I started low-carb Paleo dieting in late 2005. I ate a lot of vegetables but no starches and hardly any fruit. In retrospect, I would call it a near zero-carb diet. At that time I was 12 years into a chronic illness that got a little worse each year and was quite mysterious to me. Adopting a low-carb diet brought immediate changes: it made what I would much later recognize as a chronic bacterial infection better (in parts of the body, not the brain) and made a chronic fungal infection worse.
Within about a year I had developed scurvy. It took me an embarrassingly long time to figure out what it was. By the time knew what it was, I had 3 cavities; had lost 25 pounds; had developed diverticulitis and an abdominal aorta that visibly swelled with every heartbeat; and had minor skin wounds – scrapes and scratches – that hadn’t healed in 6 months.
Developing scurvy was a surprise, because I was eating many vegetables plus taking a multivitamin containing 90 mg of vitamin C. I had never had any signs of vitamin C deficiency before adopting a low-carb diet.
Four grams a day of vitamin C for two months cured all the scurvy symptoms. It would be several more years before I figured out the infections, but this experience taught me the importance of micronutrition. The experience persuaded me that I needed to research diets and nutrition closely, and started us down the path of writing Perfect Health Diet.
Scurvy on a Ketogenic Diet
My experience is not unique. Here’s one case we mention in the book: the story of a young girl with epilepsy.
KM was a 9-year old girl … diagnosed with epilepsy at six months old. She started a ketogenic diet in October 2003, as her multiple antiepileptic drugs were proving to be less than effective; indeed she was having as many as 12 tonic seizures per day with prolonged periods of non-convulsive status epilepticus. After the diet was prescribed the seizure frequency reduced markedly and there were a number of long periods of time in which she had no seizures.
KM’s mother gave a history of her daughter having had bleeding gums since the beginning of September 2006; she described them as being very dark red, swollen and bleeding. In addition, she explained that her daughter had dry, crusted blood peri-orally. The family’s general dental practitioner had explained that this was probably caused by erupting teeth and instructed her to use 0.2% chlorhexidine gluconate gel and to continue her regular oral hygiene regimen; however this had no effect. About a month later the patient’s right arm became swollen. It was thought that she had sustained a fracture or a dislocation; however she was discharged from the local hospital’s fracture clinic because there was clinical improvement and radiographs showed no callus formation.
In early November KM inhaled a primary molar tooth while she was having her teeth cleaned (Fig. 1). This required an emergency bronchoscopy to retrieve it; at the same time the surgeons extracted her remaining primary teeth in order to avoid a recurrence of the problem….
At that time an appointment was made to attend a paediatric dentistry consultant clinic at the Leeds Dental Institute; however this was never kept as about three weeks after the extractions the patient was admitted to hospital with low grade fever, persistently bleeding gums, oedema of her hands and feet and a petechial rash on her legs. [1]
This girl was eating a typical amount of vitamin C: her dietary intake was calculated at 73 mg/day, well above the US RDA for 9-13 year olds of 45 mg/day. Yet her blood level was only 0.7 µmol/l. Scurvy is diagnosed at levels below 11 µmol/l.
The symptoms of scurvy are sufficiently insidious that it is easy to miss the diagnosis. In KM’s case, it happened that a “senior house officer” – a junior doctor in training – from India recognized the symptoms of scurvy. Otherwise, it might have never have occurred to the doctors to test her vitamin C level. [2]
What Is the Cause of Low-Carb Scurvy?
So what causes scurvy to develop on low-carb diets even with vitamin C intake well above the US RDA?
It seems to be a confluence of two factors:
- An infection or some other stress (e.g. injury, cancer) leads to the oxidation of extracellular vitamin C; and
- On a low-insulin or glutathione-deficiency-inducing diet, oxidized vitamin C is not recycled.
Infection and Vitamin C
The immune response to infections generates reactive oxygen species, which oxidize vitamin C. Oxidation removes a hydrogen atom from vitamin C, turning it into “dehydroascorbic acid,” or DHAA. If DHAA remains in the blood, it degrades with a half-life of 6 minutes. [3]
Infections can cause vitamin C deficiency on any diet. During the “acute phase response” to infection or injury, vitamin C often becomes deficient. Here is a nice paper in which French doctors surveyed their hospital patients for scurvy:
We determined serum ascorbic acid level (SAAL) and searched for clinical and biological signs of scurvy in 184 patients hospitalized during a 2-month period.
RESULTS: The prevalence of hypovitaminosis C (depletion: SAAL<5 mg/l or deficiency: SAAL<2 mg/l) was 47.3%. Some 16.9% of the patients had vitamin C deficiency. There was a strong association between hypovitaminosis C and the presence of an acute phase response (p=0.002). [4]
So half were at least depleted in vitamin C and 17% had outright deficiency, which if it persisted would produce scurvy.
We’ve previously written of how important it is to supplement with vitamin C during infections:
- “Fighting Viral Infections With Vitamin C at Bowel Tolerance,” https://perfecthealthdiet.com/?p=636.
- “New Zealand Man Left for Dead By Doctors, Cured by Vitamin C,” https://perfecthealthdiet.com/?p=439 and “Vitamin C vs Modern Medicine,” https://perfecthealthdiet.com/?p=619.
I might add here that in sepsis, an extremely dangerous inflammatory state brought on by bacterial infections, intravenous vitamin C reverses some of the worst symptoms. [5] If you have a loved one suffering from a dangerous infection, it might not be a bad idea to get them some vitamin C.
Insulin Dependence of Vitamin C Recycling
DHAA can be recycled back into vitamin C, but only inside cells.
