Cushing's Syndrome cause by Cereal Grains (and/or Sugar)?

The dog of my mother has Cushing's – probably, we need to do more tests. Anyhow, the dog has a lot of problems, which may or may not be connected to Cushing's:

• (Probably) Cushing's, thin legs, bigger stomach
• Muscle problems: weakness, (temporary) limbing
• Fatigued
• Liver problems (I swear, he hasn't been drinking)
• Cataract
• Hearing problems
• Probably a few other small things

Now, the only things wrong in his nutrition were Cereal Grains and Sugar. No dairy that I know of. His nutrition contained probably some seed oil, but I don't know what. Possibly some chicken egg through noodles.

As his condition worsned, and the dog started limping, and dragging one hind-leg, we had to do something. The doctor first suspected arthitis, and the dog got anti-inflamatory medication and anti-pain medication. I changed the dogs diet at the same time and removed cereal grains and sugar for his diet. The result was that he improved somewhat.

Next he got anti-biotics and again anti-pain medicaiton. The dog improved again somewhat. I started giving the dog more carbs (rice and potatoes). The combination of anti-biotics and carbs seems to have done some help.

Now he is off the anti-biotics, and got less carbs, and the dog is more fatigued again.

Now, it is difficult to say whether the dog improved due to the medication, or due to the change in nutrition. But I'll be damned if cereal grains and sugar are not bad for dogs.

We'll keep looking. 

Let's see, this week the dog get another test, and then maybe some medication for Cushing's. It is really sad to see the dog like that, but at least it improved noticeably over the last weeks.

Anecdote: Paleo Diet helps for Crohn's

Robb Wolf has the details:

…
A couple weeks later, at home, bored and on Youtube, a video about the Paleo diet popped up and after watching this I was fascinated; For the next week I was locked to my laptop finding out all I could about it. I immediately decided to give the auto-immune protocol a try, and after a few trials and errors to discover what I could and couldn’t tolerate, virtually ALL my symptoms of Crohn’s were gone!

Let me break that down for you,

Joint pain-100%gone

Psoriasis-100%gone

Diarrhea-100% gone

Intestinal pain-100% gone
…

I think the note about the auto-immune protocol is important. IIRC Robb Wolf's auto-immune protocol gets rid of eggs and nightshades, among others, as I think eggs might be involved in the pathogenesis of Crohn's.

Rituximab for Behçet's

While I think that (pasterized) milk, dairy and eggs are causing Behçet's, it is interesting to see that Rituximab seems to be helping Behçet's patients.

Rituximab in intractable ocular lesions of Behcet's disease; randomized single-blind control study (pilot study).

Davatchi F, Shams H, Rezaipoor M, Sadeghi-Abdollahi B, Shahram F, Nadji A, Chams-Davatchi C, Akhlaghi M, Faezi T, Naderi N.
Source

Behcet's Unit, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

BACKGROUND:
Ocular lesions, the main morbidity of Behcet's disease (BD), are the most difficult to treat. The aim of this study was to evaluate the efficacy of rituximab.

METHODS:
Inclusion criteria were retinal vasculitis and edema, resistant to cytotoxic drugs. Twenty patients were randomized to a rituximab group (RG) or cytotoxic combination therapy group (CCTG). Rituximab was given in two 1000-mg courses (15-day interval). Subjects received methotrexate (15 mg/weekly) with prednisolone (0.5 mg/kg per day). The CCTG received pulse cyclophosphamide (1000 mg/monthly), azathioprine (2-3 mg/kg per day) and prednisolone (0.5 mg/kg per day). The primary endpoint was the overall state of patients' eyes and the Total Adjusted Disease Activity Index (TADAI). Secondary endpoints were: visual acuity (VA), posterior uveitis (PU), and retinal vasculitis (RV). The baseline data were compared at 6 months by paired sample t-test and analysis of variance.

RESULTS:
TADAI improved significantly in the RG (t = 3.340, P = 0.009), but not in the CCTG (t = 2.241, P = 0.052). For secondary endpoints (RG/CCTG), the mean VA improved in two patients versus three (2/3), remained unchanged in 1/1, and worsened in 7/6 patients. The mean PU improved significantly in the RG (t = 3.943, P = 0.001), not in the CCTG (t = 2.371, P = 0.028). RV improved, but not statistically (t = 2.027, P = 0.057 vs. t = 1.045, P = 0.31). Edema of retina, disc and macula improved significantly in both, but much better for the RG (t = 2.781, P = 0.012 vs. t = 2.707, P = 0.014).

CONCLUSION:
Rituximab was efficient in severe ocular manifestations of BD, TADAI improved significantly after 6 months with rituximab, but not with CCT.

