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Iodine and Hashimoto’s Thyroiditis, Part I

Posted by on May 24, 2011 239 comments

Mario Renato Iwakura is a Brazilian engineer and Hashimoto’s thyroiditis patient who is intimately familiar with the hypothyroidism literature. Mario has graciously agreed to do a guest series on the place of iodine and selenium supplementation in treatment of hypothyroid disorders. I’m very excited to have Mario’s thoughts, as he’s extremely smart and passionately engaged with the science. — Paul

Most doctors believe that iodine supplementation will aggravate autoimmune (Hashimoto’s) thyroiditis. This view is supported by observations that the incidence of Hashimoto’s hypothyroidism tends to increase in populations that increase their iodine intake. (The incidence of hyperthyroidism, on the other hand, increases as iodine intake decreases.). However not all epidemiological studies support this association [1][2][3][4].

Dr. Datis Kharrazian (“Dr. K”), whose 2010 book “Why Do I Still Have Thyroid Symptoms?”[5] is popular among Hashimoto’s patients, vehemently opposes the use of iodine in Hashimoto’s [5][6][7]. Chris Kresser of The Healthy Skeptic [8] has argued this point of view in his post “Iodine for hypothyroidism: like gasoline on a fire?”. And there’s little doubt that some patients have experienced bad consequences from high-dose iodine.

On the other side, doctors such as Dr. Guy E. Abraham [9], Dr. David Brownstein [10], Jorge D. Flechas [11] and Dr. David Derry [12] have claimed success prescribing high doses of iodine for Hashimoto’s and for breast and thyroid cancers.

Can these experiences by reconciled? What we will try to do is demonstrate that iodine acts synergistically with selenium, and that it is imbalances between the two that damage the thyroid.

First, Some Background

Thyroid peroxidase or thyroperoxidase (TPO) is an enzyme expressed mainly in the thyroid that liberates iodine for addition onto tyrosine residues on thyroglobulin (TG) for the production of the thyroid hormones thyroxine (T4) or triiodothyronine (T3).

The human body normally has low levels of auto-antibodies against both TG and TPO, which serve some physiological function. Autoimmune thyroiditis features high levels of these auto-antibodies, leading to immune attacks on the thyroid.

High levels of  thyroid auto-antibodies are positively associated with hypothyroidism symptoms [13][14]. TPO antibodies and TSH levels are strongly associated with progression of subclinical hypothyroidism to overt hypothyroidism [3], as can be see in Table 3 below:

Selenium Can Cure An Iodine Excess

Dr. K said in his book and site that “iodine stimulates the production and activity of the thyroid peroxidase (TPO) enzyme” [5][7]. Since TPO is a target of autoimmune attack in Hashimoto’s patients, this might worsen the disease [5][6][7]. In his book he also states that excessive iodine will shut down TPO activity [5], but he neither cites a reference nor states what level of iodine intake will cause this to happen.

In fact, excess iodine combined with selenium insufficiency will reduce (not increase, not shut down) TPO activity [15]. Let’s look at a study that had seven groups: normal iodine and lab-chow selenium only (NI), excess iodine and lab-chow selenium only (EI), and five groups with excess iodine and steadily increasing levels of selenium added to water (IS1 to IS5). TPO activity was reduced by excess iodine (EI), but returned to control levels (NI) with moderate selenium (IS1 and IS2). With excess iodine and excessive selenium (IS3 to IS5), TPO activity was also decreased, as we can see from table 2 below.

Some other studies have also demonstrated this reduced TPO activity at high iodine intakes [23][24].

This study [15] also showed a picture (fig. 1) of thyroid follicles from rats receiving normal iodine diet (NI), excessive iodine (EI) and excessive iodine plus 0.2 mg/L selenium (IS2). Thyroid follicles from the excessive iodine group (EI) are enlarged, a characteristic of goiter. But, there is virtually no difference between the first and last picture! If selenium and iodine are increased together, no goiter occurred.

Note that the IS2 level of selenium, which protects against iodine toxicity, corresponds in a person who drinks 1-2 liters per day to a selenium dose of 200 to 400 mcg per day – which happens to be the Perfect Health Diet “plateau range” for selenium.

