Let Food Be Medicine
At the risk of repeating myself too much as in former pages of this website, I want to return to discussing in some depth the fallacies incorporated in our present approach to health and disease. You may or may not remember that I have stated a number of times that Hippocrates (400 BCE) uttered the formula “Let food be thy medicine and medicine thy food”. Having been construed as the “father of modern medicine”, it has seemed to me for a long time that he has been ignored as a “parent”.
For centuries, there was no idea about disease. The early Egyptians bored holes in people’s heads “to let out the evil spirits”. Throughout medieval history the only treatment seems to have been “bloodletting”. In our modern world, horns from the rhinoceros are regarded so highly for their medical properties, that this wonderful animal is reaching the point of annihilation. Pharmaceutical drugs, with the exception of antibiotics, only treat symptoms. I ask you, does this make any sense at all in the light of what Hippocrates suggested?
Because humanity tends to follow a collective pattern and only rarely listens to an idea derived from rational deduction, I view medicine as like a traveler on a road without a known destination. In my imagination, he comes to a fork in the road, but the signpost records information on only one fork. It reads “kill the enemy”, reminding me of the story of Semmelweiss, a lone thinker in his time and who “gave thought to the message on the signpost”. Most physicians are familiar with this story but it is worth repeating.
Semmelweiss was a physician who lived at a time before microorganisms had been discovered. He presided over an obstetric ward where there were 10 beds on one side and 10 beds on the other. The physicians would deliver their patients without changing their clothes or washing their hands. As we would expect today, the death rate from infection was extremely high. Semmelweiss said to himself, “they must be bringing [the enemy] in on their hands” and he devised the first known clinical experiment. He made it a rule for the physicians on one side of the ward to wash their hands in chlorinated lime before they delivered their patient. The physicians on the other side of the ward continued to deliver their patients in the same old way. As we would easily recognize today, it did not require a statistician to see the difference between the incidences of infections on the two sides of the ward. Irrespective of the fact that this was a dramatic discovery that later had obvious meaning, Semmelweiss was accused by the medical authorities of the day of being non-scientific because he could not explain what it was that was supposed to be on the hands of the physicians. Of course the medical establishment had no idea that their model for disease was catastrophically wrong, although collectively certain that their philosophy bore all the hallmarks of scientific truth. Semmelweiss had offended the medical establishment and they threw him out of the hospital. He died a pauper in a mental hospital.
The First Medical Paradigm: Kill the Enemy
When microorganisms were discovered to be responsible for infections, it fulfilled the message on the signpost and it became the first paradigm in medicine. Kill the bacteria: kill the virus: kill the cancer cell, but try not to kill the patient. If we look at the history of this time, we find that a lot of patients were killed in the concerted attempts to find ways and means of killing the enemy. We all remember the discovery of penicillin and how it led to the antibiotic era, still the major therapeutic methodology, even though we know that it is running into bacterial resistance and has never been a good idea for viruses or cancer cells.
Although the germ theory had been around for a long time, Louis Pasteur, Ferdinand Cohn and Robert Koch were able to prove it and are regarded as the founders of microbiology. However, Pasteur was said to have uttered the words on his deathbed “I was wrong: the microbe (germ) is nothing. The terrain (the interior of the human body) is everything”. Perhaps he had unknowingly voiced the principles of the next paradigm in medicine.
The Second Medical Paradigm: Genetic Determinism
The monk, Mendel, by his work on the segregation of peas, formulated what came to be known as the genetic mechanisms of Mendelian inheritance and the discovery of DNA modeled the next stage in our collective development. The fact that each of us is built from a complex code that dictates who we are was a remarkable advance. The fact that the construction of the code sometimes contained mistakes (mutations) led us to explaining many diseases and for a long time we believed that the genes were fixed entities, dictating their inexorable commands throughout life. However, the newest science of epigenetics has shown us that the DNA that makes up our genes can sometimes be manipulated by nutrition and lifestyle, as well as by artificial means in the laboratory.
