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:
Martin,
If you had been here reading longer, you would know that as a rule we don’t count calories from vegetables, since the calorie count is low and gut bacteria and intestinal cells may intercept and consume them. So I will often call a diet whose only plant foods are low-calorie vegetables a zero-carb diet.
The Bellevue experiment found that two healthy men would not get scurvy eating 550 protein calories per day including offal. They were presumably infection free. That is not the situation I am addressing here. Two cases following the diet for only one year does not prove safety for the general population. My scurvy developed after a year on a zero-carb diet. We just did a post on GI cancers appearing in very low-carb dieters after 15-20 years. The Bellevue All-Meat Trial is very interesting but it proves only so much.
Your definition of “normal” insulin is begging the question of what a “normal” diet is.
Are you aware that we are discussing a scurvy I developed 4 years ago, and that there have been significant changes (improvements!) in my diet since then?
Your continued assertions that scurvy is not a vitamin C deficiency are, frankly, ludicrous.
I only read this blog post, nothing more. Maybe I should read more, but based only this post, it’s immediately obvious that you do not speak of the same zero carb diet that I know of. The zero carb diet I know of doesn’t count calories, but plant matter, i.e. none. That you consider your previous diet near zero carb means you don’t count plant matter, only calories. Right there is a fundamental difference in perspective. Yet your post doesn’t try to distinguish between the two, and positively tries to apply to all zero carb diets.
If you don’t count the vegetables you ate, maybe you are implying that they are safe for humans. I don’t know, I’m trying to understand. But consider the fact that you ate them yet you developed scurvy. Maybe they’re not safe for humans after all.
Based on your characterization of the Bellevue trial, it’s obvious that you are not completely aware of its intricacies. Many questions were answered. For example, the question that an all-meat diet is deficient for humans or causes deficiencies. It’s not and it does not.
In fact, the conclusion at the end of one paper says “In these trained subjects, the clinical observations and laboratory studies gave no evidence that any ill effects had occurred from the prolonged use of the exclusive meat diet.”
Note the caveat however “In these trained subjects”. Yet these same subjects were not trained from birth, they were trained when they were fully grown adults. So this is not an effect of habit, but of physiology: Their physiology is able to handle the diet and maintain perfect health all the while. Indeed, their previous habit was extremely hard to break when they were just starting to eat that diet with the natives. But only because of acquired taste, not because of some physical affliction caused by the diet. Their own accounts of more companions not involved in this experiment says that all of them, once the customary acclimation period of 6 month was done, they did just fine on an all-meat diet and would happily return to it without trouble.
This paper is called “CLINICAL CALORIMETRY.
XLV. PROLONGED MEAT DIETS WITH A STUDY OF KIDNEY
FUNCTION AND KETOSIS.” It’s available for free online.
That experiment is the best science on the subject. There is no other of that quality that I know of. There was literally an army of scientists, doctors and all kind of other people involved with it. You say it’s not enough to extrapolate to the population at large yet you extrapolate your own personal experience in the same fashion. You use inference from independent findings not directly related to your experience to support your arguments against a zero carb diet. This trial is direct evidence that a zero carb all-meat diet is completely safe for humans. With the caveat that the diet must be followed properly. The value of this paper far surpasses the value of your personal experience no matter how many other papers you attach to it.
But never mind the intellectual debate. Your post was a result of your health failing. Keep that in mind next time you argue in favor of what you believe. Don’t let your belief get in the way of your health. Or worse, don’t let your belief get in the way of the health of those who buy your book.
Paul, you say that as a species we never survived on only meat. The Bellevue experiment refutes that assertion. The experiment says that we must have lived on a diet exclusively composed of animal flesh at some crux of our evolution at least once, otherwise the trial would have shown deficiencies in short order. This is one such question the experiment was trying to answer.
The logic is that if we had needed plant matter directly to survive, and if there came a time when there was no plant matter to eat but only animal flesh in any form, then we wouldn’t be here right now discussing the subject. Rather, there must have been a time when only those who _could_ survive on an exclusive diet of animal flesh _did_ in fact survive to give us the result we see in the Bellevue experiment. Those who couldn’t, well, they’re history.
If the Inuit contribution to the human genome is so infinitesimal, then we are indeed very lucky to have found two men of such genome for the Bellevue experiment. Not to discount all their companions who also ate an all-meat diet though that wasn’t part of the Bellevue experiment yet is still recorded history.
