Instalment 2: Dietary interventions

“We are what we eat” expresses the idea that food and drink have an enormous influence on health and wellbeing. Besides the macronutrients (carbohydrates, such as sugars and starches; fats; protein; and non-digestible fibre), foods contain a huge variety of other chemical compounds, most of which have never been identified or studied.

A huge problem with studying the biological effects of plant-based compounds is our lack of knowledge about how these compounds actually work. Research on the isolated chemical extracts often gives different results from what is found when the plant is eaten. One difference is in the prebiotic qualities of the plant (non-digestible fibre which is fermented by gut bacteria to produce short-chain fatty acids (SCFAs) including butyrate1, a powerful anti-inflammatory. Another difference is that eating the plant also involves ingesting its microRNA; there is good reason to believe that this microRNA directly influences gut bacteria (microbiome). While the colon microbiome is relatively easy to study, examining the bacteria in the duodenum and small intestine is technically difficult in humans. But here is where plant microRNA might have a powerful effect, stimulating bacteria to take up and metabolize glucose from food. This glucose will no longer be available for absorption into the bloodstream and therefore will not trigger insulin secretion by the pancreas. Less insulation, so less inflammation (as well as all the other insulin-stimulated conditions such as cancer, dementia, obesity…)

But here is some of what is known.

Eat more of:

Cruciferous vegetables

Such as broccoli, cauliflower, kale, cabbage, Brussels sprouts, turnips, kohlrabi, bok choy, or radishes, contain sulforaphane, which has been shown to regulate inflammation in mice2. It also lowers insulin levels3.

Vegetables containing inulin

Inulin, a non-digestible carbohydrate, is a prebiotic dietary fibre which can be fermented by gut bacteria to produce short-chain fatty acids (SCFAs) including butyrate4, a powerful anti-inflammatory. Inulin has also been shown to reduce insulin responses after meals5.

Appreciable amounts of inulin are found in vegetables such as plantain, burdock root, chicory root, garlic, Jerusalem artichoke, jicama, leek, or onion.

Konjac noodles

Konjac is a south-east Asian plant whose edible corm can grow up to 25 cm in diameter and contains up to 40% glucomannan, another non-digestible carbohydrate. One use for the corm is to make noodles in a variety of shapes and styles. Again, gut bacteria ferment the glucomannan to produce anti-inflammatory SCFAs6. And as for inulin, insulin levels are decreased by glucomannan7

Fatty fish

Fatty fish such as salmon, trout, tuna, mackerel, and herring, are good sources of long-chain omega-3 fatty acids which are necessary to make anti-inflammatory prostaglandins and leukotrienes (don’t ask!).

At the same time, try to avoid foods rich in omega-6 fatty acids, which are building blocks for pro-inflammatory substances (prostaglandins, thromboxanes, and leukotrienes).

Modern diets often contain appreciable amounts of medium-chain polyunsaturated fatty acids. Unfortunately, these are mostly omega-6 which interfere with the conversion of omega-3s to the long-chain versions. Thus, a double whammy: omega-6s are pro-inflammatory, and they prevent omega-3s from reducing inflammation8.

You can read more about omega-3 fatty acids in my summary, or in my 2006 presentation.

Spices

A number of spices are believed to have anti-inflammatory effects9, including turmeric (containing curcumin), cumin (not to be confused with curcumin), ginger, cinnamon, and hot chili peppers (containing capsaicin). The mechanism may be through insulin lowering, which has been demonstrated for curcumin10, cumin11 ginger12, cinnamon13, and chili14.

Dark chocolate

Dark chocolate is one of a number of foods with anti-inflammatory properties15. Compared to milk or white chocolate, dark chocolate consumption decreased calorie consumption and lowered insulin levels16.