Health: The Ability to Respond Effectively to a Hostile Environment
We are surrounded by germs that exist everywhere, many of which cause disease as we are all too well aware. Nevertheless, whatever evolutionary mystery guides our development, we are all equipped with an extraordinarily complex, genetically determined, defense system. We now know that this is organized and directed by the brain. Assuming that the genetic determinations of the terrain are completely intact, we can be reasonably assured that we can defend ourselves from any germ that Mother Nature can throw at us. Built in mechanisms in the brain require a huge amount of energy when it goes into action directing the traffic of the immune system. It is a crisis and can be likened to a war between the body and the attacking organisms. Thus, if Pasteur may have stated the next paradigm in medicine, what does it mean?
As an example, a typical microbial attack causes a common disease that goes by the name of febrile lymphadenopathy (strep throat). The throat becomes inflamed, perhaps because the increased blood supply brings in white blood cells, acting in defense. An increase in circulating white cells also occurs, bringing a brigade of defensive soldiers. The glands in the neck become swollen because they catch the germs that get into the lymph system. Lastly, the increased temperature of the body is also part of the defense. Germs are programmed to have their most intense virulence at 37°C, the normal body temperature. If this temperature is increased, the attacking germ does not have its maximum efficiency. In other words, what we are looking at as the illness is really the act of brain/body defensive interaction. Besides attempting to kill the attacking germ as safely as possible, should we not be assisting the defense? The answer calls into question the relationship between genetic intactness and the required energy to drive the complex defensive action. Perhaps a genetic mistake (mutation) can sometimes be manipulated by an epigenetic approach through nutrients, just as advised by Hippocrates.
Disease: The Inability to Adapt to the Environment
If we look at health as the ability to respond effectively and adapt to environmental, mental and physical stressors, it is possible to re-conceptualize illness by the manner in which that response is carried out. A healthy individual will respond to stressors without problem, because of an efficiently effective mobilization of energy dependent mechanisms. In contrast, individuals who are not healthy will respond in one of two ways. Either the defense mechanisms will be incomplete or absent or over-reactive and inconsistent. Listed below are examples of both. Note that this is in line with the ancient philosophy of Yin and Yang or, in modern terms “everything in moderation”. Too much of anything is as bad as too little.
Exhausted Defense Systems
When I was a resident in my English teaching hospital, before the antibiotic era, I admitted a patient with pneumonia who was known to have chronic tuberculosis. He was seen to be “unconsciously picking at thin air with his fingers” and the physician for whom I was resident pointed out that it was a classic example of “a sick brain” and that he would die. He never had any fever, elevation of white blood cells or any other marker of an infection but at autopsy, his body was riddled with small staphylococcal abscesses. He had lived in the east end of London, notorious for poverty and malnutrition at that time. In fact, as an organism, he never showed the slightest sign of a defense. His “sick brain” was completely disabled in any attempt to organize his defense.
Excessive or Aberrant Defense Mechanisms
Many years ago I was confronted with two six-year-old unrelated boys who for several years had each experienced repeated episodes of febrile lymphadenopathy. Both boys had been treated elsewhere as episodes of infection. In each case the swollen glands in the neck were enormous. One of the boys had been admitted to a hospital for a gland to be removed surgically for study. It had been found that the gland was just enlarged but had a perfectly normal anatomy, only contributing to the mystery. One of the curious parts of the history was that each of these boys had been indulged with sweets. Because I was well aware that sweet indulgence could induce vitamin B1 (thiamine) deficiency, I tested them and found that both were indeed deficient in this vitamin. Treatment with large doses of thiamine completely prevented any further attacks. The mothers of the boys were advised to prohibit their sweet indulgence. I needed some evidence and asked one of the mothers to stop giving thiamine to her son. Three weeks later he experienced a nightmare, sleep walking and another episode of lymphadenopathy that quickly resolved with thiamine. A nightmare and sleep walking supported the contention that the brain was involved in the action. In addition, his recurrent illnesses had been associated with increased concentrations of two B vitamins, folate and B12, both of which decreased into the acceptably normal range with thiamine treatment. Of course, this added complexity to an explanation.
