Designs for Health



Breakfast

Smoked salmon, rice cakes, green tea

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2-3 Egg omelet from hens fed flaxseed, sweet potatoes w/rosemary, ½ cup black beans

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Organic oatmeal, milk, soymilk, or goat’s milk, 3 Tbsp. fresh ground flaxmeal

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Hot brown rice cereal w/cinnamon, green tea

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Sugar free yogurt, 1 Tbsp. flaxseed oil, ½ cup berries

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Poached organic omega-3 eggs, sweet potatoes, smoked salmon

Lunch and Dinner

Large mixed green salad, small can of tuna, chopped yellow and sweet red peppers

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Season sardines in water (green and white label), green salad

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Swordfish steak, grilled onions, green salad with flax oil dressing

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Broiled red snapper, steamed broccoli, baked yams

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1 cup cottage cheese or yogurt, 1 tablespoon flax oil, 1 Tbsp. natural preserves

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4 ounces wood-smoked or broiled salmon, brown rice Vermicelli pasta (Pastariso brand), tomato sauce w/ extra oregano, thyme, and garlic, grilled vegetables

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1 chicken breast with rosemary, ½ cup black eyed peas, roasted onions or garlic,

spinach salad.

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Salmon burger patties made with 6 oz. chopped salmon, onions, dill, an egg, and ¼ cup ground sesame seeds, and sautéed in skillet with 1 Tbsp. butter.

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Snacks

Roasted garlic or almond butter on rice cake or celery, protein shakes with freshly ground flaxseeds added, handful of raw almonds, hazelnuts, walnuts, brazil nuts, or pumpkin seeds, fresh organic fruit of any kind, 2 oz. cheese, lean hormone free meat with mustard, hard boiled egg

Avoid

Antibiotics (Crohn’s), NSAIDS (if possible), corticosteroids treatment, wheat or dairy (if sensitive or allergic), sugar, alcohol, caffeine, allergenic foods, refined and processed foods, hydrogenated oils, safflower, sunflower, and corn oils

Beverages

Green drinks: Green Magma, Kyogreen, or Green Kamut: (1 tsp. 1-3x day in water)

Herbal Teas: Chamomile, Green Tea, Slippery Elm

Suggestions And Goals

IBD & Crohn’s:

Treatment using nutrition and elimination diets has been very successful for Crohn’s and IBD. Check for immune system abnormality. It is critical for IBD sufferers to keep eating sufficient amounts of food to provide nutrition and prevent further complications. Corticosteroid treatment should be avoided (or seriously compensated for with nutrition) since it leads to nutrient depletion and malabsorption, and causes protein catabolism. Elemental diets which contain predigested or isolated proteins have been successful, as have allergen elimination diets. Also, high complex carbohydrate, high fiber diets have been successful. Regular Exercise is important, as is relaxation exercises.

Arthritis (also see Autoimmune Program A):

Often helped by physical therapy such as exercise, heat, cold, massage, diathermy, lasers, and paraffin and mineral baths. Look into improving impaired digestion due to hydrochloric acid deficiency and/or altered GI flora.

Migraines:

Perform relaxation exercises such as deep breathing, meditation, prayer, and visualization. Eliminate Food Allergies. Drink at least 48 oz. purified water daily.

Cayenne pepper for cluster headaches and migraines. Feverfew leaf 100 mg x 2 as preventive (.66-.74% parthenolide), and ginger.

Supplements

EPA/DHA 2,000-10,000 mg (this equals EPA + DHA values)

Vitamin E 400-1200 IUs (Gamma Tocopherol should be included)

GLA 240 mg capsules/2-6 per day

Acidophilus 1-2 tsp. per day for 2 weeks

Bifidobacteria 1-2 tsp. per day for 2 weeks

Vitamin C 1-20 grams

Selenium 400 mcg

Zinc 25 mg

Lipoic Acid 100-600 mg

Grape Seed Extract 50-300 mg

Curcuminoids 100-1,000 mg

Boswellia Extract 1200 mg

Quercetin 300-900 mg

Bromelain 1-2 g

Magnesium 400 mg

Copper Sebacate 2-4 mg

Taurine 1-3 grams

NAC 1-2 grams

Glutamine (IBS) 1-40 grams

Molybdenum 100-500 mcg

MSM 2-4 grams

Cayenne pepper ¼ tsp. per cup hot water or creams

Feverfew 1-2 capsules per day of extract standardized for parthenolides

In Osteoarthritis:

