Vegan-Stuffed Roasted Capsicum with Spinach patties


So I have decided to go  plant based for a while to try and reduce the inflammation in my body and I feel that eating  meat at the moment may be impacted this considerably. This could be due to the ARACHIDONIC ACID

Arachidonic acid is an inflammatory omega-6 fatty acid. … Arachidonic acid is found in animal products, like poultry and eggs. The amount of arachidonic acid found in just one egg a day can  elevated arachidonic acid levels in the bloodstream, and increase inflammation  considerably – Japanese researchers learned. ( see next blog for more information)



  •  1 cup of cooked buckwheat
  • 1/8 bunch enoki mushrooms chopped
  • 1 Ripened Roma tomato chopped
  • Bunch Fresh Thai basil- any basil will do
  •  salt & Pepper to tast
  • 1/4 teaspoon Tumeric
  • 1 teaspoon dried vegetable stock / broth
  • MIX altogether
  • 4 red or Yellow capsicum – preferably with 4 bums ( bottom of cappy)- tops cut off and insides cleaned
  • Mix all together and stuff  the capsicum
  • Place in baking tray and bake until soft.


  • one bunch of chopped and little cooked silverbeet or spinach
  • Squeeze excess water out
  • Add thyme, parsley
  • Grated vegan cheese- small handful
  • Tablespoon Chia seeds that have been soaked in 1/4 cup water 10 mins prior
  • Salt and Pepper to taste
  • 1/4 cup Tapioca or GF flour
  • Mix together – looks like a batter
  • Shallow fry until golden brown with grapeseed or Extra Virgin Olive Oil


Serve with Fresh Cos lettuce  with squeeze of lemon and dash of Truffle oil.








 Inflammation – PAIN- Chronic Disease

Focus On: Issue 3 2016

 Did you know Chronic inflammatory diseases have reached epidemic levels in industrialised countries. According to the 2014-2015 National Health Survey, half of all Australians live with a chronic inflammatory disease such as asthma, cardiovascular disease, diabetes mellitus, obesity, arthritis, Alzheimer’s disease, autoimmune disease, and cancer.4, 5, 6

It was long assumed that an acute inflammatory process was passively self-limiting, with chemotactic factors (substances that stimulate the migration of inflammatory cytokines) simply diluting or draining away.7 However this is not the case, evidenced by the development of chronic inflammatory conditions, where inflammatory mediators persist at a site, and the resolution of the inflammatory process failing to engage.8

It is  now known that the resolution of inflammation is an active process, controlled by a family of chemicals known as specialised pro-resolving mediators (SPMs).9 SPMs promote inflammation resolution, reduce pain, encourage the clearance of pathogens and mitigate pathological inflammation, without immunosuppression. Together, these qualities make SPMs an important consideration for the treatment of chronic, unremitting inflammatory conditions.

SPMs are derivatives of omega-3 essential fatty acids (EFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). They are produced during the resolution phase of an acute inflammatory response, working to switch off the inflammatory process.10, 11 Several classes of SPMs are derived from EFAs, including resolvins (e.g. RvE, RvD1), protectins (e.g. PD1), and maresins (e.g.MaR1, HDHA).12 Lipoxins, another class of SPMs, are produced from the omega-6 fatty acid, arachidonic acid.

Inflammation, initiated

At the genesis of these inflammatory states is an initial insult, such as a tissue injury, infection, or exposure to an allergen or toxin, which activates the acute inflammatory response.13, 14 Here, an influx of poly-morpho-nuclear neutrophils (PMNs) enter the affected site and produce inflammatory mediators (e.g. cytokines, chemokines and eicosanoids) needed to trigger tissue repair. PMNs also phagocytose pathogens, and finally themselves undergo apoptosis,15, 16 causing inflammation and tissue damage, which must be cleared by macrophages in a process known as efferocytosis. Clearing this cellular debris enacts the resolution of the inflammatory process,17 allowing the body to once again return to homeostasis.