Bitter melon

Traditional and indigenous medicine practices all over the world have identified certain foods that have anti-obesity and anti-diabetes effects, which suggests that they lower insulin. For example, bitter melon, which originated in India, is widely used in China and in the Caribbean, and goes by a variety of names. Bitter melon extract has anti-inflammatory properties and markedly decreases insulin levels17.

Black rice, purple cauliflower, purple corn, blue potatoes

There are varieties of vegetables and fruits which, because of a high content of desirable phytochemicals shown to reduce inflammation18, may be worthwhile seeking out and consuming in preference to the regular supermarket varieties. This includes black rice, purple cauliflower, purple corn, blue potatoes

Slow cooling of cooked foods

When starchy foods such as potatoes, beans, or white rice are slowly cooled after cooking, the links between the glucose molecules in the starch are rearranged, making the starch more difficult to digest; more of the starch becomes “resistant”. This process, called retrogradation, reduces the amount of insulin produced as a result of eating that starchy food19 and may explain why fried french fries produced lower glucose and insulin responses in children compared to pasta, rice, or boiled mashed potatoes20. Additionally, the resistant starch acts as a prebiotic, in that it feeds gut bacteria which ferment the starch to butyrate and other short-chain fatty acids with anti-inflammatory properties21.

End of instalment 2.

Please read instalment 3 of DIY:Inflammation, where I discuss what we should eat less of, and why.

  1. Boets E, Deroover L, Houben E et al. Quantification of in Vivo Colonic Short Chain Fatty Acid Production from Inulin. Nutrients. 2015;7:8916-8929. PMID 26516911
  2. Tian S, Wang Y, Li X, Liu J, Wang J, Lu Y. Sulforaphane Regulates Glucose and Lipid Metabolisms in Obese Mice by Restraining JNK and Activating Insulin and FGF21 Signal Pathways. J Agric Food Chem. 2021;69:13066-13079. PMID 34706542
  3. Tian S, Wang Y, Li X, Liu J, Wang J, Lu Y. Sulforaphane Regulates Glucose and Lipid Metabolisms in Obese Mice by Restraining JNK and Activating Insulin and FGF21 Signal Pathways. J Agric Food Chem. 2021;69:13066-13079. PMID 34706542
  4. Boets E, Deroover L, Houben E et al. Quantification of in Vivo Colonic Short Chain Fatty Acid Production from Inulin. Nutrients. 2015;7:8916-8929. PMID 26516911
  5. Lightowler H, Thondre S, Holz A, Theis S. Replacement of glycaemic carbohydrates by inulin-type fructans from chicory (oligofructose, inulin) reduces the postprandial blood glucose and insulin response to foods: report of two double-blind, randomized, controlled trials. Eur J Nutr. 2017PMID 28255654
  6. Boets E, Deroover L, Houben E et al. Quantification of in Vivo Colonic Short Chain Fatty Acid Production from Inulin. Nutrients. 2015;7:8916-8929. PMID 26516911
  7. Morgan LM, Tredger JA, Wright J, Marks V. The effect of soluble- and insoluble-fibre supplementation on post-prandial glucose tolerance, insulin and gastric inhibitory polypeptide secretion in healthy subjects. Br J Nutr. 1990;64:103-110. PMID 2169302
  8. This is more completely explained in this presentation.
  9. Aggarwal BB. Targeting inflammation-induced obesity and metabolic diseases by curcumin and other nutraceuticals. Annu Rev Nutr. 2010;30:173-199. PMID 20420526
  10. Thota RN, Dias CB, Abbott KA, Acharya SH, Garg ML. Curcumin alleviates postprandial glycaemic response in healthy subjects: A cross-over, randomized controlled study. Sci Rep. 2018;8:13679. PMID 30209353
  11. Taghizadeh M, Memarzadeh MR, Asemi Z, Esmaillzadeh A. Effect of the cumin cyminum L. Intake on Weight Loss, Metabolic Profiles and Biomarkers of Oxidative Stress in Overweight Subjects: A Randomized Double-Blind Placebo-Controlled Clinical Trial. Ann Nutr Metab. 2015;66:117-124. PMID 25766448
  12. Saravanan G, Ponmurugan P, Deepa MA, Senthilkumar B. Anti-obesity action of gingerol: effect on lipid profile, insulin, leptin, amylase and lipase in male obese rats induced by a high-fat diet. J Sci Food Agric. 2014;94:2972-2977. PMID 24615565
  13. Hlebowicz J, Hlebowicz A, Lindstedt S et al. Effects of 1 and 3 g cinnamon on gastric emptying, satiety, and postprandial blood glucose, insulin, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and ghrelin concentrations in healthy subjects. Am J Clin Nutr. 2009;89:815-821. PMID 19158209
  14. Ahuja KD, Robertson IK, Geraghty DP, Ball MJ. Effects of chili consumption on postprandial glucose, insulin, and energy metabolism. Am J Clin Nutr. 2006;84:63-69. PMID 16825682
  15. Natsume M. Polyphenols: Inflammation. Curr Pharm Des. 2018;24:191-202. PMID 29119920
  16. Marsh CE, Green DJ, Naylor LH, Guelfi KJ. Consumption of dark chocolate attenuates subsequent food intake compared with milk and white chocolate in postmenopausal women. Appetite. 2017;116:544-551. PMID 28572069
  17. Bai J, Zhu Y, Dong Y. Response of gut microbiota and inflammatory status to bitter melon (Momordica charantia L.) in high fat diet induced obese rats. J Ethnopharmacol. 2016;194:717-726. PMID 27751827
  18. Talero E, Avila-Roman J, Motilva V. Chemoprevention with phytonutrients and microalgae products in chronic inflammation and colon cancer. Curr Pharm Des. 2012;18:3939-3965. PMID 22632755
  19. Sonia S, Witjaksono F, Ridwan R. Effect of cooling of cooked white rice on resistant starch content and glycemic response. Asia Pac J Clin Nutr. 2015;24:620-625. PMID 26693746
  20. Akilen R, Deljoomanesh N, Hunschede S et al. The effects of potatoes and other carbohydrate side dishes consumed with meat on food intake, glycemia and satiety response in children. Nutr Diabetes. 2016;6:e195. PMID 26878318
  21. Wang S, Li C, Copeland L, Niu Q, Wang S. Starch Retrogradation: A Comprehensive Review: Starch retrogradation…. COMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY. 2015;14:568-585. abstract