Glucosamine HCL 1500-3,000 mg

Chondroitin Sulfates 300-2,000 mg

Manganese 5-10 mg

MSM 1-6 grams

Research Review

Gut Inflammation, Bowel Permeability and Inflammatory Joint Disorders

Ankylosing spondylitis (AS) is reportedly associated with subclinical endoscopic gut inflammation in up to 57% of patients. We sought to re-examine intestinal permeability in patients with AS and their relatives. We studied small intestinal and gastric permeability by measurement of excretion of lactulose, mannitol, and sucrose in 60 patients with AS and 24 of their first-degree relatives. Both patients and first-degree relatives had significantly increased small intestinal, but not gastric, permeability compared to controls. Among patients, current users of nonsteroidal anti-inflammatory drugs (NSAID) had significantly increased small intestinal permeability compared to nonusers, but relatives not using NSAID also had increased permeability. CONCLUSION: Patients with AS have altered small intestinal, but not gastric, permeability. NSAID use cannot explain all the abnormality. Bowel permeability abnormalities, possibly genetically determined, may antedate development of bowel or joint symptoms. Increased CD20+CD45RO+ expression suggests increased antigen exposure, which may be related to previous or current intestinal permeability abnormalities.[1]

Ankylosing Spondylitis is a form of arthritis that involves primarily the spine and joints of the extremities, such as the shoulders, hips and knees. It strikes young adults, causing pain, stiffness, and disability in severe cases.

Some of today's most exciting immunologic research relevant to the pathogenesis of spondyloarthropathies concerns the relationship between the host immune system in the gut and in the intestinal bacteria. Through transgenic and gene knockout studies in rodents and the development of appropriate experimental models, it has become clear that this relationship depends on a fine balance in the production of different cytokines. The connection between gut inflammation and spondyloarthropathy has been carefully documented by clinicians over the past 30 years.[2]

Spodyloarthropathies are also known as "spondylarthritis", "seronegative arthritis", and "seronegative spondyloarthropathy". These are a group of inflammatory arthritis that can cause joint pain and stiffness in not only the upper and lower extremities but also pain and stiffness in the neck, upper and lower back.

Since reactive arthritis is induced by specific urogenital or enterogenic bacteria, and since the gut is implicated in different forms of spondyloarthropathies, especially in IBD, it was clear that the gut could play an important role by permitting exogenous factors to enter the body. This hypothesis was the rationale for investigating the gut in the spondyloarthropathies by performing ileocolonoscopies. In the first ileocolonoscopic studies of SpA patients, histological signs of gut inflammation were found in a relatively great number of patients, mostly without any clinical intestinal manifestations. These lesions were not seen in other inflammatory joint diseases. Further ileocolonoscopic studies confirmed the strong relationship between gut and joint inflammation. In patients in whom a second ileocolonoscopy was performed, remission of the joint inflammation was always connected with a disappearance of the gut inflammation, whereas persistence of locomotor inflammation was mostly associated to the persistence of gut inflammation. The hypothesis was proposed that some patients with a spondyloarthropathy had a form of subclinical Crohn's disease in which the locomotor inflammation was the only clinical expression. This hypothesis was confirmed in prospective long-term studies in which the ileocolonoscoped patients were reviewed 2 to 9 years later: about 6% of SpA patients not presenting any sign of Crohn's disease at first investigation but demonstrating gut inflammation on biopsy, developed full-blown Crohn's disease. The discovery of subclinical gut inflammation in the SpA had therapeutic consequences. Sulphasalazine (SASP) has been proven to be an active drug in the treatment of IBD. Since the gut could play a crucial role in SpA, it was logic to use this drug in the treatment of this disease. Multiple open and double- blind studies have proven the effectiveness of this drug in SpA; recent studies concluded that the beneficial effect of the drug in this disease entity is more prominent on the peripheral arthritis than on the axial disease.[3]