SPMs: inflammation stop signs

Entering this stage of inflammatory resolution relies on the synthesis of SPMs, which reduce PMN infiltration and increase efferocytosis.18 SPMs also achieve resolution via the regulation of macrophage polarisation. Macrophages exist in two broad phenotypes; M1 macrophages, which are pro-inflammatory, and M2 macrophages, which synthesise SMPs, inhibit PMNs, and promote efferocytosis, tissue repair, and resolution. SPMs trigger the macrophage switch from the M1 to the M2 phenotype, thereby promoting resolution.19

Additionally, SPMs have specific anti-inflammatory mechanisms, decreasing pro-inflammatory and increasing anti-inflammatory mediator production.20 In animal models, resolvins demonstrate the ability to reduce the production of pro-inflammatory eicosanoids and cytokines such as prostaglandin E2 (PGE2), leukotriene B4 (LTB4), interleukin-1β (IL-1β), IL-17 and IL-6.21, 22 Resolvins have also been shown to inhibit tumour necrosis factor alpha (TNF-α) activation in vitro and in animal models.23 SPMs also counter-regulate inflammatory gene transcription, and increase the clearance of inflammatory mediators by up-regulating chemokine binding receptors on T cells and PMNs, which are then phagocytosed by macrophages.24 However, in patients experiencing chronic inflammatory conditions, SPM production can be compromised,25 preventing the resolution of their condition. Supporting their presentation with Specialised Pro-Resolving Mediators will therefore provide the body with the capacity to work toward resolution of their inflammation.

Reduce the pain too, please

Additionally, SPMs also carry standalone analgesic properties. Shown to influence signalling within the brain, the resolvin RvE1 has demonstrated capacity to inhibit glutamate release and N-methyl-D-aspartate (NMDA) receptor hyperactivity, both important targets for pain relief.26 Exhibited further in animal models of inflammatory pain, resolvins have reduced pain-associated behaviours, and produced comparable pain relieving effects to the pharmaceutical medication pregabalin.28 Whilst reducing inflammation can also provide pain relief, these additional analgesic effects of SPMs will be of particular benefit for those patients experiencing concomitant chronic pain.

The many patients of SPMs

Given their pro-resolving and anti-inflammatory actions, SPMs are indicated in any condition involving chronic, unremitting inflammation. One such example commonly presenting in clinical practice is arthritis, with the crucial role of SPMs in this condition demonstrated in several human and animal studies.29, 30, 31, 32 Beyond this, Table 1 explores further evidence-based applications of SPMs in a varying range of inflammatory conditions.

Table 1. Overview of emerging research and applications for SPMs.

Condition SPM mediator studied Research outcomes
Allergies RvD1 and 17-HDHA Inhibited immunoglobulin E (IgE) production and suppressed differentiation of naïve B cells into IgE secreting cells in vitro.33
Endometriosis RvD1 and 17(R)-RvD1 Reduced severity of vaginal hyperalgesia and reduced vascular permeability in endometrial cysts in rat model of endometriosis.34
Psoriatic dermatitis RvE1 Potently suppressed inflammatory cell infiltration and reduced expression of IL-23 in skin and dendritic cells in mouse model of psoriatic dermatitis.35
Wound healing RvD1, RvD2 and RvE1 Inhibited neutrophil migration and accelerated wound healing in mouse model; RvE1 was most effective, and caused more mature collagen organisation and reepithelialisation.36
Cancer RvD1, RvD2 and RvE1 Inhibited debris-stimulated cancer progression by enhancing macrophage phagocytosis in mouse models.37
Sjögren’s syndrome AT-RvD1 Down-regulated Sjögren’s syndrome associated inflammatory genes and reduced apoptosis in Sjögren’s syndrome mouse model.38
Periodontitis associated bone loss RvD2 Modulated gene expression, favouring bone preservation, and down-regulated interferon gamma (IFN-γ) without dampening Porphyromonas gingivalis specific immune response in mice.39
Atherosclerosis RvE1 Reduced atherosclerotic lesion size, the formation of severe lesions, and the expression of pro-atherogenic genes in mice.40
Inflammatory bowel disease RvD2, AT-RvD1, MaR1, and 17-HDHA Have been shown to help reduce intestinal tissue damage, reduce inflammation and neutrophil infiltration, maintain body weight, and increase survival in animal models of inflammatory bowel disease.41, 42, 43