In order to enter cells, DHAA needs to be transported by glucose transporters. GLUT1, GLUT3, and GLUT4 are the three human DHAA transporters; GLUT1 does most of the work. [6]
DHAA transport is crucial for brain vitamin C status. There is no direct transport of vitamin C into the brain, yet the brain is one of the most vitamin C-dependent tissues in the body. The brain relies entirely on GLUT1-mediated transport of DHAA from the blood for its vitamin C supply. Within the brain, DHAA is restored to vitamin C by glutathione.
Supplying DHAA to stroke victims (of the mouse persuasion) as late as 3 hours after the stroke can reduce the stroke-damaged volume by up to 95%:
DHA (250 mg/kg or 500 mg/kg) administered at 3 h postischemia reduced infarct volume by 6- to 9-fold, to only 5% with the highest DHA dose (P < 0.05). [7]
This is a fascinating reminder of the importance of vitamin C for wound repair and protection from injury.
Glucose transporters are activated by insulin. Thus, DHAA import into cells is increased by insulin, leading to more effective recycling of vitamin C [8]:
Insulin and IGF-1 promote recycling of DHAA into ascorbate. Source.
Confirming the role of insulin in promoting vitamin C recycling, Type I diabetics (who lack insulin) have lower blood levels of vitamin C, higher blood levels of DHAA, increased urinary loss of vitamin C metabolites, and greater need for dietary vitamin C. [9, 10]
Now we have a mechanism by which zero-carb diets reduce vitamin C recycling: by lowering insulin levels they inhibit the transport of DHAA into cells, preventing its recycling into vitamin C. Instead, DHAA is degraded and excreted. As a result, vitamin C is lost from the body.
Glutathione and Vitamin C Recycling
Once inside the cell, DHAA is recycled back to ascorbate, mainly by glutathione inside mitochondria:
Dehydroascorbate, the fully oxidized form of vitamin C, is reduced spontaneously by glutathione, as well as enzymatically in reactions using glutathione or NADPH. [11]
A GLUT1 transporter on the mitochondrial membrane is needed to bring DHAA into mitochondria, possibly squaring the effect of insulin on vitamin C recycling.
Since glutathione recycles vitamin C, glutathione deficiency is another possible cause of vitamin C deficiency.
Glutathione is recycled by the enzyme glutathione peroxidase, a selenium-containing enzyme whose abundance is sensitive to selenium status. One difficulty with zero-carb diets is that they seem to deplete selenium levels.
Selenium deficiency is a common side effect of ketogenic diets. Some epileptic children on ketogenic diets have died from selenium deficiency! [12]
So here we have a second mechanism contributing to the development of scurvy on a zero-carb diet. The diet produces a selenium deficiency, which produces a glutathione deficiency, which prevents DHAA from being recycled into vitamin C, which leads to DHAA degradation and permanent loss of vitamin C.
Conclusion
Zero-carb dieters are at high risk for vitamin C deficiency, glutathione deficiency, and selenium deficiency. Anyone on a zero-carb diet should remedy these by supplementation.
These deficiencies are exacerbated by chronically low insulin levels. Insulin helps recycle vitamin C, which supports glutathione status. Lack of insulin increases vitamin C degradation and loss.
The failure of the body to efficiently recycle vitamin C and maintain antioxidant stores on a zero-carb diet is evidence of an evolutionary maladaption to the zero-carb diet.
There was no reason why our ancestors should have become adapted to a zero-carb diet; after, all they’ve been eating starches for at least 2 million years. It seems a risky step to try to live this way.
Related Posts
Other posts in this series:
- Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
- Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers A Nov 15, 2010.
- Dangers of Zero-Carb Diets, IV: Kidney Stones Nov 23, 2010.
References
[1] Willmott NS, Bryan RA. Case report: Scurvy in an epileptic child on a ketogenic diet with oral complications. Eur Arch Paediatr Dent. 2008 Sep;9(3):148-52. http://pmid.us/18793598.
[2] Willmott NS, personal communication.
[3] “Dehydroascorbate,” Wikipedia, http://en.wikipedia.org/wiki/Dehydroascorbate.
[4] Fain O et al. Hypovitaminosis C in hospitalized patients. Eur J Intern Med. 2003 Nov;14(7):419-425. http://pmid.us/14614974.
[5] Tyml K et al. Delayed ascorbate bolus protects against maldistribution of microvascular blood flow in septic rat skeletal muscle. Crit Care Med. 2005 Aug;33(8):1823-8. http://pmid.us/16096461.
[6] Rivas CI et al. Vitamin C transporters. J Physiol Biochem. 2008 Dec;64(4):357-75. http://pmid.us/19391462.
[7] Huang J et al. Dehydroascorbic acid, a blood-brain barrier transportable form of vitamin C, mediates potent cerebroprotection in experimental stroke. Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11720-4. http://pmid.us/11573006.
[8] Qutob S et al. Insulin stimulates vitamin C recycling and ascorbate accumulation in osteoblastic cells. Endocrinology. 1998 Jan;139(1):51-6. http://pmid.us/9421397.
[9] Will JC, Byers T. Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev. 1996 Jul;54(7):193-202. http://pmid.us/8918139.
[10] Seghieri G et al. Renal excretion of ascorbic acid in insulin dependent diabetes mellitus. Int J Vitam Nutr Res. 1994;64(2):119-24. http://pmid.us/7960490.
[11] Linster CL, Van Schaftingen E. Vitamin C. Biosynthesis, recycling and degradation in mammals. FEBS J. 2007 Jan;274(1):1-22. http://pmid.us/17222174.
[12] Bank IM et al. Sudden cardiac death in association with the ketogenic diet. Pediatr Neurol. 2008 Dec;39(6):429-31. http://pmid.us/19027591. (Hat tip Dr. Deans.)
via this link:
Thanks for the answer Paul,
Are you basing your info only on “Insulin Stimulates Vitamin C Recycling and Ascorbate Accumulation in Osteoblastic Cells” ? I am not stating otherwise, I would personally like to put nail on this topic as it is of big practical value for me, especially during acute stress.