Klebsiellae Infection and Gut Inflammation in Ankylosing Spondylitis

A role for Klebsiella pneumoniae in ankylosing spondylitis (AS) has been suggested because fecal carriage of Klebsiella and serum Klebsiella specific antibodies may be increased in this disease. This study has extended the earlier findings by comparing Klebsiella specific serum IgA class antibodies with inflammatory changes in the gut. METHODS: IgA antibodies to K pneumoniae, Escherichia coli, and Proteus mirabilis in serum samples of 25 patients with AS, of eight control patients, and of 100 healthy blood donors were measured by enzyme immunoassay. Gut inflammation of the patients was studied by ileocolonoscopy. RESULTS: Increased IgA antibody concentrations to K pneumoniae associated with gut inflammation in patients with axial form of AS. Such association was not seen in patients with peripheral form of AS. These findings may provide further evidence for the role of K pneumoniae in the pathogenesis of AS. [4]

The term "enteropathic arthritis" describes joint manifestations that occur in conjunction with gastrointestinal disease. Underlying causes include inflammatory bowel disease, reactive arthritis, iatrogenic disease. Whipple's disease, and other gastrointestinal diseases. A possible association between Reiter's syndrome and human immunodeficiency virus infection also has been reported. These arthritic syndromes can be treated symptomatically, but long-term therapy should be directed at the underlying cause.[5]

Whipple's disease is a malabsorption disease. It interferes with the body's ability to absorb certain nutrients. The disease causes weight loss, irregular breakdown of carbohydrates and fats, resistance to insulin, and malfunctions of the immune system. Whipple's disease is caused by bacteria. The disease causes lesions on the wall of the small intestine and thickening of the tissue. The villi, tiny, finger-like protrusions from the wall that help absorb nutrients are destroyed. Symptoms include diarrhea, intestinal bleeding, abdominal bloating and cramps, loss of appetite, weight loss, fatigue, and weakness. Arthritis and fever often occur several years before intestinal symptoms develop. Diagnosis is based on symptoms and results of a biopsy of tissue from the small intestine. Whipple's disease is treated with antibiotics to destroy the bacteria that cause the disease.

Elimination Diet

Additions in five steps were made, as a possible therapeutic measure, to the diet of 27 patients with rheumatoid arthritis (RA) after a period of two weeks of a basal isocaloric diet free from pulses, cereals, milk, and non-vegetarian protein foods. Fourteen patients finally took part in the trial, 10 (71%) of whom showed significant clinical improvement. Only three patients (11%) adhered to the diet for a period of 10 months. The others discontinued the diet and were then treated with conventional disease modifying drugs. The study indicates that dietary factors may influence inflammatory response in RA.[6]

Vegetarian Diet

Many patients with atopic dermatitis are dissatisfied with conventional treatments based on topical steroids and have experienced some traditional remedies and alternative therapies. However, most of such therapies have not been evaluated scientifically and clinically by specialists. This study was designed to assess whether a certain vegetarian diet might be effective for atopic dermatitis and if so, to identify the mechanisms of this remedy through analyses of immunological parameters. An open-trial study was carried out in twenty patients with atopic dermatitis. An improvement of dermatitis was evaluated by SCORAD index and serological and immunological parameters were monitored. After a two-month treatment, the severity of dermatitis was strikingly inhibited, as assessed by SCORAD index and serological parameters including LDH5 activity and a number of peripheral eosinophils. A sharp reduction in eosinophils and neutrophils was observed prior to improvement in the skin inflammation. In addition, PGE2 production by peripheral blood mononuclear cells was reduced by this treatment. In contrast, serum IgE levels did not change during the same period. Although this study is an open-trial one, it suggests that this treatment may be useful for the treatment of adult patients with severe atopic dermatitis.[7]

Two patients with seropositive inflammatory arthropathies who experienced clinical improvement on the Waianae diet are presented. The scientific literature validates the usefulness of fasting in the control of joint inflammation. Elimination diets are variably successful. Fasting followed by a vegetarian diet can produce a sustained positive response measured clinically and by laboratory variables of inflammation; the efficacy of such an approach appears to hinge on the alteration of fecal flora. Swaying the balance of dietary fats in favor of the omega 3 and omega 6 fatty acids has an antiinflammatory effect, but does not appear to correct the basic immunologic processes involved in the development of the arthropathies. Practical guidelines for the application of this information are offered.[8]