SPMs and EFAs are allies

It is important to note that although EPA and DHA are precursors of SPMs, EFAs do not possess the same unique pro-resolving qualities.44 Additionally, during states of chronic inflammation,45 and with progressive ageing,46 the body’s capacity to convert EFAs into SPMs may be compromised. This is a potential explanation for why fish oil, while reducing inflammation, may not always be clinically efficacious in fully resolving established inflammatory states. Therefore, SPMs do not replace EFA therapy, and vice versa – their actions are distinct but complementary. EFA supplementation should be utilised to correct deficient dietary intake, during times of increased demand (e.g. pregnancy) and to influence the induction of the acute inflammatory cascade (preventing the development of chronic inflammation). Meanwhile, providing Specialised Pro-Resolving Mediators augments the resolution of chronic inflammatory conditions, given its targeted action in resolving chronic, unremitting inflammation. For the chronically inflamed patient, EFAs and SPMs are ideally prescribed together to resolve existing inflammation, and prevent the development of inflammation in the future.

Innovative anti-inflammatories

The reality that chronic inflammatory conditions have now reached epidemic proportions is evidenced via patients’ presentation in clinical practice. Whilst resolution of these states can often present a clinical challenge, Specialised Pro-Resolving Mediators now offer an innovative and unique solution. These lipid mediators promote the resolution of chronic, unremitting inflammation, whilst also carrying their own unique anti-inflammatory and analgesic properties. Complementing EFAs which supplement dietary intake and prevent the development of chronic inflammation, SPMs offer hope and freedom for many inflamed patients.

written by:


When taking any supplements you should seek professional advice and take only as prescribed 