Martin, is it possible you are confusing tolerated with optimal?
Hi Paul,
Thank you so much for the post. Your timing is unbelievable for me considering I just discovered, completely by accident, that I have probably been Vit C deficient for the past 3 months or so or longer. Being in a similar position as you, I discovered I also had a bacteria infection (probably for the last 10 years!) that I have been treating for the last two weeks, but despite this I was feeling pretty crap. Randomly on the weekend I started taking some good quality Vit C, and two days later I am feeling unbelievable!
I find your assertion that the bacteria infection leads to the deficiency on a low-carb diet really interesting and thanks for posting all the additional information about it. It makes complete sense in my situation. I have been doing a mostly paleo/primal diet with some occasional carbs in the form of rice and sweet potatoe, but still lots of fruit and veg and I was still deficient. I think the bacterial infection has a lot to do with it.
Raymond
Raymond,
Fantastic! I’m glad you’re on the path to health.
Best, Paul
Abby, you mean concerning the Bellevue experiment? I’m not confused. I mean, the scientists, the doctors and everybody else who worked on this experiment couldn’t all have been confused. A few perhaps, but everybody? Bear in mind that at the time, this was a huge deal. People were _dying_ from scurvy, unlike our friend Paul here. The claim was huge: Fresh meat cures scurvy! Naturally, the test was proportional to the claim. Hence the army of scientists and doctors.
The story of scurvy and vitamin C is quite a lesson in stupidity. It’s long but the gist of it is that people believed in spite of the deaths. Even after this experiment, people continued to believe, blind to the facts.
No, I’m not confused. Are you?
Abby, maybe you’re talking about the evolutionary theory? I’m not confused about that either. It’s simple really. Natural selection works by negative selection: Those who die don’t reproduce. This sieving is continuous and permanent. We’ve been sieved many times. We are not the descendants of those who died, obviously. The Bellevue experiment merely outlines one of those times when we were sieved.
Some time during our evolution, at least once, we had to go through a famine whereby the only food available was animal flesh. This famine must have lasted for long enough to span perhaps one generation or more. Those who couldn’t adapt to this limited diet died off. The rest reproduced. It didn’t need to be optimal, it only needed to be different enough that some couldn’t handle it. If this famine lasted for many generations, then the sieving would be thorough across the entire human genome and irreversible. Considering the unequivocal results of the Bellevue experiment, this scenario seems most likely.
A greater understanding of the all-meat diet and scurvy can be found by reading Fat Of The Land (alternate title, Not By Bread Alone) by Vilhjalmur Stefansson, our favorite Arctic explorer. It explains, for example, the nutritional beliefs at the time.
A notable quote which relates to our discussion:
“Specifically it was believed that without vegetables in the diet one would develop scurvy. It was a “known fact” that sailors, miners, and explorers frequently died of scurvy “because they did not have vegetables and fruits””
(quotes in the original text)
And this one:
“Under the present view, the causes of scurvy are wholly dietetic. We find it interesting, therefore, when we go as far back at we can in the literature, say, to the thirteenth century, that we have a constant recurrence of views similar to those of the present. There is the further striking similarity that only now and then are we told by the older writers that fresh meat will cure scurvy, but we are constantly told that fresh vegetables are a cure.”
Inuit/Chuchki are clever, they collect, store and eat tubers and berries in the arctic:
http://pubs.aina.ucalgary.ca/arctic/Arctic6-1-15.pdf
Very interesting Franco!
I’ll add this article (a grad thesis actually) to the mix: http://tinyurl.com/22vh5mk (Vitamin C in the Inuit Diet: Past and Present).
I discovered it a while ago, but had forgotten about it until now. It’s LONG but informative.
Nice one, Lyn!
I found an alternative download here: http://www.acrobatplanet.com/non-fictions-ebook/ebook-vitamin-c-inuit-diet-past-and-present.html
Will read now.
Thanks, Franco and LynMarie! Very interesting!
From Franco’s article: “The recent investigations by Rodahl (1944) and others, of the vitamin content of arctic plants, have demonstrated too, that it is just those arctic plants that are eaten by preference by nearly all arctic tribes, that have the highest content of ascorbic acid as well as of thiamine, and that the methods of preparation and of storing of vegetable foods used by these people are perhaps the best possible in the circumstances for the preservation of vitamins.”
