Category Archives: Disease

Disease Begins in the Mucus

Hippocrates famously said, “All disease begins in the gut.” I think we can narrow it down further: much modern disease begins in the mucus.

In a recent post, I put up this picture:

Antimicrobial peptides (AMPs), including defensins and cathelicidins, constitute an arsenal of innate regulators of paramount importance in the gut.

A depleted mucosal layer leads to inflammation and gut permeability.

It’s from a paper on the role of antimicrobial peptides in maintaining gut health. [1] The point of the left panel is that a healthy gut is characterized by a thick mucosal layer that shields our intestinal and immune cells from direct contact with bacteria. The inner mucus layer is infused with antimicrobial peptides to minimize its bacterial content. The outer mucus layer contains a population of friendly mucin-degrading bacteria – symbionts like Akkermansia who evolved to feed on our mucus. These friendly bacteria provide another layer of defense against infectious pathogens; bacteria tend to be quite good at keeping out competitors. Akkermansia has been found to prevent obesity.

In an unhealthy gut, on the other hand, the mucosal layer often gets stripped away. The image (right panel) attributes this to infection, which is one possibility, but nutritional factors also matter. For example:

  • Deficiencies of vitamins A or D will reduce production of antimicrobial peptides, making it easier for pathogens to reach our gut cells;
  • On very low-carb diets, production of mucin-2, the primary constituent of gut mucus, may be limited in order to preserve glucose for the brain (see “Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers,” Nov 15, 2010);
  • Deficiencies of dietary fiber, vinegar, choline, and other nutrients may impair gut motility, leading to concentrations of partially digested food and bacteria at specific points in the intestine.

Regardless of why it happens, once bacteria come into direct contact with our gut and immune cells, they trigger inflammation and tend to loosen the gut barrier. This allows live bacteria and cell wall components from dead bacteria to enter the body from the gut.

Endotoxins – toxic compounds released when bacteria die, such as lipopolysaccharides from the cell walls of gram-negative bacteria – are immunogenic and inflammatory. A large influx of endotoxins into the body is “endotoxemia” – poisoning by endotoxins. As little as 2 nanograms LPS per kilogram body weight will induce fever, and 1 microgram LPS per kilogram of body weight will induce shock. [2]

Diseases caused by endotoxemia include:

  • Hepatitis [3]
  • Diabetes [4]
  • Heart disease [5]
  • Obesity [6]
  • Pulmonary hypertension [7]
  • Dyslipidemia [8]
  • Chronic kidney disease [9]

Many of today’s most prevalent diseases are caused by chronic endotoxemia.

So it behooves us to avoid it. If endotoxemia is fundamentally caused by the loss of a protective mucosal layer in the gut, how do we assure healthy production of mucus?

A recent paper sheds valuable light on that question.

Natural Whole Foods, High-Fat Diets, and Gut Health

It’s well known that in mice, “high-fat diets” induce endotoxemia. But these diets aren’t necessarily high in fat – any pelleted rodent food in which fat provides more than 20% of calories may be called “high-fat.” The critical difference of “high-fat diets” from chow is that they are composed of purified nutrients – starch, sugar, oil, vitamins, and minerals – whereas chow is composed of natural whole foods such as wheat, corn, and seeds.

A recent study tried to distinguish whether the cause of endotoxemia is the fat, or the purified starch, sugar, and oil. It made up three diets of varying fat content (8%, 48%, and 74% of energy respectively), but composed of natural whole foods. [10]

The result was remarkable:

[U]sing complex [i.e. natural whole foods] HFD, no associations were observed between dietary lipid amounts and the magnitude of endotoxemia, inflammation, and physiological alterations developed.

It turns out the endotoxemia that typically develops on high-fat diets is due to getting the calories from purified sources – starch, sugar, oil – rather than from whole foods. On a whole foods diet, the amount of endotoxin entering the body is more or less independent of the amount of fat consumed.