  1. Prevete N, Liotti F, Amoresano A, Pucci P, de Paulis A, Melillo RM. New perspectives in cancer: Modulation of lipid metabolism and inflammation resolution. Pharmacol Res. 2018 Feb;128:80-87. doi: 10.1016/j.phrs.2017.09.024. Epub 2017 Oct 3.
  2. Wang X, Zhu M, Hjorth E, Cortés-Toro V, Eyjolfsdottir H, Graff C, et al. Resolution of inflammation is altered in Alzheimer’s disease. Alzheimer’s & Dementia. 2015 Jan; 11(1): 40-50.
  3. Fredman G, Hellmann J, Proto JD, Kuriakose G, Colas RA, Dorweiler B, et al. An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques. Nature Communications. 2016;7:12859.
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  7. Recchiuti A, Serhan CN. Pro-resolving lipid mediators (SPMs) and their actions in regulating miRNA in novel resolution circuits in inflammation. Front Immunol.  2012 Oct 22;3:298. doi: 10.3389/fimmu.2012.00298.
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  12. Hirahashi J. Omega-3 polyunsaturated fatty acids for the treatment of IgA nephropathy. J Clin Med. 2017 Jul;6(7):70. doi: 10.3390/jcm6070070.
  13. Gallo J, Raska M, Kriegova E, Goodman SB. Inflammation and its resolution and  the musculoskeletal system. J Orthop Translat. 2017 Jul;10:52-67. doi: 10.1016/
  14. Souza PR, Norling LV. Implications for eicosapentaenoic acid- and docosahexaenoic acid-derived resolvins as therapeutics for arthritis. Eur J Pharmacol. 2016 Aug 15;785:165-173. doi: 10.1016/j.ejphar.2015.05.072.
  15. Souza PR, Norling LV. Implications for eicosapentaenoic acid- and docosahexaenoic acid-derived resolvins as therapeutics for arthritis. Eur J Pharmacol. 2016 Aug 15;785:165-173. doi: 10.1016/j.ejphar.2015.05.072.
  16. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  17. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  18. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014; 19: 21- 36. doi: 10.1016/j.cmet.2013.10.006.
  19. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab. 2014 Jan 7;19(1):21-36. doi: 10.1016/j.cmet.2013.10.006.
  20. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014; 19: 21- 36. doi: 10.1016/j.cmet.2013.10.006.
  21. Serhan CN, Petasis NA. Resolvins and protectins in inflammation resolution. Chem Rev. 2011 Oct 12;111(10):5922-43. doi: 10.1021/cr100396c.
  22. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  23. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  24. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014; 19: 21- 36. doi: 10.1016/j.cmet.2013.10.006.
  25. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014;19:21-36. doi: 10.1016/j.cmet.2013.10.006.
  26. Sommer C, Birklein F. Resolvins and inflammatory pain. F1000 Med Rep. 2011 Oct;3:19. doi: 10.3410/M3-19.
  27. Xu ZZ, Zhang L, Liu T, Park JY, Berta T, Yang R, et al. Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med. 2010 May;16(5):592-7. doi: 10.1038/nm.2123
  28. Klein CP, Sperotto ND, Maciel IS, Leite CE, Souza AH, Campos MM. Effects of D-series resolvins on behavioral and neurochemical changes in a fibromyalgia-like model in mice. Neuropharmacology. 2014 Nov;86:57-66. doi: 10.1016/j.neuropharm.2014.05.043.
  29. Arnardottir HH, Dalli J, Norling LV, Colas RA, Perretti M, Serhan CN. Resolvin D3 is dysregulated in arthritis and reduces arthritic inflammation. J Immunol. 2016 Sep 15;197(6):2362-8. doi: 10.4049/jimmunol.1502268.
  30. Perretti M, Norling LV. Actions of SPM in regulating host responses in arthritis. Mol Aspects Med. 2017 Dec;58:57-64. doi: 10.1016/j.mam.2017.04.005.
