation seen in schizophrenia. [131-133] Pro-inflammatory cytokines and other inflammatory markers are also increased. [134-136] All this information leads to the following assertion:

Schizophrenia is Chronic Encephalitis.

Encephalitis is inflammation of the brain, typically occurring acutely in conjunction with a new viral infection precipitating widespread inflammation throughout the brain and CNS. In schizophrenia the chronically elevated inflammatory parameters indicate that ongoing inflammation is causing the signs and symptoms of schizophrenia. Schizophrenia = chronic brain inflammation = chronic encephalitis. [137] Many of the symptoms seen in acute encephalitis brain are also seen in the chronic encephalitis brain of the schizophrenic patient, including alterations in consciousness, confusion, hallucinations, and cognitive impairment. Some authors have descriptively referred to schizophrenia as "the shattered mind." [138] The steady destruction of brain tissue by the chronic inflammation also explains why schizophrenia present for years responds less readily to any nutrient or drug regimen than schizophrenia of recent onset. The chronic inflammation slowly destroying brain tissue in schizophrenia is analogous to the patient with ongoing myocarditis and death of heart muscle eventually going into congestive heart failure. The later a positive therapy is started, the less effective it will be.

The effective clinical resolution of many schizophrenics is further complicated and even impaired by the common and severe side effects seen with the drugs commonly used in its treatment. Many of these side effects are indistinguishable from many of the symptoms for which the drugs are being given. Such symptoms include restlessness, brain fog, and social withdrawal with the loss of desire to interact with others. [139] Once a schizophrenic patient has received prescription drugs for a long enough period, it can become impossible to know when the condition itself is getting worse or a drug needs to be discontinued and/or decreased in dosage. As it is, the clinical picture of an unmedicated schizophrenic patient also spans a variety of symptoms present in many different combinations. [140]

The levels of niacin in schizophrenic patients are always low, oftentimes severely so. This also means that their cellular ATP levels are significantly depressed as well. It has been clearly shown that high doses (relative to RDA or DRI recommendations) of niacin or a niacin vitamer often completely resolves schizophrenia, even in its advanced stages. And when clinical resolution is not complete, significant improvement in the major symptoms of schizophrenia is nearly always seen.

In a group of 30 acute schizophrenia patients, one gram three times daily of niacin or niacinamide were given for only 30 days, and the patients were then followed for one year. 80% of the niacin-treated group recovered versus 33% of the placebo-treated group. [141] Recovery in acute or chronic schizophrenia was only considered to have been reached when the patient

  • Had complete disappearance of disease-related symptoms and signs;
  • Was interacting normally with family members as well as members of the community;
  • Became gainfully employed.

Vitamin C, a perfect treatment for any condition involving chronic inflammation, was often given in a dose of 1 to 10 grams daily as well. As the primary antioxidant (anti-inflammatory agent) in the body, vitamin C should always be used to help resolve the brain inflammation of schizophrenia. [142] Much higher doses will always help, and sometimes dramatically so, especially in schizophrenia of recent onset.

While not typical, acute schizophrenia can spontaneously resolve. Presumably, the factors provoking the inflammation in the brain of those patients eventually resolve, or become much less pronounced (e.g., infection, toxin, autoimmune reaction, micronutrient depletion).

Six more double-blind, randomized and controlled clinical trials confirmed the positive impact of niacin on the recovery of schizophrenic patients. [143,144] Many of the most chronic patients (with the most structural brain damage) required this therapy for five or more years to derive clear benefits. [145] For the niacin treatment of schizophrenia, the starting dose was 1,000 mg three times daily, with the dose slowly increased to as much as 4,500 to 18,000 mg daily, depending on clinical response. For those treated with niacinamide rather than niacin, the daily dose rarely exceeded 6,000 mg due to the increased problems with nausea and stomach sensitivity. [146-148]

Dr Abram Hoffer treated over 5,000 schizophrenic patients with this niacin protocol. No deaths ever resulted from the administration of niacin. Furthermore, consistent with the wide-ranging positive effects of niacin on NAD levels throughout the body described above, Hoffer noted improvements in many symptoms not directly attributable to schizophrenia in his niacin-treated patients. [149] He also developed a more comprehensive orthomolecular approach to schizophrenia over the course of his years in clinical practice. [150] Currently, over 85% of chronic schizophrenic patients treated with traditional measures never resolve, even if some treatment benefits are realized. Instead, they remain sick and dysfunctional for the rest of their lives when niacin is not at least a part of their treatment program.

The following can be definitively asserted:

Niacin cures acute schizophrenia most of the time. And substantial clinical improvement is the rule even when a complete cure is not realized in acute or long-standing schizophrenia.