This is surprising in one respect. Lipopolysaccharide is fat-loving and enters the body along with dietary fat. So it stands to reason that a higher-fat diet would carry more endotoxin into the body.

But it turns out the body has mechanisms to regulate how much endotoxin enters the body. It wants a small amount so that the immune system can sample the gut microbiome, but not so much as to cause inflammation.

The primary mechanism for controlling endotoxin influx? Mucus production. The study noted that the mice eating higher-fat “had an increased number of goblet cells … [and] an increased MUC2 production.” MUC2 is mucin-2, the primary component of mucus in the gut.

Here is a picture with mucin-2 in the mucin-producing goblet cells stained red:

disease begins in mucus 02

It’s obvious that mucin production goes up dramatically as the fat content of the diet increases.

The study concludes,

“We show that, in complex HFDs based on chow ingredients and milk fat, there was no association between dietary lipid amounts and the magnitude of metabolic endotoxemia or low-grade inflammation.”

If high-fat diets are healthy, we can thank our mucin-producing goblet cells.

One last note: the fact that mice can produce healthy amounts of mucus on a 74% fat diet does not necessarily mean that humans can do the same. Humans have much larger brains than mice, and as a result our carbohydrate needs are larger. It’s possible that mice can maintain mucus production on a low-carb diet better than humans can.


[1] Muniz LR, Knosp C, Yeretssian G. Intestinal antimicrobial peptides during homeostasis, infection, and disease. Front Immunol. 2012 Oct 9;3:310.

[2] Warren HS et al. Resilience to bacterial infection: difference between species could be due to proteins in serum. J Infect Dis. 2010 Jan 15;201(2):223-32.

[3] Parlesak A, Schäfer C, Schütz T, Bode JC, Bode C. Increased intestinal permeability to macromolecules and endotoxemia in patients with chronic alcohol abuse in different stages of alcohol-induced liver disease. J Hepatol. 2000 May;32(5):742-7.

[4] Moreno-Navarrete JM et al. Circulating lipopolysaccharide-binding protein (LBP) as a marker of obesity-related insulin resistance. Int J Obes (Lond). 2012 Nov;36(11):1442-9.

[5] Lepper PM et al. Association of lipopolysaccharide-binding protein and coronary artery disease in men. J Am Coll Cardiol. 2007 Jul 3;50(1):25-31.

[6] Cani PD et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007 Jul;56(7):1761-72.

[7] Dschietzig T, Alexiou K, Richter C, Bobzin M, Baumann G, Stangl K, Brunner F. Endotoxin causes pulmonary hypertension by upregulating smooth muscle endothelin type-B receptors: role of aldose reductase. Shock. 2008 Aug;30(2):189-96.

[8] Lassenius MI et al. Bacterial endotoxin activity in human serum is associated with dyslipidemia, insulin resistance, obesity, and chronic inflammation. Diabetes Care. 2011 Aug;34(8):1809-15.

[9] McIntyre CW et al. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease. Clin J Am Soc Nephrol. 2011 Jan;6(1):133-41.

[10] Benoit B et al. Increasing fat content from 20 to 45 wt% in a complex diet induces lower endotoxemia in parallel with an increased number of intestinal goblet cells in mice. Nutr Res. 2015 Apr;35(4):346-56.


Matt Farina’s Recovery from Hypothyroidism

Matt Farina is in the process of using the Perfect Health Diet to recover from hypothyroidism, and wanted to report his progress to PHD readers. Here’s Matt! – Paul Jaminet

My hypothyroidism was discovered in 2012. I was age 30 at the time and had just moved to a new part of the UK and enlisted with a new doctors surgery. The condition was discovered by accident when a nurse at the new surgery noticed I had an irregular heart beat. I was sent for blood tests in April 2012 where it was discovered that I had an underactive thyroid. My serum TSH was 11.3. We retested a week later and it was similar, 11.7. Free T4 was 11.1 and 11.6 pmol/l, on the low side.