  31. Barden AE, Moghaddami M, Mas E, Phillips M, Cleland LG, Mori TA. Specialised pro-resolving mediators of inflammation in inflammatory arthritis. Prostaglandins Leukot Essent Fatty Acids. 2016 Apr;107:24-9. doi: 10.1016/j.plefa.2016.03.004.
  32. Perretti M, Norling LV. Actions of SPM in regulating host responses in arthritis. Mol Aspects Med. 2017 Dec;58:57-64. doi: 10.1016/j.mam.2017.04.005.
  33. Kim N, Ramon S, Thatcher TH, Woeller CF, Sime PJ, Phipps RP. Specialized proresolving mediators (SPMs) inhibit human B-cell IgE production. Eur J Immunol. 2016 Jan;46(1):81-91. doi: 10.1002/eji.201545673.
  34. Dmitrieva N, Suess G, Shirley R. Resolvins RvD1 and 17(R)-RvD1 alleviate signs of inflammation in a rat model of endometriosis. Fertil Steril. 2014 Oct;102(4):1191-6. doi: 10.1016/j.fertnstert.2014.06.046.
  35. Sawada Y, Honda T, Nakamizo S, Otsuka A, Ogawa N, Kobayashi Y, et al. Resolvin E1 attenuates murine psoriatic dermatitis. Sci Rep. 2018 Aug 8;8(1):11873. doi: 10.1038/s41598-018-30373-1.
  36. Menon R, Krzyszczyk P, Berthiaume F. Pro-resolution potency of resolvins D1, D2 and E1 on neutrophil migration and in dermal wound healing. Nano Life. 2017 Mar;7(1). pii: 1750002. doi: 10.1142/S1793984417500027.
  37. Sulciner ML, Serhan CN, Gilligan MM, Mudge DK, Chang J, Gartung A, et al. Resolvins suppress tumor growth and enhance cancer therapy. J Exp Med. 2018 Jan 2;215(1):115-140. doi: 10.1084/jem.20170681.
  38. Easley JT, Nelson JW, Mellas RE, Sommakia S, Wu C, Trump B, et al. Aspirin-Triggered Resolvin D1 Versus Dexamethasone in the Treatment of Sjögren’s Syndrome-Like NOD/ShiLtJ Mice – A Pilot Study. J Rheum Dis Treat. 2015;1(4). pii: 027.
  39. Mizraji G, Heyman O, Van Dyke TE, Wilensky A. Resolvin D2 restrains Th1 immunity and prevents alveolar bone loss in murine periodontitis. Front Immunol. 2018 Apr 25;9:785. doi: 10.3389/fimmu.2018.00785.
  40. Salic K, Morrison MC, Verschuren L, Wielinga PY, Wu L, Kleemann R, et al. Resolvin E1 attenuates atherosclerosis in absence of cholesterol-lowering effects and on top of atorvastatin. Atherosclerosis. 2016 Jul;250:158-65. doi: 10.1016/j.atherosclerosis.2016.05.001.
  41. Bento AF, Claudino RF, Dutra RC, Marcon R, Calixto JB. Omega-3 fatty acid-derived mediators 17(R)-hydroxy docosahexaenoic acid, aspirin-triggered resolvin D1 and resolvin D2 prevent experimental colitis in mice. J Immunol. 2011 Aug 15;187(4):1957-69. doi: 10.4049/jimmunol.1101305.
  42. Chiu CY, Gomolka B, Dierkes C, Huang NR, Schroeder M, Purschke M, et al. Omega-6 docosapentaenoic acid-derived resolvins and 17-hydroxydocosahexaenoic acid modulate macrophage function and alleviate experimental colitis. Inflamm Res. 2012 Sep;61(9):967-76. doi: 10.1007/s00011-012-0489-8.
  43. Marcon R, Bento AF, Dutra RC, Bicca MA, Leite DF, Calixto JB. Maresin 1, a proresolving lipid mediator derived from omega-3 polyunsaturated fatty acids, exerts protective actions in murine models of colitis. J Immunol. 2013 Oct 15;191(8):4288-98. doi: 10.4049/jimmunol.1202743.
  44. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014;19:21-36. doi: 10.1016/j.cmet.2013.10.006.
  45. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014;19:21-36. doi: 10.1016/j.cmet.2013.10.006.
  46. Arnardottir HH, Dalli J, Colas RA, Shinohara M, Serhan CN. Aging delays resolution of acute inflammation in mice: reprogramming the host response with novel nano-proresolving medicines. J Immunol. 2014 Oct 15;193(8):4235-44. doi: 10.4049/jimmunol.1401313.