As covered above, schizophrenia, with its close connection to pellagra, is a condition precipitated and worsened by multiple factors. A quality diet and a wide array of vitamin and mineral nutrients are mandatory for an optimal clinical response in all these patients. Several reasons account for the varied (but positive) clinical responses of schizophrenia patients treated with niacin. [151] Nevertheless, monotherapy with niacinamide has completely resolved schizophrenia. [152] As an important and non-toxic nutrient vitamin, niacin should NEVER be denied to any patient with any brain disorder, much less schizophrenia. As Dr. Hoffer put it: "Apparently the worst sin in orthodox medicine is to see a recovery for the wrong reason."

The production of ATP, the final physiological goal in the severely NAD-depleted brain (and body) of the schizophrenic patients is specifically nurtured and supported not only by niacin, but also by riboflavin, CoQ10, and methylene blue. These four agents directly power the different steps in the mitochondrial ETC [Electron Transport Chain] needed to optimize ATP production, which directly accounts for all healing and good health. And when permanent brain damage is minimal and the symptoms are due to ongoing neuroinflammation, an excellent clinical response can be anticipated, even if a complete cure is not realized. Niacin, CoQ10, and riboflavin comprise a nutrient triad that has been shown to benefit the antioxidant status of breast cancer patients. [153-155] And even though vitamin B3 is important to everyone, its optimal dosing is achieved by few individuals. While it is literally good for everyone, it nevertheless needs to be clearly asserted that:

Everyone with any psychological or psychiatric condition should take niacin or one of its vitamers, and the dose should be maximized before considering such a condition permanent and/or unresponsive.

Currently, the standard of care in psychiatry does not include the routine administration of niacin or niacinamide for schizophrenia or any other mental or emotional disorder.

While the established standard of practice is usually sufficient to protect a physician from malpractice, deliberately avoiding the usage of niacin for schizophrenia after being exposed to much of the literature and information cited in this article nevertheless constitutes clear medical malpractice, even if it remains unadjudicated.

Healthcare practitioners have an obligation, albeit rarely-honoured, to stay informed on the science of old, current, and new therapies. The benefit of niacin therapy in schizophrenia and most brain disorders is certainly not a new discovery. As with all other conditions that have been shown to clearly benefit from an orthomolecular approach to addressing vitamin, mineral, and other nutrient deficiencies, a healthcare practitioner should always be open to all legitimate scientific information that the patient might offer. If such a practitioner refuses to even review such information, and/or will not even discuss such information with the patient, it is time to find a new one.

You do not need a doctor to give you niacin, and there are no absolute contraindications to taking it. You can take it for yourself, and you can advise any friend or family member with a neurological or psychiatric condition that you have information indicating that it is often beneficial regardless of the precise diagnosis.  


Niacin and its related compounds have a long history of improving the mental status of a wide variety of mental and emotional disorders. It has been shown to cure or greatly improve most cases of schizophrenia for which it is properly-dosed. These disorders are primarily caused by a severe deficiency of NAD in the ATP-generating mitochondria in all cells. The primary role of niacin is to increase NAD levels, resulting in an improved or normalized amount of cellular ATP, the most important energy-providing molecule in the body. While many other nutrients will be of benefit in schizophrenia, highly-dosed vitamin C and magnesium should always be given to further control and quell the ongoing neuroinflammation.

Pellagra, the disease established to occur after severe and long-standing niacin deficiency, typically presents with significant brain dysfunction, sometimes clinically identical to schizophrenia. Niacin administration often completely resolves such states of psychosis, further supporting the concept that NAD repletion leading to optimal ATP levels in the brain is the root cause of schizophrenia.

A chronic NAD deficiency always causes increased oxidative stress in the affected tissue. This means that schizophrenia is a chronic encephalitis, as chronic encephalitis simply means an ongoing state of neuroinflammation in the brain.

The variability in clinical response of schizophrenia to niacin therapy is primarily due to how many other nutrient deficiencies are present and whether they are properly restored. How long the schizophrenia has been present and how much irreversible brain damage (decreased brain mass) has occurred is also critical in determining how much clinical benefit is realized.

Even though the psychiatric standard of care does not include niacin therapy for schizophrenia, it can only be considered malpractice not to apply it, especially considering the enormous physical, mental, and societal impact of this dreaded disease. Opting not to use a toxic therapy that might only help a little for a relatively minor condition does not apply to niacin for schizophrenia. That reasoning is reserved for many pharmaceutical agents, not natural nutrients.

Dedicated to the work of Abram Hoffer MD PhD

Dr Thomas E Levy, an OMNS Contributing Editor, is a cardiologist, attorney, and author of 13 books. He can be reached at A collection of all his OMNS articles can be easily accessed with the following link under the subheading of "Orthomolecular": )


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Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
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Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
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Victor A. Marcial-Vega, M.D. (Puerto Rico)
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Mignonne Mary, M.D. (USA)
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Tahar Naili, M.D. (Algeria)
Zhiyong Peng, M.D. (China)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
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Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
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Andrew W. Saul, Ph.D. (USA), Editor-In-Chief
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