The doctor asked if I had any of the common symptoms of hypothyroidism; I said I was tired in the day and had brain fog in the morning. I regularly go to the gym and run 10k and half marathon races, so the tiredness was noticeable. My mood was sometimes a little unstable too.

The doctor prescribed 50 mcg levothyroxine, and I began taking it daily. In July 2012, we remeasured. With the levothyroxine, my TSH had fallen to 3.0 and my free T4 had risen to 17.6 pmol/L – right in the middle of the normal range. Nevertheless, my hypothyroidism symptoms, such as brain fog and tiredness, persisted.

In early 2013, I relocated to a new part of the country and found a new doctor. They remeasured and my TSH was now 2.71. In July 2013, it was 2.6. I was still taking 50 mcg levothyroxine daily.

In early 2014, I moved again, and found a new doctor. My TSH had risen a little, to 3.3.

I decided to start researching causes and cures of hypothyroidism, and started to listen to podcasts from Ben Greenfield and Robb Wolf. Through them, I noticed that some people were successfully curing hypothyroidism through the Paleo diet. This really piqued my interest and I wanted to know more.

In May 2014, I sent Ben Greenfield an email saying I was considering starting a Paleo diet to overcome my hypothyroidism and I really wasn’t expecting a reply considering how busy he must be. He kindly responded very quickly saying, “I would say Paleo may be a bit dangerous, ideally I encourage you to follow a diet closer to this one.” He linked to the Perfect Health Diet.

A new set of blood tests were taken a few days after Ben’s email which showed a significant decrease in serum free T4 and an increase in TSH levels; free T4 was down to 12.1 and TSH was up to 6.42.

The doctor wanted to double my daily dose of levothyroxine to 100 mcg per day. I asked him why he thought I had hypothyroidism, and whether he would recommend that I change my diet to help overcome it. His responses shocked me. He said my hypothyroidism “could be genetic” and “unfortunately it’s just who you are.” He also said that he wouldn’t recommend any dietary changes because I didn’t show symptoms of food intolerance.

I decided that I would stick with the 50 mcg dose of levothyroxine, and see if diet could help me. I started the Perfect Health Diet the next day – June 2, 2014.

The first 3 months on the Perfect Health Diet yielded weight loss and other health benefits. I was never over weight but I dropped a jean size, started noticing stomach muscles and people were commenting on me losing weight in my face. As I intermittently fasted in the mornings, my clarity of thinking improved at work in the mornings with reduced brain fog. Other benefits included easier breathing through my nose, reduced tiredness in the day, and no more heart palpitations. The first few weeks were a little tough as my body was becoming fat adapted but that soon passed. The diet left me feeling satiated the vast majority of the time and the food I was having were truly delicious combinations. I used the Perfect Health Diet audiobook to scrub up on knowledge while I was at the gym.

After 3 months on the Perfect Health Diet, in late August 2014, I had a set of blood tests. My serum free T4 was back to normal at 18.0 and my TSH had dropped to 5.25. Nevertheless, my doctor still wanted to double my levothyroxine dose to 100 mcg. I politely declined as I knew the diet was working and that there would be even better results to come.

After 6 months on the Perfect Health Diet, in November 2014, free T4 was up again to 19.2 pmol/L and TSH had dropped again to 3.78. At this point the doctor had no comment except to say that I should stay at 50 mcg of levothyroxine daily.

At my next test, in March 2015, free T4 was up again to 19.9 pmol/L and TSH had dropped to 2.08. I continued to take 50 mcg levothyroxine daily, though in retrospect this would have been a good time to begin dropping the dose.

At my 12 month anniversary of adopting the Perfect Health Diet, in June 2015, I was tested again. This time free T4 was 27.6 pmol/L – well above normal – and TSH was only 0.12. I was now overdosing on thyroid hormone.

The doctor suggested cutting my levothyroxine dose in half, to 25 mcg per day, but I’ve decided to drop levothyroxine entirely and see if I show hypothyroidism symptoms. If I do I’ll try small doses of levothyroxine to see what works for me. I’m eagerly looking forward to my next blood test in three months to see if I am back to normal.