From LynMarie’s: The author, Karen Fediuk, estimates the median vitamin C intake among the Inuit at 30 mg/day, which is enough to prevent scurvy among healthy people, but would be problematic during infections.
Probably the Inuit had very few chronic infections before the arrival of Europeans.
There are plenty of Eskimo tribes who did not consume any fruits or vegetables (many saw vegetable foods as animal food not fit for human consumption).
Regardless, this information, taken with the Belleview experiments and your personal experience, Paul, seem to suggest that we blame chronic infections as the culprit of your scurvy (since you received plenty of vitamin C from your vegetable intake), not low-to-no carbs. There is much anecdotal evidence that Antarctic explorers used fresh meat too to cure and prevent scurvy, too (a mechanism that includes proline and another amino acid, I believe, which are closely linked to vitamin C cycling–would have to look it up again).
So, it seems likely that scurvy is highly unlikely to develop on a low-to-no carb diet, except when a chronic infection is draining the host vitamin C. So, maybe the blame of this thread, regarding scurvy, has been misplaced. Just my two cents.
Hi Poisonguy,
The key point of this post is that vitamin C degradation rates are increased (and therefore intake needs increased) on very low-carb diets, making scurvy more likely and infectious diseases more severe.
Your observations are largely correct. But:
Yes, chronic infections caused my scurvy. But chronic pathogens are all around us, everyone gets multiple infections by age 40.
Infectious disease rates were very low among hunter-gatherer populations, especially isolated populations in cold climates (with few, e.g., mosquitos). Among modern urban populations, they are very high.
A healthy modern diet, therefore, needs to support immunity, maintain resistance to infections, and enable recovery from infectious diseases. It needs to be robust to pathogens and small nutritional deficiencies.
Finally, I doubt very much that the 30 mg/day the Inuit got was optimal for health – thus the great efforts they took to find vitamin C containing plants.
Here’s a medical summary of the House episode featuring scurvy:
http://www.politedissent.com/archives/1369
Paul, look around, there is no such thing as a healthy modern diet. A modern diet is intrinsically unhealthy. It’s a universal observation that traditional diets are healthy while modern diets are unhealthy in comparison.
If anything, a modern diet does not support immunity, but instead attacks it at all angles from the suppression of the immune system, to the addition of inflammatory factors.
Humans don’t have the ability to produce vitamin C. That alone should give us a hint that this particular substance is not critical in great quantities, or at all. There are other substances that replace vitamin C in certain functions like uric acid as an anti-oxidant for example.
That we have lost this ability is indication that at some point in our evolution, keeping this ability was working against our survival and those who kept it died off as a result. We are the descendants of those who’s physiology was better adapted to the conditions that made a high vitamin C production lethal to us. I am reminded again of the all-meat diet. Perhaps this diet, which certainly was our sole diet at some point, is incompatible with a high vitamin C production or even a high vitamin C intake. There is evidence that vitamin C intake of only 1,000mg daily has a significant negative effect on muscle maintenance, i.e. we lose muscle. Accordingly, concurrently to the all-meat diet, we also had to get rid of the high vitamin C production.
This is all theoretical but the facts are there: We can’t produce vitamin C, and vitamin C in any significant quantity prevents normal muscle maintenance, and we can maintain perfect health indefinitely on an all-meat diet.
I’ll grant you that vitamin C may be therapeutic. That is a far cry from calling it essential, or calling scurvy a vitamin C deficiency.
These guys are making bold claims about vitamin C – and back it up with studies!
http://www4.dr-rath-foundation.org/THE_FOUNDATION/About_Dr_Matthias_Rath/scientific_publications.htm
I’m taking my last post and the link contained back!
After some more reading I have to say that guy is “controversial” at best. 😉
You may remove the link, Paul.
Supplementing 500mg of vitamin C during a no-low carb diet (50g of vegetables carbs) led me to another deficience:
After 2 months of supplementation I become anemic having normal-high level of ferritin. Blood test showed very low level of copper, after supplementing copper I was no more anemic.
Hi Kratos,
Very interesting. C and copper are among the crucial supplements we think everyone should take.
Hi Franco,
Unless you insist I’ll leave the link up. Rath was a Linus Pauling collaborator and although most of their ideas didn’t pan out, their work may be interesting to readers.
Hi Paul,
that’s okay with me. I just wanted to make clear that I don’t support most of his ideas.
