Tuesday, June 3, 2008

Wheat: Is It Evil Or Just in the Context of Vitamin D and EPA+DHA Deficiency?

I love Gladiator (yes, it's one of my all time f-a-v-e movies, next to When Harry Met Sally)... the first scene is mesmerizing... he's watching the flax and wheat fields glowing with gold, fearless in the face of death. In the dawn of time, ancient wheat probably did not cause as many autoimmune and silent/non-silent celiac diseases (or ?autism or ?coronary artery disease) as the present day. Why? In the Gladiator days, for one, sunscreen did not exist! Secondly, most people worked and warrior-ed outdoors. Toiling in the sun, hand laundering clothes, baking bread on outdoor hearths, practicing swordplay, gathering berries, fishing, preparing crops, hunting gamey-flesh (which BTW gamey-meat and grass-fed beef are enriched in EPA+DHA, much like fatty deep sea fish/fish oil), and other noble chores in the bright sunshine (because candles were scarce). All day long 24/7...

Does having enough sunlight and vitamin D give us more power to tolerate gluten and not develop damaging self-destructive auto-antibodies? It's unlikely we'll know in any good RCT (randomized controlled trials). No drug company will put up lettuce $$ to determine that good ol' cheap FREE UVB unblocked-sunshine is going to trump their $2-3/day drug (or super-sized vitamin D analogue) in a head-to-head trial. That's just absurd. And they're not stupid... because they pay staticians a lot of lettuce to figure that out for them.

Psoriasis is another celiac condition (incl autoimmune). What are the pharmacological treatments? UVB lightbox 5-10min weekly as needed and topical vitamin D derivatives in creams/ointments (and a couple of toxic Immunosuppressive injections like Enbrel for instance which has a side effect of c-a-n-c-e-r). New diagnostic techniques for celiac disease (widely used in Europe) are being employed now (check this out here). Years ago Dr. Davis figured out the value and power of oral administration of natural Vitamin D3. The recently published study impressively validates his work.

Effective tratment: Vitamin D3 (+ gluten-free lifestyle/diet plan)

Am J Med. 1978 Dec;65(6):1015-20.
Osteomalacia and celiac disease: response to 25-hydroxyvitamin D3. Hepner GW, Jowsey J, Arnaud C, Gordon S, Black J, Roginsky M, Moo HF, Young JF.
In this 54 year old woman with celiac disease, osteomalacia developed while she was on a gluten-free diet which had caused regression of her steatorrhea. She was not responsive to large doses of parenterally administered dihydrotachysterol (fake foreign synthetic vitamin D version) and calcium, but she was responsive to the oral administration of 25-hydroxyvitamin D3 (25-OHD3 = natural).

The data suggest that 25-OHD3 is the treatment of choice for patients with vitamin D deficiency due to intestinal malabsorption. PMID: 742623


Effective treatment: Fish oil!

Fish oil has been shown to be hugely beneficial due to its impressive autoimmune immunemodulating and skin-stabilizing benefits. Anything anti-inflammatory helps (like antioxidants with high ORAC scores). Fasting creates lower systemic bodily inflammation -- yes the MONKS know what they are doing. In TYP, the practice of intermittent fasting is a fast way to success.

Br J Dermatol. 2005 Oct;153(4):706-14.
Diet and psoriasis: experimental data and clinical evidence. Wolters M.