I fully intend to continue the Perfect Health Diet indefinitely, and I hope my story helps other people overcome their hypothyroidism.

Back in May 2014, when I first learned about PHD and the hope that it gave for natural thyroid healing, and heard my doctor say that hypothyroidism was genetic and incurable and that I would be living with it for the rest of my life, I left the doctors office feeling sad. If diet could heal hypothyroidism, then many people were being misled by their GPs.

Now I feel hope. I know hypothyroidism can be healed. Thanks for you hard work Paul, it’s really appreciated.

Nitric Oxide and AO+Mist Skin Probiotic at the Perfect Health Retreat

Our May Perfect Health Retreat begins on Saturday, and we’re thrilled to announce a new partner: AOBiome.

In January I blogged (“UBiome and the May 2015 Perfect Health Retreat”) about our partnership with UBiome has contributed two gut microbiome sequencing kits for each guest, and we’re sequencing gut microbiomes pre-retreat and at the end of the retreat to see if a week together in a PHD-optimized environment causes microbiomes to converge to a “Perfect Health Diet” pattern.

Now, AOBiome is donating a four week supply of their AO+Mist skin probiotic to each guest. To see why I’m excited about this, I have to say a little about nitric oxide.

Nitric Oxide and Health

Nitric oxide is a gaseous signaling molecule with powerful effects on blood vessels, nerves, the immune system, gut and skin. It has proven to be such an important molecule that the three pharmacologists who established its role in relaxing blood vessels were awarded the Nobel Prize for Medicine in 1998.

Nitroglycerin, the explosive which turned out to be an effective remedy for heart failure, works by increasing nitric oxide levels.

A list of health conditions that may be improved through better nitric oxide status would be too long to attempt, but here is a brief sampling of Pubmed links. Nitric oxide may be helpful for high blood pressure and cardiovascular disease, gut conditions like constipation and impaired gut barrier integrity, obesity and diabetes, immunity against infections, dementia, lung dysfunction / COPD, and kidney disease. Nitric oxide has been reported to improve reaction time and exercise performance. It’s been proposed that nitric oxide may slow aging.

How do we obtain nitric oxide? It is a gas so you can’t eat it. Rather, we eat green leafy vegetables and beets to obtain nitrates; nitrates and bacteria-generated derivatives like nitrites are stored in the body, especially the skin; and then sunshine on the skin, among other processes, generates NO.

Here is dermatologist Richard Weller explaining why nitric oxide may be the reason sunshine is so good for our hearts, and why Scotsmen die so young despite the benefits of malt whisky:

Ammonia-Oxidizing Bacteria

Unfortunately, most of us don’t eat enough spinach to optimize our nitrate status. It would be wonderful if there were another way to obtain nitric oxide precursors.

David Whitlock, the scientist-founder of AOBiome, realized that there is. He was wondering why horses and other animals wallow in the mud, and realized that they might be obtaining probiotic bacteria for the skin from the soil.

Investigation revealed that a class of bacteria called ammonia-oxidizing bacteria are present in soil and, when they colonize the skin, can transform ammonia excreted in sweat to nitrite which can be re-absorbed by the body. These “AOBs” not only improve nitric oxide status, they improve body odor by eliminating ammonia. But they are destroyed by soaps and chlorinated water. Since most people use soap, take chlorinated showers, and rarely wallow naked in the mud, we lack these AOBs.

So AOBiome came up with the idea of a skin probiotic – some AOBs dissolved in water that you spritz on your skin after a morning shower, to re-colonize your skin each morning.

AOBiome has a variety of information on their web site if you’d like to read more: information about the skin microbiome in general, how modern lifestyle has changed it, why having a healthy skin microbiome is an important part of health, and the basics about the bacteria in the AO+ Mist.

Thank You, AOBiome

The Perfect Health Retreats represent our best effort to develop natural ancestral healing methods based on diet, lifestyle, and a healthful environment. Microbes are an important part of our environment, and managing our microbial environment has the potential to significantly improve health.