What he has to say about vitamin C and cardiovascular health made a lot of sense and I still believe it has some merrit but when he went of to the land of conspiracy-theories…
I recently purchased your book, and I’m enjoying reading it. Like some others in this and other threads, I think a distinction should be made between VLC and ZC diets, if only because most people who are interested in these things make such a distinction. Moreover, low-density vegetables do have some impact on postprandial BG levels.
I have read that some children on KD to prevent epileptic seizures are fed large amounts of PUFA, in the form of things like mayonnaise and dressings. This would be expected to have a pro-inflammatory effect and to weaken the immune system, making infection more likely. So again, the problem may not be the absence of dietary carbohydrate, but the addition of PUFA to make up the missing calories.
If VLC or ZC presented a significant risk of scurvy, I think we’d see more evidence of this. Yet many people, myself included, report what might be called “anti-scurvy” outcomes on VLC or ZC. For example, reports of cured or much improved gum disease are fairly common.
Given current trends, people who read diet books–ANY sort of diet books–are likely to be struggling with obesity. People struggling with obesity are likely to have metabolic syndrome to some degree, and impaired glucose tolerance. My guess is therefore that most readers of your book will need to be at the lower end of the carb range, i.e., the 50g end.
Hi Ubizmo,
Those are all good points.
We try in our book to give readers the knowledge to optimize the diet for their personal situations. We do suggest that many people with obesity will benefit from the low-carb ketogenic version of the diet, 50 g / 200 calories per day.
It will be interesting to see if most readers of our book fall into the overweight/obese group. We are hoping to reach a lot of people with chronic health problems, since we think our diet will cure a lot of conditions that medicine doesn’t. Ideally, we’d like to reach healthy people who want to learn how to optimize their health or stay healthy for a long time.
The classic implementations of the ketogenic diet havea lot of problems — malnutrition high among them, and PUFA poisoning as you say — so we have to be careful in examining the problems that appear on ketogenic diets to see whether their cause is exacerbated by low-carbing, or just a result of a nutrient deficiency or food toxicity that would be equally bad with any carb intake.
Your idea that PUFA intake would suppress immunity and increase infection risk is a very good point. I think that’s right.
Best, Paul
Hi Paul,
Expanding on Ubizmo’s remark about distinguishing between VLC and ZC: I think it would be useful to explicitly define what you mean by “zero-carb diet”. This would help to focus the discussion, and to put conclusions and advice into the proper context.
Right now it appears like everyone is discussing the same thing: a “zero-carb diet”. But in reality, without an explicit definition, everyone just replaces that label by their own definition of it. And it is highly unlikely that all definitions match. So the conclusions and advice based on one definition, could very well be inaccurate for another definition.
For example, my personal definition of “zero-carb diet” is simple: any diet without carbs. So this ranges from highly inadequate diets (lots of omega 6 fat, only lean meat) to seemingly adequate diets (Bellevue trial: lean meat, fat, marrow, brain, liver, mostly boiled, some consumed raw).
Given such a broad definition, I tend to disagree with several of your conclusions, simply because they don’t hold up against my definition. And the real irony is that if I knew your definition (instead of having to guess), chances are that I would agree with the conclusions.
So, could you please elaborate a bit on what you mean by “zero-carb diet”, and what you don’t mean by it?
Is it the SAD without carbs? Or Hyperlipid Peter’s diet? Atkins? Protein Power? Some of the Northern Inuit?
John
Hi John,
I’m thinking more along the lines of the Bellevue diet and Charles Washington’s diet: http://blog.zeroinginonhealth.com/.
These are relatively healthy implementations.
However, since few people have been on such diets for long periods of time, and there’s essentially no data on Pubmed on such diets, we have to look at other diets, such as ketogenic diets for epilepsy, the Optimal Diet, Atkins, Inuit diets, and so on for clues.
Then when we see what health problems crop up on these very low-carb diets, we have to try to judge the cause. Was it nutritional inadequacy? Or some problem applicable to all low-carb diets?
Probably I was premature to put concluding thoughts from posts early in the series. It would have been better to present evidence and analysis, and then discuss my conclusions in a “summing up” post.
Best, Paul
Hi Paul,
Thanks for the information. I didn’t know about the Charles Washington diet.
I agree that more studies on the long term effects of such diets would be useful.
At the moment we have one peer reviewed experiment with 2 people, lasting a year. Plus the findings of Stefansson, although I don’t think that most of the Inuit diets he described will appeal to a lot of people.