I read the complete study and there are some suspicious in-vitro scenarios:
– Higher intake of DHAA requires pre incubation of insulin during 12 hours on 23C. This doesn’t seem much relevant for humans as I don’t know how would you keep peripheral insulin so high during such amount of time. They also didn’t xplain why they used that temperature.
– The insulin concentration used was 10nm. According to the [1] peripheral insulin concentration after 25g glucose loading is much less then 1 nM.
– The use of cycloheximide to test the hypothesis is highly questionable since it is non-selective protein synthesis inhibitor. Who knows what is rationale for the reduced DHAA uptake, only one scenario is offered.
– They say that similar conclusion of osteoblasts are probably true for RBCs, however, those cells have stomatin switch and increasing glucose doesn’t compete with DHAA [2].
– They say that “UMR-106 cells lack the facilitative hexose transporter isoform (GLUT4) associated with rapid stimulation by insulin … Instead, the maximal effect of insulin (10 nm) on facilitated hexose transport activity requires approximately 16h and is associated with increased expression of GLUT1 and GLUT3”. This might mean that such cells also might have stomatin switch.
– They also say that “Under physiological conditions in vivo, virtually all plasma vitamin C is in the form of ascorbate; therefore, accumulation of vitamin C by osteoblasts probably occurs via Na ascorbate cotransport”. THey deduced that study is related to phatophysiological conditions in which there are higher levels of DHAA due to oxidative stress, so if their finds are true, the effect dependants on personal status rather then diet alone.
Also, in paper [3] they say that “brain insulin, which is typically 10 times higher than plasma insulin concentrations, and brain receptor content, which is equivalent to receptor content on peripheral tissues, appears to be regulated entirely independently of hormone and receptor in the periphery.” which means that brain recycling probably functions differently then what is known for other tissues.
BTW, my fasting blood glucose didn’t change on 50g < CHO < 100g per day. My recordings previous 5 years are 5.7, 5.5, 5.0, 5.6, 5.4. The last value is on low carb diet. Boosted liver glucose production might occur as pathological process in specific category of people (for instance pre-diabetes). However, I do have cheat day with 'unlimited' CHO once per week, wich probably makes a big difference.
[1] Proinsulin, Insulin, and C- Peptide Concentrations in Human Portal and Peripheral Blood
[2] Erythrocyte Glut1 Triggers Dehydroascorbic Acid Uptake in Mammals Unable to Synthesize Vitamin C
[3] Concentrations of Insulin and of Insulin Receptors in the Brain are Independent of Peripheral Insulin Levels
I tend to be skeptical of the relevance of papers that refer to “the” ketogenic diet, because they so often refer to just one of the many kinds of ketonemia-inducing diets — the classic therapeutic, medically supervised, deep-ketosis, high-PUFA, semi-palatable kind.
It’s past time to retire the use of the grammatical define article here (…or perhaps to start referring to low fat diets as “the” low fat diet, the use of antibiotics as “the” antibiotic therapy, and so on).
Hi majkinetor,
A number of good points there … the effect of insulin on C recycling is not huge and it does depend on the presence of oxidative stress creating large amounts of DHAA.
However, during chronic infections oxidative stress can be substantial. That’s how I got scurvy.
So I agree these are special situations we are talking about. But a healthy diet should be robust to infections, because everyone gets them sooner or later.
Hi Google scholarly,
Agreed.
Paul,
for chronic infections, is it NAC test of any good ?
I want to check out if it out on myself (was thinking about 2.4g dose for 3 days).
I had bunch of autoimmune diseases since 16 – scleroderma, allergy to heat during winter, dermatology problems like eczema, etc… I would like to test this possibility especially as I have case of paradentosis which occurs only when my immune system is at its low (so I was thinking that some pathogen took resistance in my gums and take opportunity)
Anything else I could do at home to find out ?
Would you also like to give your input on how bacterial endotoxins are supposed to be good marker for chronic disease as your body is full of different bacteria which are not pathogens in normal circumstances. All those good/neutral bacteria will die along with bad ones so how could you say if endotoxins are related to bad bacteria.
Hi majkinetor,
Some people with chronic infections will experience a negative reaction to NAC. C. pneumoniae is one such pathogen.
But I don’t know that it is reliable as a diagnostic tool. I think your symptoms are a good indicator that you do have some kind of infection. NAC may be therapeutic.
High endotoxin levels indicate some kind of problem, either systemic or in the gut. In healthier people, endotoxins are generated in the gut and carried into the body with fat. With a leaky gut or a gut infection that the immune system is fighting this flux increases. A systemic infection also leads to increased endotoxin levels.
Dunno is this was covered in previous comments, but ketogenic patients with clinical selenium deficiency were taking anti-epileptic meds including valproate. Valproate is well-known to deplete selenium even on normal diets. Though the classic epilepsy keto diets restrict animal protein and use MCT instead of animal fat, restricting important sources of selenium, the drug toxicity factor seems the most likely culprit. Further, a modified Atkins ketogenic diet is replacing the classic keto diet in epilepsy control and this includes more sources of selenium, plus the need to supplement selenium with valproate and similar drugs is better understood.
Hi George,
Thanks! That’s very valuable background.
Best, Paul
http://www.biblelife.org/stefansson1.htm
Maybe Vilhjalmur Stefansson was the only person to test this clinically – and in that famous n=2 experiment the requirement for ascorbate if anything dropped on an all-meat diet.
“On my third expedition it happened as circumstantially related in a book called “The Friendly Arctic”, that three men came down with scurvy though disobeying the instructions of the commander and living without his knowledge for two or three months chiefly on European foods when they were supposed to be living chiefly on meat.