Selenium Can Cure Autoimmunity

Another paper, also from China, looked at the effects of selenium in an animal model of iodine induced autoimmune thyroiditis [16].

There were three groups of mice, a healthy control group, and groups with iodine induced autoimmune thyroiditis without (AIT) and with (AIT+Se) selenium. The AIT+Se group was given high iodine (AIT only) for 8 weeks to induce the disease, and then, for 8 weeks more, they were given iodine plus selenium. After 8 weeks of selenium supplementation their thyroid follicles were almost fully recovered, as we can see below, even though high-dose iodine had continued:

The AIT group has enlarged cells characteristic of goiter and dead tissue; the AIT-Se group thyroid section resembles a normal thyroid. Thyroid weight doubled in the AIT group, proof of goiter, but returned to normal after selenium supplementation.

Before selenium was given to the AIT+Se group, serum TgAb antibodies were elevated, but they returned to normal after selenium supplementation:

An interesting aspect of this study was the changing population of immune cells. A specialized subpopulation of T cells, negative regulatory T cells or Tregs, helps establish and maintain self-tolerance by suppressing response to self-antigens and suppressing excessive immune responses deleterious to the host. Deficits in Treg cell numbers or function lead to autoimmune diseases [17].

In this study, CD4+CD25+Foxp3+ Treg Cells were reduced by high iodine, but returned much of the way toward normal after 8 weeks of selenium even though high iodine intake continued. The implication is that selenium-iodine balance may be needed to maintain proper Treg cell populations, and that selenium supplementation may restore normal regulation of autoimmunity.

The researchers concluded:

“In the present study, we observed that Se supplementation increased the frequency  of CD4+CD25+Foxp3+ T cells and enhanced expression of Foxp3 in vivo. These changes were accompanied by suppressed TgAb titers and reduced thyroiditis. Thus the benefit of Se treatment may be due to the increase of CD4+CD25+ regulatory T cells.”

Under What Circumstances Does Excess Iodine Induce Autoimmunity?

In the previous study high doses of iodine were used to induce autoimmune thyroiditis. Let’s look more closely into the circumstances in which that happens.

It’s often said that excessive iodine in Hashimoto’s triggers an immune response characterized by proliferation of T lymphocytes, a disrupted Th1/Th2 axis, and altered CD4/CD8 levels. Pathogenesis of autoimmune disease is believed to begin with the activation of T cell autoaggression (turning them into “allergized T cells”).

Our next study, also from China, showed that excess iodine can indeed cause such an autoimmune pathology, but only if there is a deficiency in selenium [18].

Mice in 5 groups were orally administrated different combinations of iodine and selenium for 30 days. Four groups had no selenium but varying amounts of iodine in their water:  0 μg/L (group I), 1500 μg/L (group II), 3000 μg/L (group III), and 6000 μg/L (group IV). The fifth group had 6000 μg/L iodine plus 0.3 mg/L selenium (group V).

In Group IV, high-dose iodine at 6000 μg/L caused a proliferation of lymphocytes. But this was completely abolished by the addition of selenium to water in Group V:

Normally there are relatively stable population of T cells and their subgroups in tissue till immune function is in disorder. As we can see from Fig. 1, increasing iodine increased T lymphocytic reproductive activity, and was clearly high in group IV. But group V, which also received selenium, had the same values as the control group (I).

Subjects with Hashimoto’s also have a lower ratio of CD4+ to CD8+ lymphocytes than controls [19][20]. From fig. 2, we can see that iodine supplementation in groups II and III actually increased the CD4+ to CD8+ ratio, until the onset of autoimmune symptoms at very high doses in Group IV when the ratio decreased. However, group V, which had the highest iodine intake but with selenium as well, had the highest CD4+ to CD8+ ratio of all groups.  This suggests that high-dose iodine and selenium together may actually diminish the autoimmune syndrome compared to the low levels in the controls.