Most of the other information we have is anecdotal, like Charles Washington being on his zero-carb diet for about 3 years (if I understand correctly, he doesn’t use supplements). I saw Barry Groves mention that Lord Strathcona ate nothing but eggs, milk, and butter. And of course there is the story of Owsley “the Bear” Stanley, who has been eating just meat, eggs, butter and cheese for over 50 years. I do wonder if Stanley’s diet differs a lot from the zero-carb diets that caused problems, and if so, how it differs.
John
Hi John,
There really is a paucity of clinical evidence. Since cow’s milk is almost 40% sugar/carbs, the number of cases is even fewer than you think! Lord Strathcona’s diet wasn’t zero-carb.
Best, Paul
I was reviewing this thread again because I’m about to read a book on the history of scurvy and vitamin C, and I realized I never thanked speno for posting info on the “House” scurvy episode. So thanks; it was much appreciated!
Hi Paul,
What multi-vitamin (mineral) supplement and dosage do you use? And, is there benefit to resveratrol or astaxanthin supplementation?
Thank you,
Robert
Hi Robert,
We use an ordinary supermarket multivitamin, Centrum Silver, but any of the standard ones will do. One a day.
I personally don’t recommend supplementing resveratrol or astaxanthin. Rather I would recommend eating foods, like berries/grapes and salmon/egg yolks.
Supplementing could have benefits, could have harms, we don’t know yet, but I think the odds of benefits are greater and of harms less if you eat the foods.
Coincidentally a review just came out on astaxanthin: http://pmid.us/21089055.
Hi Paul,
What is the connection between your diverticulitis and low carb / vit C deficiency?
I’m asking because I’ve heard of someone recently who developed diverticulitis after being on a paleo diet for a couple of years.
Hi julianne,
Vitamin C is needed to make collagen, which is the main component of the extracellular matrix which is the scaffolding of tissues. No matrix, no cells: the cells can maintain a structure, like a vascular tube or a colon, only if there is a matrix behind them.
In scurvy, the extracellular matrix gradually wastes away, so the walls of the colon and of blood vessels become thin and weak. They can bulge out and diverticulitis develops.
Dear Dr. Paul Jaminet:
I know that it has been half a year since you posted this article, but I recently found a response by Lucas Tafur:
http://www.ketotic.org/2011/03/ketomyths-ii.html
English is not his first language. Apparently biochemistry is! Since biochemistry is not my first language I found it somewhat difficult going to read his article in full, but as I understand it, it looks like there are some mistakes in this article of yours.
It looks like low insulin levels don’t necessarily cause reduced uptake of vitamin C into cells in vivo and a carnivorous ketogenic diet should be expected to provide more than adequate bioavailable selenium, as well as precursors for glutathione, even if a diet of KetoCal (http://www.shsna.com/pages/ketocal.htm ) doesn’t.
See for example http://nutritiondata.self.com/facts/beef-products/3769/2 , which says that a single juicy porterhouse steak has the recommended allowance of bioavailable selenium, as well as liberal doses of methionine, glutamic acid, and glycine, and some cystine.
Are there any other reasons to be concerned about selenium deficiency in a carnivorous very-low-carb or zero-carb diet, aside from comparison to the epileptic KetoCal diet?
Thank you very much.
Regards,
Zooko Wilcox-O’Hearn
Hi Zooko,
I read Lucas’s series when it came out, but it was not an easy set of posts to respond to. I like the fact that he is promoting ketogenic diets, which we recommend as therapeutic for many conditions, and is citing the scientific literature. On the other hand, he misrepresented the point of my posts (which discussed zero-carb dangers, not ketogenic diet dangers – zero-carb being something we oppose, ketogenic diets something we favor) and wrote as if the scientific papers he cited were refuting my posts when in fact they were consistent with it.
If his belief is that in order to be ketogenic diets have to be zero-carb, he is mistaken.
To answer your question, yes, there is increased ROS production on zero-carb diets which increases the need for selenium.
Best, Paul
Hi Paul,
Thanks for sharing this post. I just got shingles after starting a low carb diet a couple months ago. I wonder if I had a vitamin C deficiency that caused my immune system to weaken. Similar to you, I have been eating primarily veggies and no starch and very little fruit.