On [restoring] this diet all pain disappeared from every joint within four days and the gloom was replaced by optimism. Inside a week both men said that they had no realization of being ill as long as they lay still in bed. In two weeks they were able to begin traveling, at first riding on the sledges and walking alternately. At the end of a month they felt as if they had never been ill. No signs of the scurvy remained except that the gums, which had receded from the teeth, only partly regained their position.
By comparing notes later with Dr. Alfred Hess, the leading New York authority on scurvy, I found that when I was getting these results with a diet from which all vegetable elements were absent, he was getting the same results in the same length of time through a diet where the main reliance was upon grated raw vegetables and fruits and upon fresh fruit juices.”
This may be the reason meat prevents scurvy despite being low in ascorbate:
ascorbate is essential because we need it to synthesise carnitine, hydroxyproline and one or two other hydroxylated compounds. Everything we need ascorbate to synthesise is found in meat ready-made.
Carnitine, for example, is well-absorbed from meat, reducing our requirement for endogenous synthesis and therefore our ascorbate requirement. The antioxidant action of ascorbate is likely not an essential requirement, with other antioxidants (uric acid, hydroxycobalamin, creatine, glutathione) being able to deputize in this role.
Hi George,
I think the vulnerability to scurvy is highly dependent on infection status. I do think meat protects against some of the symptoms of scurvy, but not all of them. I didn’t have any of the bleeding that is characteristic of scurvy on high-carb diets, but my wounds never healed and I couldn’t build new tissue, so lost weight steadily.
Let me just play devil’s advocate here for reasons of scientific purity: has it actually been proved that humans produce absolutely no ascorbic acid? The existence of scurvy on restricted diets is not final proof, as these diets may have been lacking some co-factor required for vit C synthesis.
It may be (humour me) that vit C is made rarely, but some dietary combinations are capable of supporting its synthesis (in very small but useful amounts).
The lack of an enzyme in human genes (in how many examples?) is compelling, but shunts or alternative syntheses are not unknown in biochemistry.
I’m just saying that I’ve looked for experiments testing whether ascorbate is or is not synthesised by humans and so far found nothing.
I’m sure the assumption is correct, but it seems to be mainly an assumption.
Paul, is the actual content of the diet that gave you scurvy, or the main foods, included on this site?
Dear George,
I believe that R.A. Anderson’s (et al) work with cinnamon might provide a clue to the information you seek.
http://www.ncbi.nlm.nih.gov/pubmed/14633804
It is generally believed that Homo sapiens and other simians produce no vitamin C due to a pseudogene in place of a functioning one. Has someone checked every simian on earth to see if this holds true? Probably not.
Nonetheless, because some species can produce vitamin C via other processes, it is possible that H. sapiens can too, just not in significant enough amounts.
In particular, because women lag behind men in the CVD statistics, it is surmised that women can produce vitamin C hormonally because, after menopause, they catch up with men rapidly. Has anyone checked ‘all women’? Hmm. Dunno.
All that said, kudos to the creator of this discussion group. Latent scurvy is very much a part of pathology today and localized scurvy tends to evade detection by the usual tests even when someone bothers to do them.
If I were in any chronic adverse condition, I would take Fred Klenner’s advice and overdo buffered vitamin C until the tests get back. Dr. Tom Levy has written the book on the subject and Dr. Mercola has an affordable version of a liposomal vitamin C product that mimics normal absorption processes in H. sapiens.
As to the ketogenic conundrum, I can add something to that: sugar will replace vitamin C, if none is available, according to Dr. Rath. If someone is short on vitamin C and avoids sugar (carbohydrates) the cells don’t even have a poor substitute to work with and go on strike. When the cells start to deteriorate, the clean-up crew (bacteria) moves in and goes to work because they think you’re dead. This situation should be avoided if possible.
I hope this helps…
AL
AskDrPangloss.com
Hi George,
It was a high-fat middling-protein almost zero-carb (but very high fat) Paleo diet. Basically, meat, vegetables, and oil. Ratatouille with lots of olive oil was a typical vegetable dish.
So Inuit don’t get scurvy on a carb-free diet.
Inuit also don’t exercise or work just for the sake of it. Every exertion or exposure has survival value for them, and if they’re sensible they rest at other times. This is the hunter-gatherer pattern; the exertion required for food or protection leads to rest. If the hunt is good, days may be spent doing nothing strenuous. So perhaps what is inducing the scurvy is, to use an obnoxious cliche, the high-stress modern lifestyle on top of a diet adapted to a different lifestyle.
This, come to think of it, fits with my own concept;
meat, eggs etc. and starchy roots were food; leafy plants, twigs, bark and fruits were medicines (or herbal and nutritional supplements if you like); conditionally essential, mostly just useful.
Especially as consciousness altering agents – in the broadest possible sense – sharpening or dulling vision, easing or preventing pain, providing variety of smells and tastes, altering sleep and digestion, and just alleviating boredom and satisfying curiosity.
I suppose some people might focus on the cooking of veges or the use of oil (which supplies fewer essential nutrients than fat). Olive oil polyphenols (and PUFAs) might even be prooxidant on a zero carb diet (see Kurt Harris’ ideas about hormesis). But that’s probably academic; if you had a serious untreated infection, then your immune system might be gobbling the ascorbate. On the low-carb diet the infection might never have gotten a foothold, but it did and it had before you started. Suddenly your innate immunity wakes up and fights it, and vit C is sucked into that. Say you switched, as a result of zero carb, from an ineffective mainly Th2 antibody response to an avid Th1 NK and macrophage response; that would require both ascorbate and glutathione (the macrophage “respiratory burst” both generating ROS and reducing glutathione).