Another marker of autoimmune thyroiditis is the relative strength of the Th1 and Th2 responses, as indicated by the markers interferon-gamma and interleukin-4 (Th2). Th1(IFN-γ)/Th2(IL-4) ratios are increased in Hashimoto patients [21][22], and related with severity of Hashimoto’s disease [22].

As we can see from Fig. 3, the group with the highest iodine intake but no selenium (IV) was the only group that had clearly higher Th1/Th2 ratio. High iodine plus selenium in group V had similar Th1/Th2 ratios than control group (I).

The researchers concluded:

“The results revealed that there was no significant difference in the immunotoxicity between interventional group (group V) and control group (group I), indicating that adequate selenium has a favorable interventional effect on excessive iodine intake.”

Conclusion

Excess iodine intake can cause an autoimmune thyroiditis that bears all the characteristics of Hashimoto’s. However, in animal studies this occurs only if selenium is deficient or in excess. Similarly, in animal studies very high iodine intake can exacerbate a pre-existing autoimmune thyroiditis, but only if selenium is deficient or in excess.

With optimal selenium status, thyroid follicles are healthy, goiter is eliminated, and autoimmune markers like Th1/Th2 ratio and CD4+/CD8+ ratio are normalized over a wide range of iodine intake. It seems that optimizing selenium intake provides powerful protection against autoimmune thyroid disease, and provides tolerance of a wide range of iodine intakes.

In the next post in this series (Iodine and Hashimoto’s Thyroiditis, Part 2, May 26, 2011), we’ll transition from animals to humans. Does epidemiological evidence suggest that these animal findings are transferable to humans?

References:

[1] F. Aghini-Lombardi et al. The spectrum of thyroid disorders in an iodine-deficient community: the Pescopagano Survey. J. Clin. Endocrinol. Metab. 84, 561–566 (1999). http://pmid.us/10022416.

[2] Marino MA et al. Urinary iodine in patients with auto-immune thyroid disorders in Santo André, SP, is comparable to normal controls and has been steady for the last 10 years. Arq Bras Endocrinol Metabol. 2009 Feb;53(1):55-63. http://pmid.us/19347186.

[3] Strieder TG et al. Prediction of progression to overt hypothyroidism or hyperthyroidism in female relatives of patients with autoimmune thyroid disease using the Thyroid Events Amsterdam (THEA) score. Arch Intern Med. 2008 Aug 11;168(15):1657-63. http://pmid.us/18695079.

[4] Stuckey BG et al. Low urinary iodine postpartum is associated with hypothyroid postpartum thyroid dysfunction and predicts long-term hypothyroidism. Clin Endocrinol (Oxf). 2011 May;74(5):631-5. doi: 10.1111/j.1365-2265.2011.03978.x. http://pmid.us/21470286.

[5] Dr. Datis  Kharrazian. Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal: A Revolutionary Breakthrough In Understanding Hashimoto’s Disease and Hypothyroidism.

[6] Dr. Datis  Kharrazian. Iodine and Autoimmune Thyroid — References. http://drknews.com/some-studies-on-iodine-and-autoimmune-thyroid-disease/.

[7] Dr. Datis  Kharrazian. Iodine and Hashimoto’s. http://drknews.com/iodine-and-hashimotos/.

[8] Chris Kresser. Iodine for hypothyroidism: like gasoline on a fire?. http://thehealthyskeptic.org/iodine-for-hypothyroidism-like-gasoline-on-a-fire.

[9] Dr. Guy E. Abraham. http://www.optimox.com/.

[10] Dr. Brownstein. Iodine, Why You Need It. https://www.drbrownstein.com/homePage.php.

[11] Dr. Jorge D. Flechas. http://cypress.he.net/~bigmacnc/drflechas/index.htm.

[12] Dr. David Derry. Breast Cancer and Iodine : How to Prevent and How to Survive Breast Cancer.

[13] Ott J et al. Hashimoto’s thyroiditis affects symptom load and quality of life unrelated to hypothyroidism: a prospective case-control study in women undergoing thyroidectomy for benign goiter. Thyroid. 2011 Feb;21(2):161-7. Epub 2010 Dec 27. http://pmid.us/21186954.