What I had already learned about thiamine deficiency is that it makes the part of the brain that controls automatic mechanisms much more sensitive. One or more reflexes are activated unnecessarily. No reflex activation is as bad as too much. Thus, the “trigger-happy” defense mechanisms were being activated falsely. Thiamine is perhaps the most important chemical compound derived from diet that presides over the intricacies of energy metabolism. All that was required was an improved energy input to the brain. Folate and B12 are vitamins that work in energy consuming mechanisms and I hypothesized that their respective functions were stalled for lack of energy, causing their accumulation in the blood. Whatever the explanation, the facts were as described. It is interesting that the high levels of folate and B12 had been found at the hospital where a lymph node had been removed. The mother had been accused of giving too many vitamins to her child. She had told me that she did not understand this explanation because she had not given any vitamins to him. I had measured them solely to verify this finding.
The Treatment of Disease Should Begin with Host Defenses
We exist in a hostile environment. Each day throughout life we live in anticipation of potential attack. A physical attack may be an injury, an infection or an ingested toxin. A mental attack, divorce, grieving, loneliness, generally referred to as “stress” may be virtually anything that causes the brain to go into increased action. In facing both physical and mental forces, it is the brain that organizes the defense and it demands an increase in energy output that depends solely on the ability to burn fuel. The fuel burning process is governed by a combination of genetically determined ability and the nature of the fuel. Thus, the treatment of all disease is dependent on this combination being effective. It can be seen as obvious that killing the enemy is insufficient. As our culture exists at the present time, trying to get people to understand the necessity of perfect nutrition is a pipe dream. This particularly applies to youth and the artificiality of the food industry. However, our culture is also virtually brainwashed to accept tablets as a means of treating anything.
In our recently published book “Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition“, Dr. Marrs and I have shown that thiamine deficiency is extraordinarily common and that supplementary thiamine and magnesium together balance the ratio of empty calories to the required concentration of cofactors necessary for their oxidation. The question remains, would vitamin supplementation, just as artificial, be a more successful sell as a preventive measure? We have shown that the symptoms derived from prolonged high calorie malnutrition can last for years as an unrecognized polysymptomatic illness that haunts many physicians’ offices. Early recognition represents an easy cure. There is a good deal of evidence that ignoring the symptoms and the persistence of high calorie malnutrition creates a gradual deterioration that then turns up as chronic disease. Some drugs, metronidazole being an example, will precipitate thiamine deficiency, so we have to recognize the precarious nature of the present medical approach in the use of drugs whose action in treating disease is often unknown. Although recognition of the artificiality of thiamine supplementation is implicit in this proposal, it is better than allowing a common example of continued morbidity to exist.
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This article was published originally on July 19, 2018.
I have been experimenting with thiamine for about three years now, since I began reading this blog. I would like to add a couple of things to this very important article.
First, my son was quite sick from the time he was born. He was a distressed birth, and I was not able to breast-feed him. His health was a mess for his entire childhood. He was addicted to drinking milk. He didn’t sleep through the night until he was 2 1/2 years old. We went from formula that never agreed with him, to milk—and trying to get him to eat baby foods. The problem was, he didn’t want anything except for the milk. So he drank far too much.m
Over the years, I have known many, many mothers that had this problem. The nutritionists apparently know that there is potentially a highly addictive quality to milk. And even without the addiction aspect, there are many kids who rely heavily on milk and milk products in their daily diet.
The discussion here about milk essentially neutralizing thiamine is something I feel is too often overlooked. My son has been an extraordinary responder to allithiamine, as have I. We first began allithiamine when Dr. Lonsdale began talking about transdermal allithiamine for the autism community nearly 20 years ago. My son, very young at that time, really improved on this—but the resulting sulfur smell was a dealbreaker for a little boy.