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Ibuprofen Vs Extra Virgin Olive Oil (EVOO) – Part One

Ibruprofen-like-activity in EVOO


Screen Shot 2019-06-25 at 9.19.23 am.png

Have heard of many benefits of virgin and extra virgin olive oil but did you know that one of the phenolic compounds in olive oil, oleocanthal, uses the same mechanism of action as ibuprofen and has potent anti-inflammatory actions. It decreases a number of inflammatory mediators and exhibits neuroprotective properties. Researchers are looking at oleocanthal and other phenolic compounds, such as oleuropein and hydroxytyrosol, in studies investigating their impact on atherosclerosis, obesity, blood sugar control, Alzheimer’s disease and cancer among many other conditions.

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Moqueca Brazilian Fish Stew


  • 1kg skinless firm white fish fillet (such as snapper), pin-boned, cut into 3cm cubes
  • 1/3 cup (80ml) lime juice
  • 1/4 cup (60ml) olive oil
  • 1 red onion, thinly sliced
  • 1 green capsicum, thinly sliced
  • 1 red capsicum, thinly sliced
  • 3 garlic cloves, finely chopped
  • 2 short red chillies, finely chopped
  • 2 cups (500ml) fish stock
  • 400g can chopped tomatoes
  • 270ml can coconut milk
  • 1 tablespoon virgin coconut oil (see note)
  • 6 large green prawns, peeled (tails intact), deveined ( optional)
  • Coriander leaves and steamed rice, to serve

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Why Resistant Starch ???

Resistant Starch – a concise guide to the bio hack of the decade

Resistant Starch Amylose Molecular Structure

Resistant Starch (RS for short)  is being called the bio hack of the decade and with good reason. The majority of people experimenting with it are reporting dramatic improvements in well-being across a number of measures.

Briefly the primary benefits seen are:

  • Improved blood glucose & metabolism
  • Improved sleep and “movie-like” vivid dreams
  • Enhanced energy, mood and well-being
  • Improved digestion and bowel movements

So what is Resistant Starch? Resistant starch is named so because it is a starch that resists digestion. RS is a carbohydrate with a complex molecular structure that the body cannot break down and absorb as glucose. It is a long amylose chain wrapped in a helical like structure. Because of this it bypasses digestion in the small intestine and is used as food for bacteria primarily inhabiting the large intestine/colon. Thus the purpose of taking resistant starch is to symbiotically feed your microbes which then in turn do all kinds of wonderful things for you.

There are four different types of Resistant Starch:

  • RS1 – Physically inaccessible or digestible resistant starch, such as that found in seeds or legumes and unprocessed whole grains
  • RS2 – Resistant starch that occurs in its natural granular form, such as uncooked potato, green banana flour and high amylose corn
  • RS3 – Resistant starch that is formed when starch-containing foods are cooked and cooled such as in legumes, bread, cornflakes and cooked-and-chilled potatoes, pasta salad or sushi rice. Occurs due to retrogradation, which refers to the collective processes of dissolved starch becoming less soluble after being heated and dissolved in water and then cooled.
  • RS4 – Starches that have been chemically modified to resist digestion. These are man-made and not found in nature

We are primarily interested in RS2 and also a bit in RS3 as they are the natural accessible forms of RS.

Medical science for the last century has largely ignored the human microbiome much to it’s own peril. When it comes to numbers we are in fact more mircobes than human, as microbe cells outnumber human cells 10 to 1 in and on the body. It is estimated that there are more than 1,000 species of gut microbes and more than 7,000 strains that collectively contain 150 times more genes than the human genome. These bacteria through their processes also help modulate the human genome epigenetically altering our very own genetic expression.

Microbiome genome genes 10 times cells bacteria 

In fact the very reason resistant starch works so well is that it reverse some of the damage western medicine has done. Ever since the discovery of penicillin and antibiotics western medicine has been on a crusade to kill bacteria, many of which have been wrongly demonized. Our germ-a-phobic society has installed hand sanitizers in almost every conceivable location and many cleaning products are marketed for their germ-killing properties. Antibiotics have found their way into our food and are used extensively on animals. In the words of one man what we have effectively done is conducted  “mass extinction”  which has a plethora of unintended consequences and inadvertently caused a whole host of chronic illnesses.

When people take antibiotics they tend to be broad spectrum and while they kill many “bad” guys they also kill “good” guys. Taking antibiotics is akin to taking a nuclear bomb to your gut. It kills all bacteria without discrimination. However it won’t kill fungi and with the bacterial competition eliminated fungi can grow out of control and cause conditions such as Candida. In addition to this many harmful bacteria are now also becoming resistant to antibiotics so when taking antibiotics it may often kill more good guys than bad guys, allowing the bad guys to gain even more of a foothold. Repeated rounds of antibiotics over life can then create dysbiosis which is at the root of many modern chronic diseases.