5 thoughts on “Instalment 2: Dietary interventions

  1. Pingback: On the eighth day of Christmas… – henry.olders.ca

  2. Catherine Ross

    Hello Henry,
    I am confused by the statement that omega-3 fatty acids are necessary to make anti-inflammatory prostaglandins and leukotrienes versus omega-6 fatty acids which are building blocks for pro-inflammatory substances (prostaglandins, thromboxanes, and leukotrienes). Does this mean there are “good” and “bad” prostaglandins and leukotrienes? Like there are “good” and “bad” omega fatty acids?

    1. Henry Olders Post author

      The omega-6 FA arachidonic acid (ARA) is a precursor for inflammatory prostaglandins (PGs) and leukotrienes(LTs) (collectively called eicosanoids) while eicosapentaenoic acid (EPA, an omega-3 FA) is a precursor for a different series of PGs and LTs which have less activity compared to the ones from ARA. Also, it seems that EPA and DHA displace ARA which reduces the pro-inflammatory effect of the ARA. See: Calder PC. n-3 PUFA and inflammation: from membrane to nucleus and from bench to bedside. Proc Nutr Soc. 20201-13. PMID 32624016
      It’s confusing, I know! But so is hormesis (see instalment 11).

    2. Henry Olders Post author

      Also, categorizing omega FAs into “good” or “bad” misses the point that we need both omega-3s and omega-6s; however, dose of each type and the balance between them is important. Like hormesis (see instalment 11).

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