AO+Mist has not been tested in clinical trials, and there is no direct evidence that it will be beneficial to health. But the mechanisms seem logical, and I’m delighted that our guests will have a way to obtain ammonia-oxidizing skin bacteria without nakedness or mud. Thank you, AOBiome!

You don’t have to attend the retreat to benefit from AOBiome’s generosity. For readers of our blog, AOBiome is offering a 25% discount. Go here to purchase AO+Mist and use the coupon code phd25 for your discount.

Neu5Gc and Autoimmunity: Hashimoto’s Hypothyroidism

In Part I of this series, I reviewed the biology of Neu5gc (“Neu5gc, Red Meat, and Human Disease: Part I,” January 14, 2015). Now it’s time for Part II: a look at whether mammalian meats (beef, lamb, pork, dairy) may help provoke Hashimoto’s hypothyroidism.

Background on Autoimmunity

If you only care about health and what to eat, skip to the next section; but for those who want to understand mechanisms, here is the key background:

  • Neu5gc is abundant in nearly all mammals, but is absent in humans, ferrets, and new world monkeys.
  • Neu5gc is a sialic acid. It provides the terminal end of the carbohydrates which coat cells and glycoproteins. Cells need to be coated in these acids, because in water acids become ions and give the cells a charge, which repels other cells. When sialic acids are bound by antibodies, the charge is lost, and cells clump or aggregate. In fact, clumping of cells after pig serum was injected into humans was the first sign that humans form antibodies to pig cells. The main antigens in pig cells are “alpha-gal” and Neu5gc.
  • Although humans cannot manufacture Neu5gc due to a mutation that occurred 3 million years ago, we retain the ability to utilize it. So Neu5gc from food can appear on the surface of human cells.
  • To generate a broad-spectrum immune response, the DNA of B cells is re-arranged to create novel combinations of segments on the light- and heavy-chain portions of antibodies. This enables the body to generate more than 10^12 different antibodies. [1] To avoid generating antibodies to human antigens, any B cells that generate antibodies while still in bone marrow are destroyed. But Neu5gc from food doesn’t reach bone marrow, so there is nothing to stop the formation of white blood cells capable of generating antibodies to Neu5gc.

So Neu5gc has the potential to accumulate in human cells, especially intestinal cells which are directly exposed to food; and we can form antibodies to Neu5gc, which then may react to human cells which have incorporated Neu5gc into their carbohydrate coat.

One might think that this would be enough to generate autoimmunity, but more is needed. Although everyone has antibodies that can react to Neu5gc, the “preimmune repertoire” of antibodies binds to Neu5gc with very low affinity, and “low concentrations of anti-Neu5Gc antibodies do not seem to have any effect on Neu5Gc containing cells.” [4] In order to make high affinity antibodies, B cells must be repeatedly stimulated by Neu5gc-containing antigens.

The best stimulation is provided by bacterial cell wall components. As one paper states,

Bacteria are potent immunogens because they express a number of factors that can act as immune stimulants. Gram-negative bacteria universally produce endotoxins that have been shown to be powerful immune system modulators through the Toll-like receptor 4 (TLR4) on a variety of human immune cells. Lipoproteins on Gram-positive and Gram-negative cell surfaces can also interact with TLR2, resulting in release of cytokines involved in B cell and T cell proliferation. In addition, bacterial DNA has been known for many years to have the capability to stimulate the immune system. [2]

So to generate autoimmunity against Neu5gc incorporated in human cells, B cells must first be triggered to form high-affinity anti-Neu5gc antibodies by meeting bacterial pathogens who have incorporated Neu5gc into their cell walls.

This can happen because some bacteria do incorporate sialic acids from their local environment into their cell walls; and thus gut bacteria will incorporate Neu5Gc from food into cell walls.

