Stress, Inflammation & Diet

How Flush GBI Fits Into the Bigger Picture

The basics

Stress is your body’s response to a challenge. Nutritionally, some foods can provoke that response (pro-inflammatory), while others can moderate it (anti-inflammatory). When stress pathways activate, the immune system releases mediators (e.g., cytokines), producing inflammation.

Why inflammation happens

Inflammation can follow infection, injury, or subtler triggers. It may be:

• Acute (short-term) or chronic (persistent), and

• Local (one area) or systemic (body-wide).
  Chronic, smouldering inflammation is linked to a higher risk of adverse outcomes over time. [1–3]

Measuring it

Clinicians often assess:

• CRP (C-reactive protein): a sensitive, short-lived marker of inflammatory activity. [4–6]

• Cytokines such as IL-6 and TNF-α (sometimes alongside CRP). [7–10]
  Testing is medical (not at-home) and done when clinically appropriate.

Diet’s role

Diet can clearly influence inflammatory activity—dramatically in some conditions (e.g., coeliac disease with gluten) and modestly in others (e.g., rheumatoid arthritis). [11–12]

The “anti-inflammatory diet” idea

There’s no single template, but consistent, evidence-aligned themes include:

• Emphasise oily fish, nuts, seeds, colourful produce, leafy greens, olive oil, herbs/spices.

• Limit excess calories, refined carbs/sugars, and saturated fat. [13–15]

Dietary Inflammatory Index (DII) – what it suggests

A literature-derived scoring approach indicates diets richer in omega-3s and phytonutrients tend to be less inflammatory; patterns high in refined carbs, sugar, calories, and saturated fat tend to be more inflammatory. [16–21]
Mediterranean-style patterns align with lower inflammatory markers; typical Western patterns do not. [22–24]

Where Flush GBI fits

Nutrients can only help if they’re absorbed and tolerated well. Flush GBI is designed to reset the gut, bowel, and intestinal environment, which may support:

• More comfortable digestion and regularity

• A cleaner “terrain” for dietary strategies (omega-3s, fibre, polyphenols) to do their job
  Flush GBI isn’t a treatment for inflammatory disease; it’s a foundational gut-reset protocol intended to complement an anti-inflammatory eating pattern.

Beware the hype

• Isolated “miracle” compounds rarely translate from cell/animal data to meaningful human outcomes. [25–28]

• Some antioxidant megadoses can even blunt exercise adaptations. [29]

• Fish-oil and similar tools can help, but effects at dietary doses are typically modest, not magical. [30]

Practical takeaways

1. Build the base: plenty of plants (especially colourful, non-starchy veg), whole grains, legumes, nuts/seeds, and regular oily fish.

2. Dial down ultra-processed load: less refined carbs/sugars and excess saturated fat.

3. Reset the terrain: use Flush GBI to clear the gut and support comfortable, regular elimination so your diet can work harder for you.

4. Think pattern, not products: results come from what you eat most of the time, plus sleep, movement, and stress management.

References

1. Pahwa R, et al. Chronic Inflammation. 2020.

2. InformedHealth.org. What is an inflammation? 2010.

3. Furman D, et al. Nat Med. 2019;25(12):1822–32.

4. Luan Y-Y, et al. Front Immunol. 2018;9:1302.

5. Sproston NR, et al. Front Immunol. 2018;9:754.

6. Pepys MB, et al. J Clin Invest. 2003;111(12):1805–12.

7. Bautista LE, et al. J Hum Hypertens. 2005;19(2):149–54.

8. IL6R MR Consortium. Lancet. 2012;379(9822):1214–24.

9. Diez-Pina JM, et al. Int J Gen Med. 2009;2:9–14.

10. Monastero RN, et al. Int J Inflam. 2017;2017:4309485.

11. NHS. Coeliac disease. https://www.nhs.uk/conditions/coeliac-disease/causes/

12. Vadell AKE, et al. Am J Clin Nutr. 2020;111(6):1203–13.

13. Marcason W. J Am Diet Assoc. 2010;110(11):1780.

14. WorldCat search “anti inflammatory diet”: https://www.worldcat.org/search?qt=worldcat_org_bks&q=anti+inflammatory+diet&fq=dt%3Abks

15. Ricker MA, et al. Nutr Clin Pract. 2017;32(3):318–25.

16. Li J, et al. J Am Coll Cardiol. 2020;76(19):2181–93.

17. Shivappa N, et al. Nutrients. 2018;10(2).

18. Hansen PR. Curr Pharm Des. 2018;24(3):281–90.

19. Zwickey H, et al. J Restor Med. 2019;8(1):e20190107.

20. Cavicchia PP, et al. J Nutr. 2009;139(12):2365–72.

21. Shivappa N, et al. Public Health Nutr. 2014;17(8):1689–96.

22. Neale EP, et al. Nutr Res. 2016;36(5):391–401.

23. Schwingshackl L, et al. Nutr Metab Cardiovasc Dis. 2014;24(9):929–39.

24. Kiecolt-Glaser JK. Psychosom Med. 2010;72(4):365–9.

25. Epstein J, et al. Br J Nutr. 2010;103(11):1545–57.

26. White CM, et al. Pharmacol Res. 2019;146:104280.

27. Bast A, et al. Trends Pharmacol Sci. 2013;34(8):430–6.

28. Bjelakovic G, et al. JAMA. 2007;297(8):842–57.

29. Ristow M, et al. PNAS. 2009;106(21):8665–70.

30. Patel K. Examine.com. Inflammation. https://examine.com/topics/inflammation/#