[14] Díez JJ, Iglesias P. Relationship between thyrotropin and body mass index in euthyroid subjects. Exp Clin Endocrinol Diabetes. 2011 Mar;119(3):144-50. Epub 2010 Nov 17. http://pmid.us/21086247.

[15] Xu J et al. Supplemental Selenium Alleviates the Toxic Effects of Excessive Iodine on Thyroid. Biol Trace Elem Res. 2010 Jun 2. http://pmid.us/20517655.

[16] Xue H et al. Selenium upregulates CD4(+)CD25(+) regulatory T cells in iodine-induced autoimmune thyroiditis model of NOD.H-2(h4) mice. Endocr J. 2010 Jul 30;57(7):595-601. Epub 2010 Apr 27. http://pmid.us/20453397.

[17] Sakaguchi S et al. Foxp3+CD25+CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol Rev. 2006 Aug;212:8-27. http://pmid.us/16903903.

[18] Chen X et al. Effect of excessive iodine on immune function of lymphocytes and intervention with selenium. J Huazhong Univ Sci Technolog Med Sci. 2007 Aug;27(4):422-5. http://pmid.us/17828501.

[19] Gopalakrishnan S et al. The role of T-lymphocyte subsets and interleukin-5 blood levels among Indian subjects with autoimmune thyroid disease. Hormones (Athens). 2010 Jan-Mar;9(1):76-81. http://pmid.us/20363725.

[20] Zeppa P et al. Flow cytometry phenotypization of thyroidal lymphoid infiltrate and functional status in Hashimoto’s thyroiditis. Anal Quant Cytol Histol. 2006 Jun;28(3):148-56. http://pmid.us/16786724.

[21] Colin IM et al. Functional lymphocyte subset assessment of the Th1/Th2 profile in patients with autoimmune thyroiditis by flowcytometric analysis of peripheral lymphocytes. J Biol Regul Homeost Agents. 2004 Jan-Mar;18(1):72-6. http://pmid.us/15323363.

[22] Nanba T et al. Increases of the Th1/Th2 cell ratio in severe Hashimoto’s disease and in the proportion of Th17 cells in intractable Graves’ disease. Thyroid. 2009 May;19(5):495-501. http://pmid.us/19415997.

[23] Müller K et al. Effect of iodine on early stage thyroid autonomy. Genomics. 2011 Feb;97(2):94-100. http://pmid.us/21035537.

[24] Man N et al. Long-term effects of high iodine intake: inhibition of thyroid iodine uptake and organification in Wistar rats. Zhonghua Yi Xue Za Zhi. 2006 Dec 26;86(48):3420-4. http://pmid.us/17313856.

Chicken Tikka Masala

Posted by on May 22, 2011 13 comments

Chicken Tikka Masala is chicken tikka, or chicken chunks marinated in spices and yogurt and roasted or baked in a tandoor oven, and served in a masala (mixed spices) sauce. It is so popular in Britain that the British Foreign Secretary once called it “a true British national dish”. Some think it may even have been invented in London.

There are many ways to make it, and traditional Indian cooking methods are quite time-consuming; they may involve grinding the spices on the day of cooking for freshness, and long cooking to produce very tender meats.

We chose to make it in the quickest possible way. Here’s our approach to Chicken Tikka Masala.

Ingredients

Here are the main spices we used:

In the center is a masala curry powder that we bought from a local Indian shop. Unfortunately we no longer know the ingredients, but we would expect it to contain cumin, pepper, cloves, cardamom, and coriander among other spices.

Clockwise from upper left are jalapeno peppers, ginger root, garlic, onion, parsley, paprika, turmeric, and xylitol which we included for a bit of sweetness. Quantities were 1 tbsp of each spice and 1 tsp of the xylitol.