Psoriasis is considered as a T-cell-mediated inflammatory skin disease which is characterized by hyperproliferation and poor differentiation of epidermal keratinocytes. While susceptibility to psoriasis is inherited, the disease is influenced by environmental factors such as infections and stress. Diet has been suggested to play a role in the aetiology and pathogenesis of psoriasis. Fasting periods, low-energy diets and vegetarian diets improved psoriasis symptoms in some studies, and diets rich in n-3 polyunsaturated fatty acids from fish oil also showed beneficial effects. All these diets modify the polyunsaturated fatty acid metabolism and influence the eicosanoid profile, so that inflammatory processes are suppressed. Some patients with psoriasis show an elevated sensitivity to gluten. In patients with IgA and/or IgG antigliadin antibodies the symptoms have been shown to improve on a gluten-free diet. The active form of vitamin D, 1,25-dihydroxyvitamin D(3), exhibits antiproliferative and immunoregulatory effects via the vitamin D receptor (HOW ABOUT TAKING VITAMIN D3 ORALLY DAILY??), and thus is successfully used in the topical treatment of psoriasis. In this review, dietary factors which play a role in psoriasis are assessed and their potential benefit is evaluated. Furthermore, the risk of drug-nutrient interactions in psoriasis therapy is discussed (WOULDN'T IT BE NICE IF...SOMEDAY THEY SAY...WHEAT-CESSATION IS KEY TO PREVENTING PROGRESSION AND TO REVERSING PSORIASIS ?!?). PMID: 16181450


(These are many of the same strategies in TYP of course)


Are all autoimmune conditions (including Grave's and the frequently diagnosed Hashimoto's thyroiditis) just silent or non-silent celiac disease?

Why are wheat/gluten antibodies implicated so often?

Why is Vitamin D deficiency and a lack of dietary EPA+DHA commonly associated with celiac conditions (and autism and coronary artery disease)? And improve these conditions? Which came first? The chicken or the egg?? Does maternal health and in utero environments affect not only the fetus, but even the following generation as they do in rat experiments?

At least TrackYourPlaque provides answers.... Including the below...
--Optimize your vitamin D3 level (25)OHD = 60 ng/ml
--Optimize your fish oil EPA + DHA 3000 mg daily (supplements + dietary fish, shellfish, pasture-fed protein -- see last study) (or more if you have elevated Lp(a) > 30 mg/dl)
--Wheat-cessation program (yes.. that's all pasta, noodles, mac-n-cheese, bread, cereal, croissants (omg very hard), crackers, cookies, even soy sauce, etc)
--Optimize optimism (vitamin 'O')


Clin Rheumatol. 2006 Mar;25(2):240-5.
Association of systemic and thyroid autoimmune diseases.Biró E, Szekanecz Z, Czirják L, Dankó K, Kiss E, Szabó NA, Szucs G, Zeher M, Bodolay E, Szegedi G, Bakó G.

OBJECTIVE: There are few large cohort studies available on the association of systemic and thyroid autoimmune diseases. In this study, we wished to determine the association of Hashimoto's thyroiditis (HT) and Graves' disease (GD) with systemic autoimmune diseases.
METHODS: One thousand five hundred and seventeen patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), mixed connective tissue disease (MCTD), Sjögren's syndrome (SS) and polymyositis/dermatomyositis (PM/DM) were included in the study. The HT and GD were diagnosed based on thorough clinical evaluation, imaging and fine-needle aspiration cytology (FNAC). The frequency of HT and GD in these diseases was assessed. In addition, 426 patients with HT or GD were assessed and the incidence of SLE, RA, SSc, MCTD, SS and PM/DM among these patients was determined. Prevalence ratios indicating the prevalences of GD or HT among our autoimmune patients in comparison to prevalences of GD or HT in the general population were calculated.

RESULTS: Altogether 8.2% of systemic autoimmune patients had either HT or GD. MCTD and SS most frequently overlapped with autoimmune thyroid diseases (24 and 10%, respectively). HT was more common among MCTD, SS and RA patients (21, 7 and 6%, respectively) than GD (2.5, 3 and 1.6%, respectively). The prevalences of HT in SLE, RA, SSc, MCTD, SS and PM/DM were 90-, 160-, 220-, 556-, 176- and 69-fold higher than in the general population, respectively. The prevalences of GD in the same systemic diseases were 68-, 50-, 102-, 76-, 74- and 37-fold higher than in the general population, respectively. Among all thyroid patients, 30% had associated systemic disease. In particular, 51% of HT and only 16% of GD subjects had any of the systemic disorders. MCTD, SS, SLE, RA, SSc and PM/DM were all more common among HT patients (20, 17, 7, 4, 2 and 2%, respectively) than in GD individuals (2, 5, 5, 1, 2 and 1%, respectively).
CONCLUSION: Systemic and thyroid autoimmune diseases often overlap with each other. HT and GD may be most common among MCTD, SSc and SS patients. On the other hand, these systemic diseases are often present in HT subjects. Therefore it is clinically important to screen patients with systemic autoimmune diseases for the co-existence of thyroid disorders. PMID: 16247581