Here we go; bacteria found in the gut can synthesise ascorbic acid. So potentially scurvy could relate to probiotic (and prebiotic) factors as much as dietary; puts a new spin on the hygeine hypothesis if the amounts can be significant.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC91626/
In some lower eukaryotes, d-erythroascorbic acid (EASC) is present instead of l-ascorbate (ASC; 10, 15). EASC is very similar to ASC in structure and physicochemical properties (21), suggesting that it may take the place of ASC in lower eukaryotes. We have previously reported that EASC is synthesized from d-arabinose through d-arabinono-1,4-lactone by a concerted reaction of d-arabinose dehydrogenase and d-arabinono-1,4-lactone oxidase (ALO) (10, 13, 14) and is an important antioxidant molecule in Saccharomyces cerevisiae (11). We also found that our proposed biosynthetic pathway for EASC is very similar to the biosynthetic pathway for ASC in plants, in which l-galactose and l-galactono-1,4-lactone are involved (23). It is worth noting that ALO can oxidize l-galactono-1,4-lactone as efficiently as d-arabinono-1,4-lactone (10). This means that both EASC and ASC can be produced by ALO, depending upon the substrate used. Here we report the success in the functional expression of ALO and the overproduction of EASC and ASC in Escherichia coli, which is inherently devoid of ALO and can normally make neither EASC nor ASC. This is the first description about functional expression of an enzyme catalyzing the biosynthesis of EASC and ASC in Escherichia coli.
They seem to be saying that the yeast is the natural producer of ascorbate. So to rule out endogenous ascorbate, we have to rule out its production by any of myriads of microbiota species…
…just saying…
Hi George,
I do think infections are the most likely cause of oxidative loss of vitamin C, and were responsible for my case.
Re the gut microbiota making C, it seems unlikely to be a significant source. The E coli don’t do it in nature, and the Saccharomyces cerevisiae make it for themselves and presumably don’t release it.
We know that microbiota produce vitamin K2 and that this can prevent deficiency of vitamin K, but no-one has ever calculated the extent of this contribution or its parameters. There’s a lot we don’t know, in other words, and some of it is stuff we still haven’t tried to find out. Which is my point, not that this actually does happen, but that we can so easily build an edifice of knowledge on an uncertain basis.
Carnivores seem to synthesise ascorbate at much the same levels as herbivores; there doesn’t seem to be a low-carb differential.
What about nitrates? One can end up consuming animal nitrates (as opposed to natural vege ones) when eating meat every day, and there is evidence that these increase requirements for ascorbate, which detoxifies peroxynitrite.
P.S. I found a conservative medical source online which quotes requirement for ascorbate in bacterial infections as 30-200+ mg. This would meet your case.
Of course, antibiotics would reduce any putative ascorbate synthesis by microbiota… can we find cases of antibiotic-induced scurvy? I’ll let you know. That I suppose is one way to test the hypothesis…
I really appreciate this article and your website in general which is newly discovered to me. I went low carb about 7 months ago, I experimented with dr mercola’s nutritional typing plan and as his quiz told me i was a protein type (high protein/high fat/low carb) that was the plan i tried to stick to but also experimented with the mixed and carb type plans. However even his carb type plan only counts carbs from veg with a few legumes. Anyway I always had the most intense carb cravings, esp on the protein plan and had to give in to them several times. I should have listened to my body more but I thought we could get all the carbs we need from veg. I think i developed scurvy in this time as my skin has been worse since going low carb, my hands a lot more wrinkled and old looking, and my gums have gotten in very bad shape, I never had any gum problems before this. They are often sore and I have only noticed recently they have receeded in places, I have had dreams about loosing my teeth on more that one occassion. I also had dry eyes and my vision has worsed but I’m not sure if that is related. I went paleo about 3 weeks ago but was still low carb with 1 or 2 bits of fruit a day. I started supplementing vitamin c a few weeks ago but this article is making sense. I heard your interview with dr mercola about a week ago and have upped my potato, sweet potato and fruit intake in the last few days 🙂
Hi Scott,
Dry eyes are another symptom of going too low-carb, see http://perfecthealthdiet.com/?p=1077. I’m glad you found us and I expect your skin, eyes, and gums will improve soon!
Dreams about loose teeth are in my opinion the very first sign of scurvy, also a kind of itchyness of the teeth where they seem to be squirming in their sockets often preceeds actual looseness.
However, you could supply adequate vitamin C with few carbs by consuming rosehip powder, or supplements, or fresh lemons. I don’t see how eating carbs from sweet potato etc. is going to increase uptake or retention of ascorbate – if anything the opposite is true.
(Paul, if you have a theory about this, please direct me to the page).
Capatain Cook prevented scurvy on his voyages by regularly resupplying with fresh veges, fresh fruit, and fresh meat. If one of those was unavailable (there was no fruit in New Zealand, for example) the others sufficed.
What improved my skin noticably was eating lots of saturated animal fat, beef and dripping, instead of the vege oils I had used. My skin got firmer and thicker and stopped burning easily. In fact, saturated fat had a similar effect to vitamin E supplements.
But then, I’ve always supplemented vit C, so collagen was never the issue, rather peroxidation and poor circulation from PUFAs and carbs.
Wouldn’t a diet supplying lactose (galactose plus glucose) be more efficient at providing mucus (per carb) than a diet supplying just glucose and/or fructose? Cream, milk, cheese? Lactose supplies 2 of the sugars used in mucus, veges just supply one (glucose).
What about Chinese edible mushrooms? They are full of these sacharrides, but very low carb.
It occurs to me that, while we may well be discussing symptoms of mild vitamin C deficiency, we are not actually discussing scurvy at all. Scurvy is a life-threatening disease characterised by tumour growth, re-opening of old healed wounds and fractures, hyperplasia of gums (sometimes), and extreme fatigue (generally considered to be the first symptom, and due to carnitine deficiency).