We also diced 3 large tomatoes (weighing about 1.5 pound) and a chicken breast into bite-sized pieces:

Preparing the sauce

We melted some beef tallow in a wok and stir-fried the pepper, onion, ginger, and garlic for 5 minutes to bring out some of the flavor:

The ginger and garlic should be minced finely. After 5 minutes we added all the spices:

After another 2 minutes we added the tomato and cooked for 15 minutes:

Then we transferred the cooked sauce to a food processor and pureed it:

In another wok, while the sauce was cooking, we browned the chicken pieces in olive oil:

Once the chicken was browned, but well before it was cooked through, we added the pureed sauce and parsley:

Cook the chicken in the sauce for 15 minutes, and then add some Greek yogurt:

That’s it — it took us about 40 minutes. Serve it over rice:

Conclusion

The sauce was delicious! We kept some extra and tried it over salmon — it was even better with the salmon.

Around the Web; It’s Anthropology Week!

Posted by on May 21, 2011 44 comments

Here’s what caught my eye this week:

[1] Interesting posts this week: Paleo Pepper has compiled an online encyclopedia: the top 120 Paleo blog posts. Richard Nikoley asks: is optimality in diet a fool’s errand? He takes the view that individuals have an optimum, but not humanity. Via Seth Roberts, a fascinating story of how even doctors cannot get good care out of today’s medical system: How modern medicine killed my brother.

Also from Seth, his “morning faces therapy” has produced a great result for a man with bipolar disorder. We believe that “circadian rhythm therapies,” and bio-rhythm restoring techniques generally, are an underappreciated therapy. See, for instance, Intermittent Fasting as a Therapy for Hypothyroidism (Dec 1, 2010) and Seth Roberts and Circadian Therapy (Mar 22, 2011).

Emily Deans offers up a surprising danger of smoking pot – fungal infections of the lung:

[S]moked joints could easily be adulterated with natural fungi that grow into big nasty (and deadly) fungus balls in the lung.  I saw a case of this fungus ball in medical school in a patient immunosuppresed with HIV who also happened to smoke a lot of pot.  It could have been from other sources, of course, but my attendings assured me they had seen it several times in AIDS patients who were heavy pot users.  It’s not a pleasant way to go, and the treatments are horrible.

In a more controversial post, Emily argues that greater dopamine in the male brain creates “Genius and Madness,” while the lower dopamine feminine brain promotes sociability and social stability. But I wonder if a world led by “Generation XX” is really going to be more stable.

Mark’s Daily Apple notes that city living can be a brain drain. It certainly is for Shou-Ching and I; our nightmare would be living in New York City. Curiously I didn’t have the same sense of oppression in Tokyo, a much more open city. Boston is better than New York but we would prefer the country.

Robert Krulwich discusses the “loneliest plant in the world”: a male tree that can’t find a mate, as it is the only known surviving member of its species. Scientific American discusses how gut bacteria shape the brain. Chris Kresser suggests ways to keep your brain from aging.

Finally, if you’ve never seen a deer eat a bird, and would like to, Bix has you covered.

[2] Music to read exercise by:

The video can’t be embedded but is great. I wonder if the gymnastics were influenced by Parkour?

[3] My Favorite Posts This Week: The best posts this week were by Melissa McEwen of Hunt Gather Love, who has been running a series on “The Human Colon in Evolution.” All posts are great – I loved today’s (part 5) because it was new to me, and part 4 because it argues our “safe starches” are great foods for the gut – but they’re all outstanding:

[4] Human origins elucidated:

An important paper on human origins came out this week. “A Revised Root for the Human Y Chromosomal Phylogenetic Tree: The Origin of Patrilineal Diversity in Africa” used Y-chromosomes to trace the male “Adam” back to 142,000 years ago and northwest Africa, in what is now the Sahara but was then an open woodland environment. This is significant for many reasons, but one is that this region had easy communications with the Middle East along the Mediterranean coast and supports the possibility that interbreeding between Neanderthals and Africans, with significant back-migration into Africa proper, may have been an important process in the evolution of modern humans. Dienekes (here and here) and Razib Khan comment.