My son also turned a dramatic corner when I took milk out of this diet. I was given a book written by a woman who appeared on the Phil Donahue show so many years ago, who said milk allergy could be a big problem in children. He was a new kid, in less than a week! I have wondered if the milk-free diet which is the standard in the autism community could be tied in any way to problems with thiamine.
Chandler, I would love to know if there might be a similar problem with wheat as well. We got good gains for my son when we took wheat out of his diet, as do many kids with autism spectrum issues and ADHD issues. He is grown now, but wheat and milk make him feel depressed and tired.
What I would like to say here is that all these years later, I am betting that thiamine deficiency has been his primary problem from the time he was born. I suspect that the formula he was drinking may have been nearly as damaging as cow’s milk was later in his life. The more I learn about thiamine deficiency, the more I recognize it as a problem in my whole family, and not just in my son. Perhaps we have the genetic component that has been talked about here on this blog. My father was a textbook case of acute thiaminek deficiency when he died; the old pictures from the Japanese Navy look just like my dad did at the end. My mother died of complications from hydrocephalus; the doctors wouldn’t even have a discussion about thiamine deficiency being the cause, as they are sure that’s only a problem in alcoholics.
Thank you for your blog here. It has been invaluable .
I am sorry, but why would you think that pyridoxine kinase is thiamine dependent? It only involves transfer of a phosphate group using ATP. The reaction is ATP + Pyridoxal -> ADP + PLP. Thiamine is not involved there albeit only if you say that ATP requirement could be unmet due to low PDHC activity?
It is needed for the enzyme pyridoxal kinase which takes pyridoxine to pyridoxine 5 phosphate.
What do those diffenent snps mean? Have found a few when compare to Snpedia(what other site has good info?) If only find a few snps from a gene that is homozygous for a pathogenic possibility , does that mean only if its turned “on” will it effect the body? SLC19A3 i5006224 am CC, = ? rs137852958 , according to snpedia is a risk but is hard to find info that backs that up.
Dr. Lonsdale…
I am doing wonderful since supplementing with Allithiamine… after 5 years of chronic illness I am seeing the light at the end of the tunnel… I just had to tell you this… I love reading your blogs and comments too… I don’t always follow along well on everything because some of it is above my head but I still like to read it. My question is when you said this above in response to Ron:
“Since the gene depends on thiamine pyrophosphate as cofactor, finding increased blood PA is a possible new way of ascertaining thiamine deficiency”
I am a milk drinker would this work for most people who are milk drinkers or only in Ron’s particular case with the SNP’s ect… A lot of what you two discuss is a bit beyond me but so interesting. 🙂
Ron is a special case because of his gene profile
Ok thank you. I thought so.
Do not drink milk if you are thiamine deficient a substance called phytanic acid is produced
Hi Derrick just reporting back. Unfortunately I was unable to obtain a phytanic acid test. In my country the test is only undertaken in the public sector and is subsidised by the government, they will only approve of it for more ‘orthodox uses’ and if referred by a specialist.
One strange symptom I forgot to mention was that my ability to read has deteriorated. I am unable to smoothly pace my eyes from word to word. I have trouble adjusting between fixations and saccades (I think this is the correct terminology). When moving my vision away from a word my eyes want to randomly dart around the paragraph skipping words in the process and I struggle to control this. I have found that if I read aloud I am better able to follow a sentence, as if the speech delays me and reaffirms where I am in the page but it still is a struggle maintain. I’m not sure if it’s damage to the portion of my brain responsible for control of eye movement or if its a reduction in my attention but I feel that its a bit of both. Have you had patients who were in need of B1 and had their control of eye movement deteriorate? I’ve never read of b6 toxicity disturbing eye movement, perhaps I haven’t looked hard enough.
Thiamine hcl gave me energy but had little impact on my reading capability so I was thinking of taking TTFD with biotin to see if things improve, starting small and increasing slowly. I was interested in your ‘Back Pain and B Vitamins’ post ( https://www.hormonesmatter.com/back-pain-b-vitamins-notes-personal-experience ) from 2016 as it is in line with the research and cases I found from the 1940’s regarding singular large doses of a B vitamin could cause an imbalance in the B complex. I will probably add a B complex to see if the nausea and red eye effects of b1 and biotin diminish and then tweak accordingly.