And one more study:

Treatment of retinal vasculitis in Behçet's disease with rituximab.

Sadreddini S, Noshad H, Molaeefard M, Noshad R.

Tabriz University of Medical Sciences, Golgasht St., Tabriz, Iran.

Abstract

Behçet's disease (BD) is more common in eastern than western countries. Physicians have frequently encountered problems in its treatment, especially eye involvement. Recurrent oral and genital aphthous ulcerations are the hallmarks of Behçet's disease but other organs can be involved and ocular disease is one of the most disabling manifestations. Up to now, there are some problems in treatment of the retinal vasculitis due to Behçet's disease. We reported one patient, with visual loss due to retinal vasculitis that was resistant to prednisolone and azathioprine. Our patient was treated successfully with rituximab and his remission was sustained for 24 months of follow-up. Rituximab is a chimeric monoclonal antibody that acts against the specific B cell antigen, CD20. The recent success of rituximab in autoimmune diseases, which is considered to be T cell-mediated, indicates that B cells must have a much broader role in the pathogenesis of autoimmune diseases than generally appreciated.

Behçet's is a rare disease, so very few studies are being done.

However, if you have disease that might be helped by Rituximab, my (slightly educated) guess is to try consume no milk, no dairy and no eggs for at least 4 weeks to see if it helps – it's worth a shot.

Type 1 Diabetes – Dairy and Gluten to blame?

Environmental agents and type 1 diabetes
…
The most investigated dietary component associated with type 1 diabetes is cow-milk protein. Exposure to cow milk in early life (e.g. because of lack of breast feeding) has been linked with type 1 diabetes in humans and diabetes-prone BB rats. However, there is inconsistency in the studies, perhaps due to the variable composition of milk, with genetic variation in cow proteins. The findings are also consistent with the existence of a subset of milk-sensitive diabetes-prone individuals. Immune tolerance to insulin might also be compromised by early exposure to cow milk, which contains much less insulin than does human milk.

Wheat gluten is a potent diabetogen in BioBreeding (BB) rats and NOD mice, animal models of type 1 diabetes. Between 5% and 10% of type 1 diabetic patients have gluten-sensitive enteropathy (coeliac disease) and many more have antibodies to transglutaminase, a circulating marker of coeliac disease. Wheat may therefore be involved in the pathogenesis of type 1 diabetes, possibly inducing subclinical gut inflammation.
…

Or how about this:

An abrupt change in the incidence of type 1 diabetes after the migration of Polynesians to New Zealand was suggested most likely to result from the early introduction of dairy products into the infant diet, accompanied by an earlier weaning in New Zealand (Elliott 1992). A positive correlation has been reported between per capita consumption of unfermented milk proteins in populations worldwide (Scott 1990) or fluid cow milk consumption in children aged 0 to 14 years and incidence of type 1 diabetes (Dahl-Jørgensen et al 1991, Fava et al 1994). In addition, countries with the lowest prevalence of breast feeding at 3 months of age had the highest incidence of the disease (Scott 1990).

The occurrence of Celiac Disease has increased in the US

Natural history of celiac disease autoimmunity in a USA cohort followed since 1974.
…
During a 15-year period CD prevalence increased 2-fold in the CLUE cohort and 5-fold overall in the US since 1974. The CLUE study demonstrated that this increase was due to an increasing number of subjects that lost the immunological tolerance to gluten in their adulthood.

ME/CFS is a Women's Disease

Some people (mainly male doctors?) have the misogynistic perception that because ME/CFS affects more women than men, it must therefore be some form of female hysteria ("It's the vapors."). Well, I say bullshit to that. There are several autoimmune diseases that affect more women than men – a slight hint (not more, I'm afraid) that ME/CFS might share some disease mechanisms with autoimmune diseases:

Ratio of female/male incidence of autoimmune diseases:
Hashimoto's thyroiditis 10/1
Systemic lupus erythematosus (SLE) 9/1
Graves' disease 7/1
Rheumatoid arthritis 5/2
Multiple sclerosis (MS) 2/1
Myasthenia gravis 2/1

The 23andme blog this topic:

Why women are disproportionately affected by autoimmune disease is not fully known or understood, although the hypotheses are numerous. Some research suggests that estrogen may help antibody production and immune system response, but can also lead to an overly active immune system. Other research indicates that genes on the X chromosomes may play a role in these immune system mutinies, and women — who have two X chromosomes — may thus be at an increased risk over men who have only one X chromosome.