Mark
This is an important text on your knowledge promoted for years by the drug. Kwasniewski, MD, John! therefore does not refer to the link, and I quote in its entirety.
For the record, I’ve included a few authors biochemistry textbooks, that the only calculating the antioxidants in the body and are protective proteins, glutathione, and resorbed bile pigments, as mentioned many times on this forum!
Apart from these there are still dozens of specific antioxidants (especially vitamins and trace elements), which neutralize radicals generated solely and exclusively in specific areas of metabolism, such as: Vit. C – for the synthesis of collagen.
http://forum.dr-kwasniewski.pl/index.php?topic=3389.msg66881 # msg66881
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Translated from Polish into English
The swallowing of dietary supplements should not be overdone. Antioxidants contained in them can eat cancer cells.
http://www.rp.pl/artykul/351266.html
Wit-and C-o? – That the Spanish impression.
Ladies and Gentlemen,
On training in Spain, I learned that in a brochure posted: Vitamin C enrichment of!
This finding prompted me to write a few words about ascorbic acid (proton donor), because the chemistry shows that the enrichment of a base (proton acceptor).
Vitamin C as a “odkwaszacz” and “antioxidant” – a look biochemist.
http://forum.dr-kwasniewski.pl/index.php?topic=3313.msg53894 # msg53894
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Bilirubin and glutathione have antioxidant and cytoprotective’s complementary roles
http://www.pnas.org/content/early/2009/03/12/0813132106.abstract
Antioxidant capacity contributes to protection of ketone Bodies against Oxidative damage induced hypoglycemic During Conditions.
http://www.ncbi.nlm.nih.gov/pubmed/18339375
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Supplied in the diet, glutathione is always spread across prime factors – glutamic acid, cysteine ??and glycine – that is digesting!.
And if there is no dietary glutathione is glutamic acid formed from ketoglutarate, a-ketoglutarate is always available, because it is an intermediate metabolite of the Krebs cycle, and cysteine ??and glycine are amino acids always found in the valuable protein food!, So what is the problem with the synthesis of glutathione!. Well, no such numbers!, Because even after you send it to the pharmacy Coin-cell glutathione!
Well, unless anything to them … For example: x five fruits and vegetables!.
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Question:
I wonder what is the glucose produced in Gluconeogenesis Starvation?.
Answer:
mainly to support two vital routes.
Mention:
a) trail pentozo (phosphate)
b) glucuronic acid pathway.
The first maintains the integrity of cell membranes by maintaining an appropriate amount of reduced glutathione, and the other cleanses the body of poisons g?odówkowych
And what is the glutathione?.
And this is a tripeptide formed from Glu, Cys and Gly. With Sulfuric bridge connects with the other particles of active glutathione (oxidized form) or by joining the sulfur proton – reduced form. Thanks to this property glutathione is one of the key relationships governing the oxy-redox state of cells!, Amino acids are actively transported across the cell membrane and strongly detoxifies peroxides.
The latter is very important not only in fasting!.
And so, on the water are created all the particles are necessary for life – until exhaustion “magazine.”
And the water had to be “magazine supplement on an ongoing basis, because its molecule converts fumarate to malate, and is not recovered after this!
On the occasion to remind that the DNA helix rozplecenie takes 10-6 s, and synthesis of molecules of most proteins takes about a second! – It’s just for awareness of some of the intensity of metabolism!
Route pentozowy in hunger “lost” its main function (in addition to the synthesis of pentoses needed to run … genes in the “sickness”) – the production of NADPH, needed to convert glucose into fat, which in higher organisms (those that can not convert acetyl- CoA to pyruvate) is the primary energy substrate, a carbohydrate is used mainly as a buffer for the deacidification of the body for exertion stress
http://forum.dr-kwasniewski.pl/index.php?topic=2269.msg34389 # msg34389
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I recall that the salts of cholesterol is one of the best antioxidant glutathione side!
As far as receptors go, there are also GLUT2 and GLUT10.
GLUT2 has highest afinity to DHAA (from what I know its afinity to C is higher then to Glucose) and is thought to be evolutional adapatation of RBC to loss of C synthesis since primates are only mamals that expose GLUT2 on RBCs. Since cells push ascorbate back to the blood, this probably influences blood levels of AA quite a lot. GLUT10 is recently discovered to have a role in sceletal muscle ascorbate utilisation.
