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Table 1 Summary of the immune impacts of dietary components and the nutritional impacts of various disease states

From: Fast food fever: reviewing the impacts of the Western diet on immunity

Macronutrient Immunologic impact In vitro evidence Animal models Human evidence Reviews
Simple sugars - Reduced phagocytosis 24 25, 9495, 100, 101, 102 92, 103, 104
- Increased inflammatory cytokines production
- Dysbiosis
Complex sugars - Reduced inflammatory cytokine production 27 33 27, 28, 29–30, 31 26, 32
- As part of intact food substance, may reduce risk of certain diseases
- Reduced dysbiosis
Artificial sweeteners - Mostly unknown or unproven 36-37, 104-107 35, 40 34
- Potential contributor to inflammatory bowel disease
- Stevioside may enhance phagocytosis and T/B-cell mitogen responses
Salt - May increase IL-17 and worsen autoimmune disorders 41-42
Saturated fat - Alterations in prostaglandin pathway and antioxidant mechanisms 45, 47–49, 59, 61–62, 161-163 50-52, 55, 60 54, 56, 5758, 164 43-44, 53, 63
- TLR2, and TLR4 activation; CD14 alterations
- Increase gut inflammation and reduce gut barrier function
- Worse outcomes in sepsis; Increased risk of autoimmunity, allergy, certain neoplasms
- Dysbiosis
Trans fat - Mostly unknown 64
- Increased IL-6 and CRP levels
Omega-6 fatty acids - Increased inflammation via TLR4 activation 67 52, 66 65, 68 53, 64
- Dysbiosis
Omega-3 fatty acids - Reduced inflammatory cytokines and transcription factors 48, 74 80-82, 136 75-77 63, 72–73, 79
- Increased resolvin and protecin production
- Increased IL-10
Gluten - Possible TLR4 activation; studies limited to animal models 83 83 84-87 88-89
- Induction of Celiac symptoms in patients with HLA-DQ2 or HLA-DQ8
Red meat - Mostly unproven; studies limited to animal models 145 142, 147 64, 149
- Increased endothelial inflammatory, activation of foam-cell macrophages
Genetic modification - Mostly unknown 209-211 212-218 202, 207, 219
- Reduction vitamin A or calorie deficiency depending on modification/location of deployment
- No apparent impact on allergic disease
- Increased exposure to pesticides
- Potential for transmission of functional genes into small bowel bacteria
Pathologic disorder Effect on nutrition and/or immunity In vitro evidence Animal models Human evidence Reviews
Obesity - Increased inflammatory cytokines, immunologic tolerance to inflammatory cytokines 12 19 11, 1315, 16–18, 21, 169-171 7, 20, 149
- Reduced leukocyte numbers and function
- Reduced control of infection, heightened rates of certain neoplasms
- Overproduction and eventual tolerance of leptin
- Dysbiosis
Anorexia and bulimia - Reduced monocyte, neutrophil, and T-cell numbers and function 22 23
- Reduced complement function
- Any disorders related to micronutrient disorders
Dysbiosis - Maternal transmission leading to immune alterations in the offspring 47, 96–98, 104–107, 198-199 52, 93, 111, 139, 144, 196 94-95, 100, 101, 102, 109, 110, 116, 131135, 138, 141–143, 197 91-92, 99, 103
- Epigenetic changes altering offspring immunity via paternal inheritance
- Reduced regulatory T cell numbers
- Worse outcomes in sepsis; Increased risk of autoimmunity and allergy
- May increase likelihood of obesity
- May increase risk of certain neoplasms
Chronic inflammation - Reduced appetite and weight loss 155 2
- May increase risk of certain neoplasms
Food allergy - Avoidance diets predisposing to deficiency in calcium and omega-3 222, 223, 224, 226
  1. Citations are organized by the primary models used in the research, cell culture (In vitro), animal, or direct human effects. For studies involving human data: further notation indicates cross-sectional studies (standard font); longitudinal study designs both prospective or retrospective or reviews discussing longitudinal evidence (italic font); or interventional trials or reviews discussing intervention studies (bold font). The citations provided are not meant to be all-inclusive and thus additional cited reviews of note are also provided; no additional annotation is provided in the review article column.