There is still no reason to believe that someone on a low-carb diet, eating mostly fresh fatty meat with some green veges or fruit, would ever develop scurvy.
(Whereas cases are still seen in people who eat high-carb diets lacking in fresh food).
@George, I am no expert but I think Paul makes the case that illness/infection significantly increases vit C requirement, thereby contributing to deficiency.
Agreed. I just wanted to bring define terms more rigourously.
The fact is, we are, mostly, not Inuit. We did not imbibe all-meat diets at our mothers breast. Most of us came to this diet with mitochondrial or metabolic damage from carbs, long standing inflammations, chronic infections, etc, due to our previous high-carb lifestyles. An Inuit would be permanently expressing the genes for PPAR-alpha and FGF21, whereas ours have ben quiescent for long periods. Perhaps we can put this right with years of low-carb, but the sicker we are, the less we can expect this to happen overnight.
So we need, at least at first, more ascorbate, magnesium, and so on – but it doesn’t prove that we need more carbohydrate.
Chronic infection or inflammation, or reductive stress from mitochondrial disfunction, will result in elevated peroxynitrite levels, which may well persist for some time into low-carb; and quenching peroxynitrite will use up ascorbate, B12, creatine.
So this overhang from inflammation might eat into the benefits of low-carb re: conserving these nutrients at first.
Hi Paul and others,
I was reading through this post again and had a question about rDNA insulin injections with regard to the vitamin C recycling. I don’t know if you can answer this question or not (and it might be a dumb question, but I don’t know the answer) so thought I would throw it out there… My question is related to what you wrote here:
“Glucose transporters are activated by insulin. Thus, DHAA import into cells is increased by insulin, leading to more effective recycling of vitamin C [8]:”
“Confirming the role of insulin in promoting vitamin C recycling, Type I diabetics (who lack insulin) have lower blood levels of vitamin C, higher blood levels of DHAA, increased urinary loss of vitamin C metabolites, and greater need for dietary vitamin C. [9, 10]”
I am a type1 diabetic but of course I do take daily insulin injections. Do you (or anyone else) have any idea if manufactured insulins perform all the same functions (ie, vitamin C transport into cells) just as normally produced insulin inside a non-diabetic body? (I know there are different kinds of manufactured insulins– long-acting, fast-acting, time-released, etc, so my question may be difficult to answer, but generally speaking, is it the same?) I’m just curious and have never looked into this… is my convenient little bottle of insulin just about the same as the insulin of non-diabetics? Or does it possibly lack some necessary biological characteristics?
In any case, I do take vitamin C daily, usually at least 1-2g (more if I have any kind of injury or cold, etc.).
Thanks for any thoughts or input… or pointers as to where to look… maybe the manufacturers website? Just wanted to ask here first because this site seems so much more user-friendly than other places 🙂
Thanks!
KH
Hi KH,
I’m certain all the insulins will work. I think you’re safe with 1-2 g C per day.
Best, Paul
Ok, thanks! I just wasn’t sure… I used to only focus on insulin’s role in lowering my blood sugar and had not thought much about the other roles it plays. Surely I should start to learn these things!
Thanks!
Yes, vitamin C shortage can produce scurvy ………in carb-adapted people. In fat-adapted people? …..not so much.
Scurvy is not defined by the lack of any essential nutrient. Scurvy is defined by a set of symptoms associated with the damage caused by free radical oxygen and associated reactive oxygen species (ROS’s). Yes, vitamin C is *one* antioxidant beneficial for removing ROS’s.
However, nobody is saying that ketogenic diets produce levels of vitamin C comparable to non-ketogenic diets. Low carbers are saying that people on ketogenic diets only have a tiny fraction of ROS’s displayed by high carbers. So they only have a tiny fraction of ROS damage. In general, the lower the carb intake, the lower the ROS concentration and ROS damage.
There is no need for vitamin C where there is no ROS damage to treat. Cells produce free radical oxygen as a byproduct of burning sugars for fuel. If you eat fat instead of sugar, then you only produce a fraction of the free radicals.
You invented a marker for a health condition, then tried to convince us of the advantage of one diet over another by showing which diet improved the marker. It’s a straw man argument. The marker is irrelevant to the condition.
The level of ROS production varies greatly with infections status. It’s just not the case that people on ketogenic diets are guaranteed to have low oxidative stress. In fact, the high rate of kidney stones on clinical ketogenic diets indicates that those diets produce extraordinarily high levels of oxidative stress.
The cause of elevated kidney stones among low carb dieters is not well studied, either in populations or in pathways. I got kidney stones as a result of ingesting some cheap Asian coffee. I’m convinced it contained cyromazine, a commonly used pesticide in Asia. Cyromazine metabolizes into melamine plastic in the kidneys. Does carb ingestion protect kidneys against cyromazine? Does cyromazine only affect kidneys which function properly?
You don’t know, and you can’t say.
I don’t think it’s that mysterious: http://perfecthealthdiet.com/2010/11/dangers-of-zero-carb-diets-iv-kidney-stones/
At cell walls GLUT sugar transporters don’t respond just to insulin. They also respond to insulin mimetic proteins. Concavalin A (con A) from legumes, and wheat germ agglutinin (WGA) from wheat are well-studied examples.
GLUT transporters transport glucose into cells. Insulin mimetic proteins do not. They simply clog cell walls, and usurp GLUT transporters which would otherwise be used for transporting glucose.
The blood fills with unused glucose, and elicits higher insulin levels from the pancreas.
Insulin mimetic proteins from commonly ingested starches pose a much greater risk of metabolic disease than the starches themselves.
Great observation, Uncle Roscoe. Would go well on a wheat or legume dangers page.