GLUT4, the main transporter of DHAA can be downregulated by numerious factors – insuline resistance, lack of resources, glucose competition and so on. It looks like liposomal variant is hence the best form to be taken (surrogate of which could be created at home as it is pretty expensive) as it doesn’t depend on transporters but on endocitosis. It also protects C in harsh gut environment. The form used should be sodium ascorbate to avoid blood acidosis.
Since insuline is mandatory for absorption of DHAA form of ascorbate and glucose competes with it, its the best to use non liposomal forms of C with protein meals as those will also rise insuline levels (depending on amino acid content) without rising glucose blood levels.
One potential problem with protein + C might be iron in man. Since C boosts iron absoroption and red meat is full of iron, if your diet is composed primarly of that combination (and or spinach, neetle etc…) you might get high iron levels and evidence shows that it can promote infections and joint problems. By switching to low carb with lots of meat and 8g/day of C my iron levels doubled, although they were sitll within normal range. Now I avoid C after red meat and use coffie/IP6 instead to chelated iron.
Bioflavonoids are shown to both inhibit and boost C absorption so I am not sure about benefit (this includes plant sources) but its probably OK to take them together. So I don’t think that lowcarb diet is primary cause of C deficiency, but inadequate lowcarb diet and inadequate supplementation. There isn’t much C in plants anyway as plants depend on celulose for structural support, not collagen.
As for selenium, I would suggest 1-4 Brazil nuts per day providing more of Se then supplements, some little radiation in the form of Boron (which is good as of hormesis) and substantial amount of saturated fat.
Good supplements to take in combination with C are Mg, E, ACC, ALA.
As for scurvy, it seems that speed it develops, or its occurance at all depends on several factgors including microbiota. Bifidobacteria can produce some small amounts of C if one has healthy gut flora. Its not enough but little is needed to prevent clinical scurvy.
IMO, the best way to take C is according to dynamic flow hypothesis. In short, its frequency that is important, not the dose. 4x2g per day seems like a good dose in maintance. In stress, the dose is larger, and it depends on BT. It can be as high as 100g/day for common viruses.
If you are interested in references, I can dig them up for every claim up there but I really hate to that since there are lot of claims up there and my time is limited so choose what interests you the most.
Also, probably the most important thing to notice is that C is unlike other vitamins in that it is often destroyed in the chemical processes it acts as a substrate.
2 James
“I vaguely remember hearing that scurvy was almost non-existent in the inuit, so I don’t think it is low carb per se.”
AFAIK, Inut often eat eyes of animals which are the greatest source of C aside of adrenal glands. Apart from that, many native communities eat animal organs. For instance, indians were consuming adrenal glands recognising that there is something curative in them.
2 Levac
“There is evidence that vitamin C intake of only 1,000mg daily has a significant negative effect on muscle maintenance, i.e. we lose muscle.”
This evidence is scarse and almost non existant. Its part of “antioxidants are bad” theory. I searched a lot about it and couldn’t find anything conclusive. Also, most bodybuilding supplements contain large doses of C (>=1g) along with coctails of other oxidants and it doesn’t seem to make a problem.
“We can’t produce vitamin C, and vitamin C in any significant quantity prevents normal muscle maintenance, and we can maintain perfect health indefinitely on an all-meat diet.”
Genetic defects are not uniformly present in entire population. Some people are shown to be capable of producing Vitamin C.
“That is a far cry from calling it essential, or calling scurvy a vitamin C deficiency.”
Scurvy is final stage of C deficiency. The name of VItamin C – “Ascorbate” – is derived from its property to cure scruvy (anti scorbutic factor = ascorbate). Subclinical or localised forms of deficiency are visible before final metldown – artheorosclerosis, paradenthosis, joint problems, immunity problems, hypertension etc.
Hi majkinetor,
Thanks. What’s ACC? Did you mean ALC for acetyl-l-carnitine?
ACC is ACetyl L Cysteine [also abbreviated as NAC]
ALC is sometimes took along as they seem to have synergistic influence on each other. There is caution on lef site :
When taking N-acetyl-cysteine it is recommended that two to three times as much vitamin C be taken at the same time. Failure to do so may result in more harm than good from taking this product because of the prolonged presence of the oxidized form of L-cysteine.
http://www.lef.org/Vitamins-Supplements/Item00314/Mega-L-Glutathione.html
I don’t know if that is true and couldn’t find any scientific reference, but that is often repeated here and there … I would appreciate any more info.