Still other research suggests that “fetal-maternal microchimerism” may be the root cause. In this strange-sounding phenomenon, a small number of the baby’s cells pass through the placenta into the mother and continue to live within the mother. The presence of these foreign fetal cells within the mother may result in an incorrect immune system response and autoimmune disease. More research, however, is needed to establish which of these hypotheses (if any) are correct.

Autoimmune diseases are serious medical concerns for women; indeed, when taken together, autoimmune diseases constitute one of the top ten causes of death among young and middle-aged women. The irony of these conditions is that the immune system, which should be a woman’s greatest ally in fighting disease, becomes her worst enemy. Why and how a body’s betrayal occurs needs to be better understood through further research.

Interview with Ian Lipkin

An interview with Ian Lipkin in the Disco-Mag:

… LCMV, a cause of meningitis in humans, shuts down the ability of the pituitary gland to make growth hormone. The virus doesn’t kill the cell, 
but it suppresses transcription and translation of genes, so the organism as a whole suffers but the individual cell looks OK. My contribution was showing that there were specific effects on neurotransmitters linked to the behavioral manifestations of the 
disease. This became a model for understanding how persistent viral infections affect the central nervous system. …

Haven't read it all yet. Some of the interview questions are a bit "woo", and Ian Lipkin comes off as a bit woo too – but I guess this comes with having an open mind and even Newton studied Alchemy. It is definitely interesting to see were he comes from, what he learned about different diseases and how he learned to see them.

How can an infection cause a mental illness?

How can an infection cause a mental illness? It's an autoimmune issue. Mady Hornig at Columbia University has a mouse model that shows how it works. They give strep to mice, then give them another agent that breaks down the blood–brain barrier, and that induces a neuropsychiatric syndrome: the mice have trouble running mazes, and so on. Then they purify the antibodies from those mice, inject them in another mouse that never had strep, and that mouse gets the neuropsychiatric symptoms, too. That shows it's the antibodies doing the damage.

A possible route for auto-immunity

Grand total 1374 potential pathogens, counting Salmonella once. This is, obviously a gross estimate, probably a gross underestimate, of the number of pathogens that can infect us. Obviously, not everyone is exposed to every one of these pathogens. Keep in mind that each organism makes dozens of proteins and carbohydrates for the immune system to recognize and to respond with a specific antibody. I would bet the list represents more than 13,740 antibodies.

This reservoir of 10k of antigens/antibodies is a reservoir for molecular mimicry like auto-immune problems, as far as I understand it. What I don't understand: we should have with micro-assays now the tools to screen auto-immune diseases for identity of auto-immune antibodies to anti-pathogen anti-bodies.

Prevalence and sociodemographic correlates of antinuclear antibodies in the United States

Prevalence and sociodemographic correlates of antinuclear antibodies in the United States.

Satoh M, Chan EK, Ho LA, Rose KM, Parks CG, Cohn RD, Jusko TA, Walker NJ, Germolec DR, Whitt IZ, Crockett PW, Pauley BA, Chan JY, Ross SJ, Birnbaum LS, Zeldin DC, Miller FW.

Source
Department of Medicine, University of Florida, Gainesville, Florida.

Abstract


OBJECTIVE.:
To estimate the prevalence, types and sociodemographic and biobehavioral correlates of antinuclear antibodies (ANA) in the United States (U.S.).


METHODS.:
Cross-sectional analysis of 4,754 individuals from the National Health and Nutrition Examination Survey (NHANES) 1999-2004.

ANA by indirect immunofluorescence, including cellular staining patterns and specific autoantibody reactivities by immunoprecipitation in those with ANA.


RESULTS.:
ANA prevalence in the U.S. population ages 12 years and older was 13.8% (95% CI, 12.2% to 15.5%).

ANA increased with age (P = 0.01) and were more prevalent among females than males (17.8% vs. 9.6%, P < 0.001), with the female to male ratio peaking at 40-49 years of age.

ANA prevalence was modestly higher in African Americans than whites (adjusted prevalence odds ratio [POR], 1.30; 95% CI, 1.00 to 1.70).

Remarkably, ANA were less common in overweight and obese (adjusted POR, 0.74; 95% CI, 0.59 to 0.94) individuals than persons of normal weight.

No significant associations were seen with education, family income, alcohol use, smoking history, serum levels of cotinine or C-reactive protein.

In ANA-positive individuals, nuclear patterns were seen in 84.6%, cytoplasmic patterns in 21.8%, and nucleolar patterns in 6.1%, and the most common specific autoantibodies were anti-Ro (3.9%) and anti-Su (2.4%).


CONCLUSION.:
These findings suggest that over 32 million persons in the U.S. have ANA and the prevalence is higher among females, older individuals, African Americans and those with normal weight.