Oops, I guess I started this discussion by linking to Paul over here around the bottom: http://www.wheatbellyblog.com/2012/05/eat-more-sugar/#comments
@ Uncle Roscoe,
your statement about Vitamin C is inaccurate. Ascorbate is not just an antioxidant, but an essential co-enzyme (the meaning of “vitamin”. gamma-tocopherol, for example, is an antioxidant but not a vitamin; alpha-tocopherol is a vitamin because it is unconditionally required for some still-unknown reason)
Ascorbate is required to synthesise creatine, carnitine, hydroxyproline and other hydroxylated compounds that also rely on (from memory) ketoglutarate and iron.
Some of these compounds are found in meat, which may be one reason why Vit C requirements can go down on carnivorous diets.
However, ascorbate is a sugar that can be fermented by some bacteria, including E. Coli, so that gut infection – or a high-carb diet which increases E. Coli numbers – could reduce availability.
The subject was scurvy, a disease defined by the cell damage done by reactive oxygen species. The hypothesis was that this disease is caused by a shortage of vitamin C. *Via this pathway* vitamin C shortage is not a cause of scurvy in fat adapted people.
You’ve named two ways to accomplish L-conversion with ascorbic acid in the gut, natural bacteria and ingested ascorbic acid. Are there other ways? We don’t know because we’ve mostly studied these ways. Modern medical science exists in a carb-centric culture, and assumes all its victims …..errrr subjects …..to be carb adapted. It’s hard to imagine that carnivorous animals which evolved over millions of years are all deathly ill because they failed to ingest fruit.
Common successful elements among healthy carnivorous human and animal cultures include eating the stomach lumen and abdominal organs of prey animals. I’m not experienced enough to try it. I am experienced enough with fructose, carb opioids, polyphenols and bioflavonoids to steer clear of them. They do make me deathly ill.
Hi Uncle Roscoe,
Scurvy can manifest itself in multiple ways. In my case the major symptom was an inability to form collagen. I had scratch wounds that didn’t heal for six months, and lost weight despite eating 6000 calories a day.
I didn’t have the classic bleeding symptoms however. Perhaps the bleeding only occurs on high-carb diet scurvies.
2 known effects of scurvy – weak collagen (deficiency of hydroxyproline) and fatigue (carnitine deficiency, and likely creatine too) are directly related to ascorbate’s vitamin (co-enzyme) role, not its antioxidant function, which can be covered by uric acid, glutathione, and so on.
This is probably an example of the “triage” system for rationing scarce nutrients. Only if there is adequate ascorbate is it preferred to uric acid for the AO role, even though it is probably superior in this role.
see B below:
http://mcb.berkeley.edu/index.php?option=com_mcbfaculty&name=amesb
Wow! I’ve just discovered your site this week. I have been trying to implement GAPS for the past 8 months. The biggest improvement I’ve experienced has been in my skin… acne has almost totally cleared up. But I now suffer from chronic constipation, bloating, etc. and the WORST symptom is constant tooth ache, my teeth feel constantly shifty and loose, and my front teeth are forming hard, white surfaces near the gums. I kept thinking ‘oh my gosh, it must be that binge on banana the other day!’etc….. blaming every bit of sugar I’ve introduced…but I think I have all the symptoms of no starch diets your site points to…….. super interesting. The weird thing is, of course now I see I should add some starches, but I’m … afraid to, or something. I’ve so carefully and adominantly restricted starches for so long, I have developed some kind of phobia of adding them back in!! …. wish me luck!
Good luck!
“These deficiencies are exacerbated by chronically low insulin levels.”
What level would you consider low? I realize it fluctuates and a blood test is but a snapshot in time…..Trying to interpret a fasting level of 4 uIU/ mL.
Hi Paul,
I’ve been familiar with the first book, and now that your updated version is out, I’ve been revisiting your blog – and what perfect timing! I believe I have developed scurvy. I thought my carb intake was sufficient, but alas, perhaps some infection is eating up my vitamin c. My gums have been bleeding, and I developed a cavity. I’m working on increasing carb intake and increasing vitamin c. I was wondering why you didn’t take higher doses of vitamin c to heal your scurvy. Did you simply take to bowel tolerance? Today I took 15 grams with no problem.
Thank you so much!!! What a lifesaver you are!!!
Alex
Hi Alex,
Glad to hear you figured it out. I had three cavities and lost a lot of weight before I figured mine out.
I should have taken higher doses, if I had known then what I knew now I would have taken it to bowel tolerance until my bowel tolerance started coming down. As it was it took me about a month to become replete.
Dr. Jaminet,
Did you ever consider that the fibers/vegetables you were consuming on an almost ZC diet affected your health thru your gut/gut flora? I notice a difference between eating VLC with a significant amount of fibers/vegetables vs a ZC only animal based diet.
Just my 2 cents. Just bought your new book, have your old one. Merry Christmas to you and your wife!
Dan
Hi Dan,
I don’t see how vegetables, assuming they would cause a dysbiotic flora which I doubt as I had no such symptoms and in the literature common food vegetables aren’t known to produce that result, could have generated my specific set of symptoms, which boiled down to a flare of a pre-existing disseminated fungal infection. Vegetables are usually anti-fungal so I think they probably helped.
Merry Christmas!
Hi Paul,
Two questions..
1) The previous poster said they took 15 grams in one day (possibly in one single bolus?). At what dose, if any, would you be concerned that taking large quantities of vitamin-c would begin to act as a pro-oxidant instead of an anti-oxidant ?
2) Speaking of bowel tolerance, do you have any thoughts about the use of calcium ascorbate (buffered; and about 10% calcium by weight) over regular ascorbic acid ?
thanks
Hi Justin,
In sickness vitamin C needs can be quite high. See http://perfecthealthdiet.com/2010/09/fighting-viral-infections-by-vitamin-c-at-bowel-tolerance/
For a healthy person I think 500 mg to 1 g/day is sufficient. In sickness I think one must experiment, but recovering from illness is more important than oxidative status.