JS Stanton at gnolls.org had a nice essay. I don’t agree with everything in it; in particular, JS underestimates the violence of Paleolithic society. The work of Lawrence Keeley is helpful in this regard:

In browsing the comments to JS’s post I saw a link to a weird book by Danny Vendramini called Them and Us. A video by the author presents his case: Neanderthals were chimp-like super-predators and predation and rape by Neanderthals killed all the dumb humans, until the smarter humans figured out how to kill all the Neanderthals. Here’s how Vendramini imagines the Neanderthals:

There is plenty of evidence indicating that this view of the Neanderthals is wrong. I will just note that the fraction of Neanderthal genes in present-day humans is of the same order of magnitude as the level of mixing African-Americans and European-Americans have achieved in 200 years – this despite 30,000 years of selection which will have tended to work against survival of most Neanderthal genes. The idea that such extensive mixing came about through rape conducted by radically different species in perpetual warfare is, I think, totally untenable. There must have been extensive voluntary interbreeding.

Curiously, the Vendramini view recapitulates one of the earliest hypotheses about Neanderthals. This talk by Carl Zimmer shows that (at 2:40) in 1909 leading anthropologists shared Vendramini’s view of the Neanderthals, whereas today they seem — ahem — considerably more attractive:

[5] We’re glad it’s helping! Chris Kresser on Twitter:

I’ve been having some success w/modified ketogenic diet a la Paul Jaminet w/50g CHO, 6 TBS MCT oil 5g leucine.

This method of producing ketosis is much healthier than the zero-carb low-protein diets sometimes used.

UPDATE: It’s mood disorders generally, and depression specifically, that the ketogenic diet has been helping with.

[6] More on Food Deserts: Beth Mazur of Weight Maven has written of the significance of “food deserts” in the obesity epidemic. Basically, where fresh whole foods are difficult to buy, obesity rates are high.

Now the USDA has a cool interactive map showing the locations of food deserts:

Via Razib Khan

[7] Did monkeys keep pets?:

Via Yves Smith.

[8] Our book on sale: I know of at least one store that offers our book for sale: The Grainery in Baraboo, Wisconsin. Their web site has a great line from Thomas Edison:

“The doctors of the future will give no medicine , but intrest their patients in care of the human frame, diet and the cause and prevention of disease.” — Thomas A. Edison

The proprietor of The Grainery, John Kessenich, spoke recently on “Eating for Perfect Health” and might have used some of our ideas. If you happen to find yourself in Baraboo, check out The Grainery and ask John for health tips!

[9] Why the Kindle version isn’t available: I have too much brain.

[10] Primal Fashion Week: No, this is definitely not Paleo re-enactment. I doubt Neanderthal women ever wore a Sperm Coat or paired it with a Heart Tube Hat.

Personally I would prefer a cheetah skin.

[11] Low-dose naltrexone is great for Crohn’s: On my editorial calendar is a discussion of the role of endorphins and enkephalins in immunity, and the opportunity to increase their levels and circadian variability and thus modulate immunity through low-dose naltrexone (LDN), with beneficial effects against certain diseases.

While I dither, clinical studies of LDN are progressing. This week, a report came out on LDN for Crohn’s disease:

Eighty-eight percent of those treated with naltrexone had at least a 70-point decline in Crohn’s Disease Activity Index scores compared to 40 percent of placebo-treated patients.

[12] Shou-Ching’s Photo-Art:

© 2011 Shou-Ching Jaminet.

[13] Not the weekly video: Ducks Against the Wind:

Via erp, who says, “It’s getting harder and harder to keep your ducks in a row!”

[14] Weekly video: Marriage is health-improving and life-extending, especially for men, so I consider this (done in moderation!) an exemplary health practice:

Via Orrin Judd

An Osteoarthritis Recovery Story

Posted by on May 17, 2011 84 comments

Jacqueline wrote us in late March asking for tips for osteoarthritis.

She had experienced continuous pain and stiffness in her thumbs for the last year, and occasional pain when gardening for more than 10 years. Her younger sister also has joint pain and can’t turn her neck. Her father, now 73, has had pain in his thumbs for decades which eventually spread to his fingers, and a shoulder spur which had required surgery. Jacqueline’s dad says that osteoarthritis “runs in the family.”