I’m interested if you resolved the eye issues as, among many other things, my eyes do the same. The optician said I had a tic in both eyes but doesn’t know why
Hi Dr Lonsdale,
Thank you for the work you do, I have recently discovered your blogs and really appreciate them.
I was hoping you could give me some insight into my case. I went to an integrative GP for a number of non-specific symptoms and was diagnosed and treated for pyrrole disorder whereby I was given 200mg pyridoxine and 50mg pyridoxal-5-phosphate. The B6 had a devastating effect on me. I was diagnosed with B6 toxicity by my family GP and am currently recovering.
I had some of the usual B6 toxicity symptoms:
-burning sensations in the arms and legs
– some tingling in feet
– stiff jaw
-chronic fatigue (most debilitating symptom).
-cognitive impairment, focus etc
Unusual symptoms that occurred were:
-worsening of dermatitis on hands
-small lines of alopecia in my beard
– stool coming out in round pellets
– toe nails became very thick , also developed bumps with large white marks on them
I was interested to find out some people became toxic off just 10mg of B6 over a few months while others took 200mg for years and were fine. I found research and clinical cases showing doctors in the 1940’s were aware of certain vitamin b deficiencies being induced or perhaps unmasked through large doses from other vitamin b’s ( PYRIDOXINE DEFICIENCY CAUSED BY ADDITIONS OF ANEURIN AND CHALK by MARION B. RICHARDS
https://6sd6hj41ya-flywheel.netdna-ssl.com/images/pdfs/IMBALANCE_OF_VITAMIN_B_FACTORS_-MB_RICHARDS_RPRNT_10.pdf ) . So I decided to self experiment with individual B vitamins thinking perhaps the B6 ramped up the need for something I had little of. I found that the different vitamin B’s have a very powerful effect on me.
I tried sulbutamine 200mg for 7 days and got an astoundingly large boost of energy which lasted 3 days and then steadily declined until I was back to my former fatigued self. Interestingly from the 3rd day the blood vessels in my eyes dilated massively and they became bloodshot and dry. In addition I became nauseous. This all disappeared after a week upon stopping. I tried thiamin hcl 200mg a while later but the same reaction occurred although it took 2 weeks for the negative effects to just start manifesting. I was wondering if you knew what could be the possible cause to me reacting to B1 like that?
5000mcg of biotin gave me boosts of energy even larger than that of B1, this lasted for just over a week. It also improved by nails and dermatitis but then just like with the B1 the effects subsided and I became nauseous but with no red eyes. I have a few heterozygous and one homozygous SNPs in the SLC19A3 and HACL genes, I don’t know if that would be relevant to my positive reactions to B1 and biotin.
B3 increases my fatigue massively and B5 causes nausea. B2, B12 and folate had no noticeable effect although I didn’t spend too long on them as I’m used to quick reactions with the other B vitamins.
I currently take 400mg of magnesium malate which completely relieves muscle twitches I get and have been taking it for months. I would like to know your thoughts on why B1 and biotin might have such a peculiar effect and if improvement may be possible with them. I was thinking of testing riboflavin with biotin and thiamine supplementation to see if the red eyes diminished.
Kindest regards,
Ron
This is a most interesting post. The SCL19A3 gene is a transporter for thiamine and appears also to be a transporter for biotin. Ron says that he has SNPs for the SCL19A3 gene. Recent medical research has given rise to finding that a mutation in this gene causes thiamine-biotin-dependent basal ganglion disease. (look it up on PubMed). This disease is epigenetically responsive to a combination of biotin and thiamine as therapeutic supplements given together. I would deduce from the information given here that the SNPs in the gene are giving rise to an eminently treatable relatively minor version of the basal ganglion disease. What is interesting is that he responds to both thiamine and biotin for only a short time, given singly The question obviously is, would he respond to both supplements given together? He also has SNPs in the HACL gene and this gene requires thiamine pyrophosphate(TPP) as its cofactor. The action of this gene is in the peroxisome and is absolutely dependent on TPP for alpha oxidation, a necessary step in providing a fuel for brain function. Before taking advantage of this post, Ron, please ask your physician to request an assessment of your urinary concentration of phytanic acid and let me know.