Biomed Pharmacother. 2007 Feb-Apr;61(2-3):105-12.
Dietary omega-3 fatty acids for women. Bourre JM.

This review details the specific needs of women for omega-3 fatty acids, including alpha linoleic acid (ALA) and the very long chain fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Omega-3 fatty acid (dietary or in capsules) ensures that a woman's adipose tissue contains a reserve of these fatty acids for the developing fetus and the breast-fed newborn infant. This ensures the optimal cerebral and cognitive development of the infant. The presence of large quantities of EPA and DHA in the diet slightly lengthens pregnancy, and improves its quality. Human milk contains both ALA and DHA, unlike that of other mammals.
Conditions such as diabetes can alter the fatty acid profile of mother's milk, while certain diets, like those of vegetarians, vegans, or even macrobiotic diets, can have the same effect, if they do not include seafood.

ALA, DHA and EPA, are important for preventing ischemic cardiovascular disease in women of all ages.

Omega-3 fatty acids can help to prevent the development of certain cancers, particularly those of the breast and colon, and possibly of the uterus and the skin, and are likely to reduce the risk of postpartum depression, manic-depressive psychosis, dementias (Alzheimer's disease and others), hypertension, toxemia, diabetes and, to a certain extend, age-related macular degeneration.
Omega-3 fatty acids could play a positive role in the prevention of menstrual syndrome and postmenopausal hot flushes. The normal western diet contains little ALA (less than 50% of the RDA). The only adequate sources are rapeseed oil (canola; CAVEAT THIS ALSO CONTAINS OMEGA6'S WHICH IS PRO-INFLAMMATORY WHEN EXCESSIVE), walnuts and so-called "omega-3" eggs (similar to wild-type or Cretan eggs). The amounts of EPA and DHA in the diet vary greatly from person to person. The only good sources are fish and seafood, together with "omega-3" eggs. PMID: 17254747



Asia Pac J Clin Nutr. 2003.12 Suppl:S38
Feeding regimes affect fatty acid composition in Australian beef cattle. Mann NJ, Ponnampalam EN, Yep Y, Sinclair AJ.

Background - There is growing evidence that red meat contributes significantly to the intake of omega 3 long chain PUFA in western diets. The type of feeding regime used in animal production, can influence the lipids in red meat due to the fatty acid composition of the feed. Pasture feed being relatively rich in a-linolenic acid (18:3 n-3), while grain is relatively rich in linoleic acid (18:2n-6).
Objective - To determine the effect on beef fatty acid profile of varying length of grain feeding compared with grass feeding.
Design - Samples of rump, strip loin and blade cuts were obtained from eighteen cattle from each of three feeding regimes (pasture fed, short term grain feeding STGF, and long term grain feeding LTGF). All samples were analysed in triplicate as lean tissue only, using a standard chloroform - methanol extraction and capillary column gas-chromatograph fatty acid quantification.
Outcomes - Total fat, saturated and monounsaturated fatty acids were all significantly higher in the LTGF animals. The grass fed animals had higher levels of omega 3 PUFA in all three cuts, with combined EPA + DHA reaching levels in blade and strip loin that would meet Australian Food Standards classification as a ' source' of omega-3, with the rump cut reaching this level in the STGF group also. Rump from the grass fed animals was a relatively rich source of EPA + DHA and would qualify as a 'good source' of omega 3.
Conclusions - This study was able to show that pasture feeding of Australian cattle maximises omega-3 PUFA content and minimizes trans 18:1 fatty acid levels relative to grain feeding. Furthermore, LTGF results in elevated total fat and saturated fat content relative to STGF or grass feeding in lean cuts of Australian beef. PMID: 15023647

-G

10 comments:

Gyan said...