I would not want to get too much calcium, but if the dose you’re taking is low then calcium ascorbate is fine.
I notice you recommend white rice. Why would it be better than brown?
Hi Katie,
Brown rice contains some protein toxins, while white rice lacks toxins after cooking. The nutritional content of rice bran is fairly minimal, so in a balanced diet with other foods providing micronutrition, there’s no nutritional reason to favor brown rice over white rice.
Just a note of curiosity; in Good Calories Bad Calories, Gary Taubes writes about the Inuit (eskimos) who (until recently) consumed nothing but whale and seal meat and blubber–there are no fruits and vegetables in the arctic. At first the anecdotal observations were dismissed as genetic adaptation, although the question of how a homo sapien develop the ability to create ascorbic acid was never answered. Then european researchers spent years living with them and ate their meat and fat diet exclusively, and none had problems with scurvy or any other nutritional deficiency. The conclusion was, in a very simplified way, that a high carbohydrate diet and the consequent metabolic syndrome destroy the vitamin c present in meat and fat.
I’m interested in whether you are familiar with this research, and what your response is.
Thanks,
Steve
Dear Steve,
Keep up the good work.
The Low-Carbohydrate cadre doesn’t talk much about vitamin C except when it suits them. The scurvy question was supposedly answered by an experiment done at New York’s Bellevue Hospital by Stefansson et al in 1926 in which the participants limited their diet to a supposedly Eskimo regime of mostly meat. The Low-Carb people regard this as definitive proof that we can survive without very much vitamin C as found in sweet fruits. Thus we can avoid the “carbs” and not suffer from scurvy if we are prudent in other ways.
http://blog.zeroinginonhealth.com/2009/01/05/bellevue-the-all-meat-trial-part-1/
I determined that Stefansson ultimately died of a stroke at a relatively old age so this cause cannot be laid at the feet of the Bellevue experiment…necessarily. After all, he didn’t die prematurely, did he?
My take is that the condition known as “constitutive inflammation” (Phinney S) is adaptive. There is good evidence that when collagen is not properly constituted, the arteries are compromised and begin to separate. Somatic signaling causes swelling (inflammation) and concurrently brings calcified cholesterol plugs and plaques to the sites to prevent leakage and prolong life. Since L-ascorbate is a known anti-inflammatory, we can extrapolate that strengthening the collagen, reducing the inflammation (histamine: see Clemetson] and closing the gaps with properly constituted muscle tissue will repair the damage and reduce the signaling for calcified cholesterol to zero, thus lowering cholesterol readings. Q.E.D. (Rath M.)
Back to our friends the Inuit. Until quite recently, the People of the North ate mostly raw flesh. Research indicates that they gave the muscle meats to the dogs and shared the rest of the kill out among the band. Nowadays, if they have some income from the government, they can eat what the Explorers ate which is available at the Super-Valu. Almost needless to say, the old standards have gone by the board.
I think Stefansson proved something, though. Namely that caloric restriction (CR) and avoiding processed foods will help one avoid scurvy. The key is oxidative stress. The assimilation of food is described by physiologists as “combustion” which produces free radicals. If a large quantity of food is eaten, a great number of free radicals result and must be quenched lest they damage cells and hence tissues. Limit food (without starvation) and less L-ascorbate will take care of the free radicals handily. More food, more free radical activity and hence more vitamin C is required. You may have noticed that our society works just the opposite way. We eat mountains of food and little (if any) vitamin C. As Irwin Stone explained, vitamin C isn’t a vitamin at all but rather a liver metabolite meant to quench free radicals and build collagen structures in the body. [It does other things too and has help from various sources. —Ed]
http://www.proteomicsresearch.org/showabstract.php?pmid=18502597
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647905/
I have covered a good deal of this material in my book, Slow Suicide, but this is a fair synopsis. I would direct you to the work of Walford R at UCLA and urge you to seek out the photo’s of both his daughter and him online to see what the physiologic results of CR are on the human body. I also direct you to the work of McCarrison R and his followers and to the work of Feinman (sic) R, one of Gary Taubes’ friends and supporters.
Sorry so long, but it’s complicated. I won’t even mention that a surplus of blood glucose will cause cells to incorporate it structurally instead of L-ascorbate and that protein-glucose combinations are implicated in a number of diseases. Oops…
Best of health and just enough wealth,
AL
P.S. If you don’t have time to open and read the links I cite, at least add them to your reading list. Every one is a gem, I guarantee it. AL
Dear Paul Jaminet,
This article has been a lifesaver for me. I very much thank you for publishing this article. I believe the things you have talked about in this article are things many “Paleo” or other health experts have missed and have no idea about.
If you would be so kind as to offer your opinion on a related matter, I would very much appreciate it:
I also began to suffer very similar scurvy symptoms after following a zero carb diet. I was simultaneously trying to do a barefoot walking adaptation. Given my flat feet and pre-existing scurvy symptoms, the activity was too much too soon. I tore a muscle in my foot. This has prevented me from being able to walk without a limp for 8 months. Now I am finally starting to see a faster improvement in recovery by increasing food carbohydrates, selenium and vitamin C. However, I am not yet healed.
How, in your opinion, could I increase the repair even further? This muscle tear has gotten in the way for a long time and ideally I would like to drammatically increase my recovery time. I thought of Vit C megadosing. Do you have any other ideas or anecdotes on faster wound repairing?
Thanks in advance for any help you can give,
Kindest Regards,
Dom S
Hi Dom,
You might try adding vitamin E (mixed tocotrienols) and bone/joint/tendon based soups and stews. Maybe some hot baths.
Ok Paul,
Thanks a lot!
Did you get wrinkles during your scurvy, did it go away with treatment?