I’ve done some searching and have found that there seems to be one lab in my city that does phytanic acid testing and its a blood test. If my doctor is unable to find a lab that does urinary concentration of phytanic acid would serum or plasma tests be a viable alternative?
Interestingly I’ve just put some of my gene data through a template that looks at beriberi related genes according to malacards.org/card/beriberi and the results showed:
SNP rsID Minor Allele Your Genotype Phenotype
SLC19A2 rs1983546 A AA +/+
SLC19A3 rs10933203 A AC +/-
SLC19A3 rs11682956 T GG -/-
SLC19A3 rs4973216 C CT +/-
SLC19A3 rs7585481 C CT +/-
TKT rs12493802 T CT +/-
TKT rs4687717 T TT +/+
TKT rs4687718 A GG -/-
TRPV3 rs395357 T CT +/-
TRPV3 rs7217270 A AA +/+
I have quite a few SLC19A3 SNPs not listed above. One, rs863224204, took my interest as it’s clinical significance on the National Center for Biotechnology Information SNP database listed it as pathogenic which is the first time I’ve seen a SNP’s clinical significance not listed as NA when searching.
The HACL1 SNPs I have are below. I’m not sure if they are the problematic ones, there are quite a few that 23andme is missing data on.
HACL1 rs2271021 T / T
HACL1 rs62243579 T / T
HACL1 rs17485446 T / T
HACL1 rs115033840 G / G
HACL1 rs78403907 G / G
HACL1 rs76945801 T / T
Blood phytanic acid (PA) is right. I was wrong. The point here is that the HACL gene processes phytanic acid derived from chlorophyll and found in milk from feed. The result is an “upstream” effect of HACL gene failure. It may not increase in a non-milk consumer but it is at present the only clinical lab marker of a dysfunctional HACL. Since the gene depends on thiamine pyrophosphate as cofactor, finding increased blood PA is a possible new way of ascertaining thiamine deficiency
It’s much worse than that.
Pyridoxine HCl **directly** causes vitamin B6 deficiency!
However:
Pyridoxine kinase, the enzyme that converts pyridoxine to pyridoxal phosphate is thiamine dependent and so if someone has insufficient thiamine, pyridoxine will build up and become a functional B6 deficiency. If this person then takes high dose B6 or really any dose B6, without first correcting the thiamine, toxicity will build up B6 deficiency worsen.
For someone with B6 toxicity, will increasing thiamine resolve the toxicity? For years my daughter showed signs of B6 deficiency and every test we did (OAT, NutrEval, etc) showed signs of deficiency so I was told to increase her B6. She has been on B6 for years at what seems a rather high dose for a 12 year and still shows signs of deficiency. Now I think her symptoms (no knee jerk reflex, hair loss, constipation) are signs of B6 toxicity. I’m hoping to get a blood level to confirm. But I’ve read that recovering from B6 toxicity involves a lot more than reducing the B6 level in the blood and was hoping adding thiamine would be helpful. Any advice would be greatly appreciated.
B6 toxicity is because it is inactive and needs thiamine
Thank you for the response. My daughter was taking pyridoxine B6 but stopped just a few days ago when I realized she may be toxic. As you mentioned, I will add additional thiamine. Should I use P5P/B6 with her or completely stay away from any form of B6 until her thiamine has increased? I guess I’m not clear if P5P/B6 will contribute to toxicity or is it just the pyridoxine/B6 that causes toxicity (in light of a thiamine deficiency).
Will the inactive B6 stored in the body from many years of supplementation slowly get activated upon the addition of thiamine?
I’m so worried about how to handle this for my daughter. thank you for your help
Just add thiamine and don’t worry re activation.