Wheat is meant to be eaten freshly milled (the flour should be consumed within a week of milling) and should be of 100% extraction.
Now how many moderns eat such wheat.

Anonymous said...

I read the article and it doesn't say autoimmune disease can be reversed simply by going gluten free...

It said only the patients positive for Celiacs antibodies improved.

Quote:

"In patients with IgA and/or IgG antigliadin antibodies the symptoms have been shown to improve on a gluten-free diet. "

I was once thought to have Celiacs (before Graves dx). I am negative for IgA and IgG antigliadin abs and I had no change in my symptoms whether I was on gluten free or not.

Getting my Graves disease under control resolved my bowel problems fully.

Dr. B G said...

Reversibility probably depends on the degree of physical damage from auto-antibodies. For instance, in rheumatoid arthritis, if the joints have already become deformed, the likelihood of reversibility from nutritional factors is not going to be likely, unfortunately. For Grave's and other autoimmune conditions, the antibodies to gluten are not found 100 % which probably means there are other triggers including other environmental factors like viral illnesses. That is interesting you noticed a GI connection with Graves.

-G

Dr. B G said...

Here is the link with poor glycemic control with synthetic Vitamin D2 (ergocalciferol)

Dr. Gerry Schwarfenberg, MD, CCFP
http://www.cfp.ca/cgi/reprint/53/9/1435

Stephan said...

I don't think we can say people were tolerating wheat well in ancient times. True, their wheat was presumably lower in gluten, and they probably had better processing methods (like soaking and fermentation), but the switch to wheat-based agriculture was accompanied by a decline in multiple measures of health. This includes reduced stature, which may be indicative of abnormal mineral metabolism. Could be the phytic acid or something else.

I don't think wheat has ever been a healthy food, it was simply a deal with the devil to get more population density. Although I bet adequate vitamin D did mitigate its effects.

Dr. B G said...

I've been reading about phytic acid from wheat. Sprouted wheat at least seems a little better (but am not aware of the resultant effects from B5 and other peptides).

Gout, gallbladder and kidney stones are probably closely related to the higher acidity from high-wheat-consumers.
-G

Gyan said...

Dr b.g,
Could you amplify your last comment about acidity problem in high-wheat eaters.
I have a sister-in-law who suffers from a chronic acidity plus gout and recently had gallbladder removed, so I am very much interested in the connection.
She is also sufferering from irregular (and dmissed) pulse.

Dr. B G said...

Gyan,

Phytic acid is from the outer shell of wheat (and other gluten-containg grains) which affects our body chemistry after consumption (lowers pH, acidifies). Not all phytic acid is bad (in fact most are good and anti-inflammatory like from soy) -- the not so great ones are those accompanied by high carbs! The resultant pH change can affect individuals with high uric acid in the blood by causing the uric acid to 'crystallize' out which is painful when this happens in your ear or big toe. (Like a super-saturated sugar solution -- remember? making sugar crystals at school or with your mom?)

Uric acid is also secreted in sweat -- an 'exercise deficiency' may also allow some to build up.

Or high uric acid is involved with metabolic derangements. I couldn't find the link between phytic acid/high-wheat-intake and blood acidification. But the other two articles below demonstrate a link between high carb diets (ie, wheat including bread chappati cereal etc + HFCS) and gout/hyperuricemia (and insulin resistance). For gallbladder stones, it's the same story. Fatty gallbladder leads often to more gallstones these days. Hope that helps!