Plants are rich natural sources of antioxidants in addition to other nutrients. Interventions and cross sectional studies on subjects consuming uncooked vegan diet called living food (LF) have been carried out. We have clarified the efficacy of LF in rheumatoid diseases as an example of a health problem where inflammation is one of the main concerns. LF is an uncooked vegan diet and consists of berries, fruits, vegetables and roots, nuts, germinated seeds and sprouts, i.e. rich sources of carotenoids, vitamins C and E. The subjects eating LF showed highly increased levels of beta and alfa carotenes, lycopen and lutein in their sera. Also the increases of vitamin C and vitamin E (adjusted to cholesterol) were statistically significant. As the berry intake was 3-fold compared to controls the intake of polyphenolic compounds like quercetin, myricetin and kaempherol was much higher than in the omnivorous controls. The LF diet is rich in fibre, substrate of lignan production, and the urinary excretion of polyphenols like enterodiol and enterolactone as well as secoisolaricirecinol were much increased in subjects eating LF. The shift of fibromyalgic subjects to LF resulted in a decrease of their joint stiffness and pain as well as an improvement of their self-experienced health. The rheumatoid arthritis patients eating the LF diet also reported similar positive responses and the objective measures supported this finding. The improvement of rheumatoid arthritis was significantly correlated with the day-to-day fluctuation of subjective symptoms. In conclusion the rheumatoid patients subjectively benefited from the vegan diet rich in antioxidants, lactobacilli and fibre, and this was also seen in objective measures.[9]

We have previously reported that a significant improvement can be obtained in rheumatoid arthritis patients by fasting followed by an individually adjusted vegetarian diet for one year. The patients who changed their diet could be divided into diet responders and diet nonresponders. After the clinical trial the patients were free to change diet or medication and after approximately one year they were asked to attend a new clinical examination. We compared the change from baseline (i.e. at the time of study entry) to the time of the follow-up examination for diet responders, diet nonresponders and controls who ate an omnivorous diet. The following variables favored diet responders: pain score, duration of morning stiffness, Stanford Health Assessment Questionnaire index, number of tender joints, Ritchie's articular index, number of swollen joints, ESR and platelet count [corrected]. The difference between the three groups were significant for all the clinical variables, except for grip strength. There was no significant difference between the groups with regard to laboratory or anthropometric variables. At the time of the follow-up examination all diet responders but only half of the diet nonresponders still followed a diet. Our findings indicate that a group of patients with rheumatoid arthritis benefit from dietary manipulations and that the improvement can be sustained through a two-year period.[10]

The beneficial effect of a 1-yr vegetarian diet in RA has recently been demonstrated in a clinical trial. We have analyzed stool samples of the 53 RA patients by using direct stool sample gas-liquid chromatography of bacterial cellular fatty acids. Based on repeated clinical assessments disease improvement indices were constructed for the patients. At each time point during the intervention period the patients in the diet group were then assigned either to a group with a high improvement index (HI) or a group with a low improvement index (LI). Significant alteration in the intestinal flora was observed when the patients changed from omnivorous to vegan diet. There was also a significant difference between the periods with vegan and lactovegetarian diets. The fecal flora from patients with high improvement index and low improvement index differed significantly from each other at 1 and 13 months during the diet. This finding of an association between intestinal flora and disease activity may have implications for our understanding of how diet can affect RA.[11]

Fasting

Otherwise healthy and well-nourished patients with rheumatoid arthritis show significant clinical improvement from practicing prolonged fasting for 7 to 10 days. The improvement is reversible and lost when eating is taken up again. Although of little therapeutic value, the anti- inflammatory effect of short-term fasting is of significant interest and better understanding of the mechanisms is desirable.[12]

Total fasting induces within a few days a substantial reduction of joint pain, swelling, morning stiffness, and other arthritic symptoms in patients with rheumatoid arthritis. This remission subsides slowly after discontinuation of fasting. Its mechanisms are complex and involves diminished activation of neutrophils and lymphocytes and decreased generation of leukotrienes and of concentrations of serum complement factors, as well as of other proinflammatory systems.[13]