Of course, even if there is some sort of genetic basis for osteoarthritis, it will be modifiable through diet and nutrition.

Jacqueline had been eating low-carb since 2003: meat and vegetables for dinner, fruit and yogurt or eggs, bacon, and sausage for breakfast, but an occasional sandwich for lunch. Around 2007, Fitday gave her macronutrient ratios as near 65% fat, 17% carb, 17% protein. In 2009 she gave up wheat entirely. At that point she developed dry eyes.

Upon reading our “low-carb dangers” series which discussed dry eyes (see Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers, Nov 15, 2010), she decided to add some carbs back to her diet. Potatoes and bananas cured her dry eyes.

But the joint pain remained, and she asked for any further suggestions. My reply was:

Shou-Ching had a condition like that and it got better with regular vitamin K2 supplementation. Presumably it was caused by improper calcification. Magnesium, vitamin D, and vitamin C are the next most likely to be important.

I think malnutrition is probably the major cause of osteoarthritis. (We know it can cause it in moose!)

For rheumatoid arthritis the cause is usually infectious. Low-dose antibiotics, as suggested by the Road Back Foundation, often work.

The dry eye indicates a glucose and/or vitamin C deficiency. Either will contribute to joint problems too, since the joint lubricants are all made from essentially the same materials as tear lubricants / mucus. So it’s good you’ve re-introduced starch, but I would add more than just some potatoes and tubers. After you’ve gotten used to very low-carb it can be hard to re-orient yourself to the quantities you may need. If glucosamine helps, that suggests you don’t have enough glucose to make your own glucosamine. I would eat more starches and take more C also.

I think you’re probably close and a little more diet experimentation should be able to fix the problem. Rice and vitamin K2 are probably your best friends.

Jacqueline implemented that advice. She wrote back in early May:

What I did:

I kept on taking the 1.5g glucosamine daily and tried, really tried to up my carbs (as starch) intake – you’re right, once you get used to not eating them, it can be quite hard to do. I seem to have succeeded somewhat as I have gone back to using Fitday a bit and have managed (on the days I was checking) about 100g carbs a day. If I didn’t manage with the carbs, I consciously tried to eat a bit more protein on the day instead.

I have increased the frequency with which I take magnesium and vitamin K2 … and started taking a vitamin C (1g) every day. I’m easing off on vitamin D though as summer and some sunshine is finally here. I’ve also pretty much stopped the fish oil – this is of course related to your recent posts – because I do eat oily fish weekly and other fish and seafood regularly….

I have also cut out my addiction to cashew nuts since I was in Paris for a few days before Easter….

Results:

The aching and stiffness has been receding steadily. The right thumb was already improving with my trying to increase carbs (because of the dry eyes) and taking the glucosamine. The right thumb now feels pretty much back to normal. The left thumb has also stopped aching especially over the last 2-3 weeks although it is still a bit prone to ‘catching’ with sudden pain – and a sort of pulling in the ligaments  – as if it can’t react quickly enough to a sudden move e.g. when driving. I am now – over the last few days – playing the piano a lot more (got a bit out of practice with the Paris trip etc.)  – and my thumbs are recovering well – not sore the next day like they were before.

Conclusion

There are basically three kinds of arthritis:

  • osteoarthritis, which I associate with nutrient deficiencies, is a loss of cartilage and lubricating fluid in the joints, or an improper calcification or ossification of the soft tissue;
  • reactive arthritis, which is due to infections; and
  • rheumatoid arthritis, which is an autoimmune disorder but the autoimmunity is usually caused by an infection and clearing the infection will usually clear the autoimmunity.

Food toxins can also collect in the joints and cause immune reactions that produce arthritis-like joint symptoms. Foods that frequently cause allergies, such as tree nuts, may be worth eliminating as a test, as Jacqueline eliminated cashew nuts.

Since diagnosing the cause of arthritis symptoms is an art more than a science, and nutrient deficiencies are easily remedied, they’re almost always a good place to start with any joint pain and stiffness.

I’m glad they’re working for Jacqueline! It’s nice when the easy fixes work.