-G

Nippon Rinsho. 2008 Apr;66(4):669-74.[Physiology and dynamics of uric acid in hyperuricemia][Article in Japanese]
Takagi K, et al.
Gout is a type of inflammatory arthritis that is triggered by the crystallization of monosodium urate (MSU) within the joints and is often associated with hyperuricemia. Further understanding the physiology and dynamics of uric acid in human is required to make sure the disease mechanism of both gout and hyperuricemia in clinic. The amount of urate in the body consists urate pool, and which depends on the balance between dietary intake, synthesis, and excretion. Uric acid is a weak acid that exists largely as MSU, the ionized form, in urate pool at physiologic pH. But the solubility of MSU is influenced of pH, temperature and protein of blood and tissue. PMID: 18409512


++++++++++++++++++++++++
Int J Obes Relat Metab Disord. 1996 Nov;20(11):975-80.
Relationship of uric acid concentration to cardiovascular risk factors in young men. Role of obesity and central fat distribution. The Verona Young Men Atherosclerosis Risk Factors Study.Bonora E, et al.
OBJECTIVE: To examine the relationships of serum uric acid concentration with several risk factors of cardiovascular diseases (CVD). SUBJECTS: 957 men 18 y old participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study. MEASUREMENTS: Body mass index (BMI), waist/hip ratio (WHR), serum uric acid, serum lipids, blood pressure, fasting insulin and behavioural variables. RESULTS: Serum uric acid concentration showed positive associations with BMI (r = 0.24; P < 0.0001), WHR (r = 0.19; P < 0.0001) and serum triglyceride levels (r = 0.19; P < 0.0001); it was also significantly correlated to systolic (r = 0.08; P < 0.01) and diastolic (r = 0.11; P < 0.001) blood pressure, fasting insulin (r = 0.11; P < 0.001), total (r = 0.12; P < 0.001) and LDL cholesterol (r = 0.10; P < 0.01) plasma concentrations. Life-style characteristics, such as smoking and physical activity did not show any significant association, while daily alcohol intake was positively associated with uric acid concentration (r = 0.09; P < 0.01). While the adjustment for fasting insulin did not substantially change these results, the magnitude of the correlations between uric acid and CVD risk factors markedly decreased when allowance was made for BMI and WHR. Only triglycerides maintained an independent correlation with uric acid levels (r = 0.17; P < 0.0001). In multivariate regression analysis, serum triglycerides, BMI and WHR (at borderline significance) were independent positive predictors of uric acid (R2 of the model 0.122, P < 0.001), while fasting insulin concentration did not give any independent contribution to explain the variability uric acid levels. CONCLUSIONS: These data indicate that, already in young, essentially health subjects, hyperuricaemia associates with several components of the so-called insulin resistance syndrome, thus suggesting that increased levels of uric acid might be another member of this syndrome. In addition, these data suggest that obesity and central body fat distribution, rather than hyperinsulinaemia/insulin resistance, play a major role in linking hyperuricaemia with CVD risk factors clustering in the insulin resistance syndrome. Nevertheless, hypertrigliceridemia is related to hyperuricemia independently of obesity and central body fat distribution. PMID: 8923153

Am J Physiol Renal Physiol. 2006 Mar;290(3):F625-31.
A causal role for uric acid in fructose-induced metabolic syndrome.Nakagawa T, Johnson RJ et al.
Division of Nephrology, Hypertension, and Transplantation,
The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid. PMID: 16234313

-G

Gyan said...

The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup) .

What does it mean?. That fructose consumption in form of whole fruits is OK?

Dr. B G said...

Table sugar is a di-saccharide consisting of glucose-fructose. Fructose creates a lot of havoc metabolically because it does not go throught the same biochem pathways the way normal carbs do.

Fructose is like a criminal -- it gets a 'get out of jail' CARD -- do you play Monopoly Gyan?

Fructose (esp alone -- like in soda and in fruit that is consumed unmatched, no protein or no fat) will fail to trigger an insulin surge the way that normal complex carbs and glucose and lactose would. Eventually, in a simple chemical rxn, fructose gets converted to glucose for energy.

The resultant surge in blood glucose does not get countered by insulin which allows tissues to be damaged by the elevated glucoses. Later the insulin kicks in... and whoa the glucoses have already naturally begun to decline. People can experience ravenous hunger, a failure for satiation and subsequent tissue damage (from glucoses hanging around) with fructose.

-g