A primary reason for doing this is that, by coating themselves in sialic acids acquired from their host, they look like a “host cell” and are shielded from immune attack. [5] Many pathogens have learned this trick:

Many pathogens secrete a sialidase that releases sialic acid from [nearby cells] … [O]ther sialic acid-utilizing bacteria, such as the respiratory pathogen H. influenzae, lack genes for a sialidase …. Presumably free sialic acid is made available to such pathogens by other, sialidase-expressing bacteria living in the same niche, or … by host sialidases that are activated in the course of inflammation. [3]

Among the pathogens known to use host sialic acids to shield themselves from human immunity is Neisseria gonorrhoeae, the pathogen that causes gonorrhea. It is possible that gonorrhea infection could lead to autoimmunity through this mechanism.

To date, the published research on this topic has focused on the possibility of pathogens incorporating Neu5Ac, the primary human sialic acid, from human cells into their cell walls, and subsequently triggering autoimmunity against Neu5Ac. There has been little study of the possibility that gut pathogens will incorporate Neu5Gc from food into their cell walls, potentially triggering autoimmunity against Neu5Gc incorporated in human cells.

Yet a recent study [4] comparing the levels of Neu5Gc antibodies in human blood against the prevalence of Hashimoto’s hypothyroidism suggests that this may be a significant pathway for autoimmunity.

Hashimoto’s Hypothyroidism and Neu5Gc Antibody Levels

This is one paper in which it’s almost enough just to present the data. Here are levels of anti-Neu5Gc antibodies in patients with hypothyroidism vs healthy controls:

Neu5gc hashis fig 1

This is Figure 1. [4] Patients with Hashimoto’s have, on average, 7-fold higher anti-Neu5Gc antibody levels than the general population. Patients with hypothyroidism, some of whom have Hashimoto’s and some don’t, have an intermediate level of anti-Neu5Gc antibodies.

Here are antibody levels in the healthy population (Figure 2a):

Neu5gc hashis fig 2a

Few healthy patients had more than 16 mcg/mL of anti-Neu5Gc antibodies, and none had more than 24 mcg/mL.

Here are antibody levels in Hashimoto’s patients (Figure 2c):

Neu5gc hashis fig 2c

Only 3% of Hashi’s patients had less than 12 mcg/mL of anti-Neu5Gc antibodies, and 57% had more than 24 mcg/mL.

This is a very good separation of the two groups. It looks like if you can generate large numbers of anti-Neu5Gc antibodies, then you are almost certain to get Hashimoto’s hypothyroidism.

About 50% (in this study, 47.9%) of hypothyroidism cases are autoimmune in origin. The 52.1% of hypothyroid patients who didn’t have Hashimoto’s generally had low levels of anti-Neu5Gc antibodies, similar to the healthy controls. This observation strengthens the association between anti-Neu5Gc antibodies and autoimmune hypothyroidism. It looks like anti-Neu5Gc antibodies are strongly linked to autoimmunity.

Adding plausibility, “both autoantigens related to Hashimoto disease [thyroid peroxidase and/or thyroglobulin] are glycoproteins and N-linked carbohydrates containing sialic acids have been detected in both molecules.” [4] So it’s possible Neu5Gc is incorporated directly into thyroid peroxidase and thyroglobulin.

The study authors state, “this is the first study investigating the association of anti-Neu5Gc antibodies with autoimmune diseases such as hypothyroidism.” [4]

They also tested for anti-Neu5Gc antibodies in rheumatoid arthritis patients, but found no connection there. Rheumatoid arthritis patients do not have elevated levels of anti-Neu5Gc antibodies.

Their paper has not yet been cited by any other papers. It looks like the investigation of Neu5Gc-mediated autoimmunity is at its very beginnings.

Jim Beecham’s Experience

Jim Beecham, MD, responded to my previous post with a personal story:

I read with interest your post about Neu5Gc. I am anxious to read Part 2 which I understand is coming. Meanwhile I have been doing a little research on the subject.