Vitamins E, B2 and C

Vitamins E, B2, and C have been shown to exert an inhibitory effect on osteo-arthritis in animals, and it has been found that supplementation therapy, particularly with vitamin E and the combination of vitamins B1, B6, and B12, can exert a beneficial effect on the symptomatology of human degenerative joint disease. Mineral deficits in calcium, zinc and selenium (Kashin-Beck disease; endemic osteo-arthritis deformans) can provoke skeletal damage in humans and animals.[14]

Vitamins B

OBJECTIVES: To investigate the effects of treatment with B vitamins on homocysteine (Hcy) levels in patients with RA, and to analyse the relationship between Hcy levels and inflammatory variables, and/or MTX treatment. METHODS: Sixty-two patients with RA and levels of Hcy > or = 12 mumol/L were randomized to receive placebo or a combination of vitamins B6, B12 and folic acid. The patients were treated and evaluated in a double-blind manner over 12 months. RESULTS: The Hcy level decreased significantly in the B-vitamin treated patients compared with the placebo treated patients. In a simple regression model, the Hcy level at inclusion was associated with IL-2sR alpha. In a multiple regression model there was an association between the alteration in Hcy level over 0-12 months and MTX treatment, as well as the alteration in CRP, adjusted for B-vitamin treatment. CONCLUSIONS: In patients with RA, Hcy levels can be reduced by treatment with B-vitamins. The Hcy levels were related to markers of inflammation and MTX treatment.[15]

Fatty Acids

The n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are found in high proportions in oily fish and fish oils. The n-3 PUFA are structurally and functionally distinct from the n-6 PUFA. Typically, human inflammatory cells contain high proportions of the n-6 PUFA arachidonic acid and low proportions of n-3 PUFA. The significance of this difference is that arachidonic acid is the precursor of 2-series prostaglandins and 4-series leukotrienes, which are highly-active mediators of inflammation. Feeding fish oil results in partial replacement of arachidonic acid in inflammatory cell membranes by EPA. This change leads to decreased production of arachidonic acid-derived mediators. This response alone is a potentially beneficial anti-inflammatory effect of n-3 PUFA. However, n-3 PUFA have a number of other effects which might occur downstream of altered eicosanoid production or might be independent of this activity. For example, animal and human studies have shown that dietary fish oil results in suppressed production of pro-inflammatory cytokines and can decrease adhesion molecule expression. These effects occur at the level of altered gene expression. This action might come about through antagonism of the effects of arachidonic acid-derived mediators or through more direct actions on the intracellular signalling pathways which lead to activation of transcription factors such as nuclear factor kappa B (NFB). Recent studies have shown that n-3 PUFA can down regulate the activity of the nuclear transcription factor NFB. Fish oil feeding has been shown to ameliorate the symptoms in some animal models of chronic inflammatory disease and to protect against the effects of endotoxin and similar inflammatory challenges. Clinical studies have reported that oral fish oil supplementation has beneficial effects in rheumatoid arthritis and among some patients with asthma, supporting the idea that the n-3 PUFA in fish oil are anti-inflammatory. There are indications that inclusion of n-3 PUFA in enteral and parenteral formulas might be beneficial to patients in intensive care or post-surgery.[16]

BACKGROUND: Patients with rheumatoid arthritis (RA) improve on a vegetarian diet or supplementation with fish oil. We investigated the effects of both dietary measures, alone and in combination, on inflammation, fatty acid composition of erythrocyte lipids, eicosanoids, and cytokine biosynthesis in patients with RA. METHODS: Sixty-eight patients with definitive RA were matched into two groups of 34 subjects each. One group was observed for 8 months on a normal western diet (WD) and the other on an anti-inflammatory diet (AID) providing an arachidonic acid intake of less than 90 mg/day. Patients in both groups were allocated to receive placebo or fish oil capsules (30 mg/kg body weight) for 3 months in a double-blind crossover study with a 2-month washout period between treatments. Clinical examination and routine laboratory findings were evaluated every month, and erythrocyte fatty acids, eicosanoids, and cytokines were evaluated before and after each 3-month experimental period. RESULTS: Sixty patients completed the study. In AID patients, but not in WD patients, the numbers of tender and swollen joints decreased by 14% during placebo treatment. In AID patients, as compared to WD patients, fish oil led to a significant reduction in the numbers of tender (28% vs 11%) and swollen (34% vs 22%) joints (P0.01), 11-dehydro-thromboxane B(2) (15% vs 10%, P ................
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