The biggest question for me is ALA.
Alpha lipoic acid is very effective when used in addition to vitamin C.
I fell for the story of the Andy Cuttler that ALA’s chelating properties could be dangerous for specific category of people and he doesn’t advise to use it if you have amalgams. Since ALA is one of the best known antioxidants with tremendous health benefits (which is the reason why it is used with [diabetic] neuropathy) and it has well defined synergistic behavior with C, I started to replace all my amalgam fillings in order to be able to use it in the future.
You can read the problem here:
http://onibasu.com/archives/am/259260.html
Hi majkinetor,
with regards to your comment on ALA & amalgams;
are you saying that you did not need to replace your amalgam fillings?
Hi Darrin
No, I am saying that I am afraid to take ALA with amalgam in my mouth. I am in the process of replacing them with composite fillings. I don’t have any particular reason to use ALA so far, but I would like to have that option in the future.
I don’t know if Cuttler is right, he is certainly qualified to have opinion on this and altho I am not chemist, his reasoning is compiling to me. Other mercury toxicity experts don’t agree with Cuttler on the other hand. I know people who have amalgams and use ALA without any perceivable problems. Probably the reason is that not everybody have obvious symptoms from amalgam and other mercury exposure – there are for instance sex related differences, its probable that testosterone makes toxicity worst.
I think that I have problems with such toxins, even chlorine in water makes my skin itchy and dry so I don’t want to risk it. Also, USA recently started phase down of amalgam fillings which will speed up production of new safer materials in dentistry in entire world.
I made a mistake above. I wrote that RBCs use GLUT2 for AA transport while it is GLUT1. The relevant research is:
Erythrocyte Glut1 Triggers Dehydroascorbic Acid Uptake in Mammals Unable to Synthesize Vitamin C
thanks majkinetor,
found this over at the Mercola web site;
http://articles.mercola.com/sites/articles/archive/2007/09/25/this-common-antioxidant-supplement-could-cause-you-loads-of-trouble.aspx
“Glutathione, along with vitamin E, vitamin C and alpha lipoic acid are the basic antioxidants. Some nutritional authorities recommend you take it as a supplement, or take an NAC supplement. There are problems with both. First, the form of glutathione that works best is the reduced form, which is very difficult to absorb orally. Secondly, I advise against using NAC if you still have mercury amalgam fillings because it could interfere with the detoxification of the mercury.”
so he seems to be saying that he thinks ALA is okay, but to avoid NAC if you have amalgam fillings.
The study reported is on mice with ridiculously high doses of NAC.
NAC should be taken on first sign of disease, IMO.
I experience no bad efects with 1-2 g doses with several days usage. Bodybuilding supplements have large doses and are taken on daily basis.
I wouldn’t bet on Mercola’s opinion on ALA. Cuttler is more qualified (doesn’t mean he is right tho, but I don’t see why wouldn’t I replace amalgam, especially since recent phase down in USA). Also, regarding to supplements, Mercola has conflict of interest.
Hmm… after reading the text Insulin – understanding its action in health and disease, covered already in the blog, it looks like your recycling limitation of vitamin C can no longer be explained by lower levels of insulin – authors state that the main action of insulin is inhibition of liver glucose production which leads to drop of glucose in the blood and reduced peripheral tissue uptake. They claim that higher absorption is related to ‘mass effect’ of glucose and that base number of GLUT receptor is adequate for normal metabolic functions (demonstrated by MIRKO mouse model). This means that graphic you posted above about insulin dependent DHAA uptake should explained not by insulin action on transporters but on glucose drop in blood stream which makes probability of DHAA to bind to the same receptor higher.
So, lower CHO intake leading to lower insulin levels lead to higher ascorbate recycling, not the opposite.
What do you think ?
Hi majkinetor,
I don’t agree.
Lower CHO intake doesn’t lower blood glucose levels; at the low intakes we’re talking about it raises them. Zero-carb dieters often have fasting glucose levels around 100 mg/dl, whereas 400 calorie/day carb dieters tend to be in the 80s.
So there’s no lessened competition for receptors upon reducing carb intake from 400 calories/day to 0 calories/day; rather the opposite.
Insulin has many functions and one of them is inhibition of liver glucose production but another is DHAA transport. So insulin does assist C recycling.
So it looks to me like you’ve got considerably more C recycling at 400 carb calories/day than at 0 carb calories/day.