I suffered badly with childhood asthma, and I still get a sort of asthmatic tightness of my breathing once in a while. In the past few weeks have I realized this is on days after I eat cheese and/or beef. This has ceased upon my cutting out red meat and dairy this past week.

I also get hypothyroid symptoms of cold face and backs of hands from time to time. I wonder if this is also linked to Neu5Gc …

In a second comment Jim added:

Here’s another thought re: Neu5Gc…which I cannot prove but think is likely.

When an upsurge of titer of anti-Neu5Gc antibodies float in body fluids, they have opportunity cause inflammatory reaction.

One researcher postulated this mechanism for hemolytic uremic syndrome.

My own experience is I develop a groin ‘heat rash’ type reaction and irritable bladder a day or so after eating too much cheese and red meat.

Jim’s personal experiences add further evidence that Neu5Gc-driven inflammation and autoimmunity is a real phenomenon.

The paper linking Neu5Gc to hemolytic uremic syndrome is [6].


There’s an excellent chance that Hashimoto’s hypothyroidism is brought about by a complex of factors:

  1. An infection in the gut by bacterial pathogens that acquire Neu5Gc from food (primarily beef and pork) and incorporate it into their cell walls.
  2. A leaky gut that (a) allows Neu5Gc from food to enter the body for subsequent incorporation into human cells, such as thyroid cells, and (b) creates either a systemic invasion of Neu5Gc-bearing gut pathogens, or a “metabolic endotoxemia” in which Neu5Gc-bearing cell wall components of gut bacteria enter the body, triggering formation of high-affinity anti-Neu5Gc antibodies.
  3. Significant consumption of beef and pork, providing the Neu5Gc to drive the autoimmune process.

If this is the case, then the strategy for overcoming Hashi’s would involve:

  1. Improving gut barrier integrity and mucosal immunity,
  2. Normalizing or diversifying the gut flora, and
  3. Reducing dietary Neu5Gc by replacing beef, dairy, lamb, and pork with seafood and bird meats.

Neu5Gc-mediated autoimmunity does not play a role in rheumatoid arthritis, but it may play a role in other autoimmune diseases. The most likely organ to be affected is the gut, which is directly exposed to food; endothelial cells, which line blood vessel walls, and immune cells which circulate in blood, as blood is the next location after the gut exposed to food molecules entering the body; and lastly organs which interact closely with the blood, such as the thyroid. Hemolytic uremic syndrome is a condition of endothelial cell dysfunction.

So: it looks like reduction of mammalian meats, replacing them with seafood and bird meats, may be a prudent part of a “Hashimoto’s protocol.” In autoimmune disorders affecting the gut, blood vessels, or immune cells, it may be worth trying a 30-day elimination of mammalian meats.

Perfect Health Retreat

We have a few spots remaining for the May 2-9 Perfect Health Retreat, and will soon be taking reservations for the October retreat, either October 3-10 or 10-17 (or both). If you are interested, visit here for more info or email me at



[1] “Generation of Antibody Diversity,” in Alberts B, Johnson A, Lewis J, et al., Molecular Biology of the Cell, 4th edition, New York: Garland Science; 2002,

[2] Harvey HA, Swords WE, Apicella MA. The mimicry of human glycolipids and glycosphingolipids by the lipooligosaccharides of pathogenic neisseria and haemophilus. J Autoimmun. 2001 May;16(3):257-62.

[3] Severi E, Hood DW, Thomas GH. Sialic acid utilization by bacterial pathogens. Microbiology. 2007 Sep;153(Pt 9):2817-22. Full text:

[4] Eleftheriou P et al. Prevalence of anti-Neu5Gc antibodies in patients with hypothyroidism. Biomed Res Int. 2014;2014:963230.

[5] Varki A, Gagneux P. Multifarious roles of sialic acids in immunity. Ann N Y Acad Sci. 2012 Apr;1253:16-36. Full text:

[6] Löfling JC et al. A dietary non-human sialic acid may facilitate hemolytic-uremic syndrome. Kidney Int. 2009 Jul;76(2):140-4.