These data will serve as a useful baseline for future investigations of predictors and changes in ANA prevalence over time

"Study demonstrates that 95% of ME/CFS Patients have Anticardiolipin Antibodies, suggesting that ME/CFS may be an autoimmune condition"

A survey of the literature reports ACAs as commonserological markers in many different types of diseases,including viral diseases such as illnesses resulting fromchemical (1) and marine toxin exposure (4,5,6), HIV(7,8) and Epstein-Barr virus (9), hematological cancersincluding CLL and acute myelocytic leukemias, exposureto fungal organisms, malaria, and staphylococcusinfections (10,11), and autoimmune diseases such asmultiple sclerosis, systemic lupus erythematosus, autoimmunehepatitis, and more (2). This study demonstrates that a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition.As a possible autoimmune disease, CFS patients maybe treated by suppression of the ACA or by diminishingthe antigen CL in serum. Previous studies have shownthat treatment with monoclonal antibodies to B cellsreduces ACA levels to normal in patients with autoimmunedisease, leading to clinical improvements.

Specifically, Rituximab, a chimeric monoclonal CD20antibody, has been shown to normalize high ACAserum titers of patients with autoimmune systemic lupuserythematosus, rheumatoid arthritis, autoimmunethrombocytopenia, and autoimmune hemolytic anemia.Rituximab may serve as an effective therapeutic agentfor ameliorating the symptoms of CFS (11,13).

Therefore,classification of CFS as an autoimmune disordermay serve to increase the availability of treatmentoptions for patients suffering from the disease.

A study from 2009. Nice find, Dr. Speedy!

The problem with the "autoimmune" label

Oh, how I hate the press for their ignorance…

Chronic fatigue syndrome, which affects one in 250 Britons, may be caused by a faulty immune system attacking the body.

That is the problem with the "autoimmune" label: People think "well, if the immune system attacks its own body, then the cause must be a faulty immune system". No. Coeliac is an "autoimmune" disease, yet its cause is gluten (which is found ceral-grains).

That is one part of the problem with journalism: They try to explain things they don't understand. The other part is that people take what is reported in the press at faith value.

And, oh, by the way, the incidence for ME/CFS is closer to one in 200, if not more common. Doctors do underreport, it comes with the territory.

Cell Types and Diseases

There are several hundred distinct human cell types. … Cell types can be classified by their tissue of origin. However, it is possible for some cells to have their behavior induced by surrounding tissue.

So, if there are several hundred distinct human cell types, how many distinct autoimmune antibodies can there be? I know, this comparison is a bit lopsided, but still: Do we know all possible autoimmune diseases?

What kind of disease could we cause, if we would pick one cell type, target it with inflammation and/or antibodies? Is early hair-loss a autoimmune disease of certain hair-cells? Is tinnitus a autoimmune disease of certain auditory cells?

And do we know all hormones? All hormone producing cells? Or just the "important" ones? What happens if the cells responsible for a lesser hormone fail?

Sjögren's Syndrome

“In comments to the press, Ms. Williams expressed disappointment at being unable to compete because of severe fatigue and pain, but gratitude for recently receiving a diagnosis of Sjögren’s syndrome that explained symptoms she had been feeling for some time,” said Ms. Dowd. “Unfortunately, her experience is not uncommon; proper diagnosis can take years.

Blood tests can be done to determine if a patient has high levels of antibodies that are indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid factor (because SS frequently occurs secondary to rheumatoid arthritis), which are associated with autoimmune diseases. Typical Sjögren's syndrome ANA patterns are SSA/Ro and SSB/La, of which SSB/La is far more specific; SSA/Ro is associated with numerous other autoimmune conditions but are often present in Sjögren's.

So these tests are "indicative".

Loren Cordain on Autoimmunity and Nightshades

… experiments in animals confirm that organ specific autoimmune diseases can be caused by injecting a self-antigen with a powerful adjuvant such as Freund’s [33, 34]. Neither the adjuvant alone nor the self-antigen typically results in autoimmunity in animals [33-35].
…

33. Fairweather D, Kaya Z, Shellam GR, Lawson CM, Rose NR. From infection to autoimmunity. J Autoimmun. 2001 May;16(3):175-86.

34. Fairweather D, Frisancho-Kiss S, Rose NR. Viruses as adjuvants for autoimmunity: evidence from Coxsackievirus-induced myocarditis. Rev Med Virol. 2005 Jan-Feb;15(1):17-27.

35. Fairweather D, Rose NR. Women and autoimmune disease. Emerg Infect Dis 2004;10:2005-2011.