Antibiotics Microbiome wired Resistant Starch

The goal of using Resistant Starch is to help restore the balance of microbes in the gut. This is done by providing a prebiotic food (RS) that feeds the good guys and crowds out the bad guys.

n=1 Case Study – Tim Steele

Over at Free The Animal blog, commentator Tim Steele (aka. tatertot) had been experimenting with the potato diet some time ago and became interested in resistant starch. After doing further research through older published journal articles he found a mountain of evidence showing the benefits of using resistant starch. So in line with those previous studies he began experimenting on himself with high dose RS and feeling the benefits convinced other to follow suit. Soon a whole movement had started as person after person tried it out and had enormous success. Diabetics were reducing their insulin and many people were reporting lifelong health ailments being drastically improved or cured.

After 6 months of daily 4 TBS of raw potato starch in addition to 20g of RS from foods and some dietary changes Tim had his gut micrbiome tested via The American Gut Project. The following are his results:

What is profound about these results is the reduced frequency of Proteobacteria. Proteobacteria are considered pathogenic and consist of species such as E. Coli, Salmonella, Vibrio and Helicabacter. Everyone has small amounts of these bacteria in their gut however the quantity and degree of proliferation is an important indicator of health.

Tim had the lowest amount of all comparable samples! In addition to this his most enriched microbes were all of the beneficial kind. The highest being Bifidobacteria notable for their health promoting properties.

Tim never did a test before taking the RS so we don’t know what his gut profile looked before the RS, however the improvements in health and well being speak for themselves. After many people have taken on the RS challenge they have seen similar improvement in well being as well.

Short video showing how Resistant Starch works internally

Instructions on how to take Resistant Starch

All the published studies show that a person needs about 20 grams of resistant starch minimum before meaningful benefits are seen and that at about 50 grams diminishing returns are in full effect providing no additional benefit. Thus ideally you want to get about 20-50 grams of RS per day. It is highly unlikely that you will get there by food alone because most cooking/heating and food processing destroy the RS found in food. So therefore supplementing is almost always done to reach the minimum necessary amount to see beneficial effects.

Ideal Supplement Options

Currently the easiest way to get to the minimum 20 grams necessary of RS a day is to use several Tbsp of raw unmodified potato starch in a glass of water. It is about 75% RS by weight. It is very important you do not get regular potato flour. This will not work as the heating process almost entirely destroys the resistant starch.

When starting RS it is best to start slow. The gut will be undergoing some drastic ecological shifts as RS is added. Some people start at sub-tsp doses. Everyone is different in terms of their own microbiome so only you can decide how much to take and how long it takes to reach full dose.

Raw unmodified potato starch resistant starch – quality in grams 

You want to eventually reach at least 2 Tbsp a day and most people opt for settling around 4Tbsp a day. Some heroic people take up to 8Tbsp a day.

It would appear taking more at once may be better than spreading doses throughout the day. The reason being is that taking RS in a larger bolus dose increases the chances more will make it to the large intestine where it is thought it is needed most. That said a maximum of 4 Tbsp is recommended at one time.

The biggest side effect of taking RS is increased gas. This is very normal and almost everyone doing this protocol experiences this. If the the gas becomes too much, stop taking supplemental RS for 1-2 days. This will give the gut a break and a chance to do some of it’s own re-balancing. Most people have found that the additional gas goes away after using RS for at least one month so therefore expect it to take that long for your gut biome to do most of it’s re-balancing.

Ideal Foods high in RS

  • Green Bananas or unripe Plantains
  • Cooked and cooled potatoes
  • Cooked &  cooed Rice as in Sushi Rice & also Parboiled rice
  • Specifically Mung Beans and also various other legumes

The average western person on a SAD consumes about 3-5 grams of resistant starch per day. Where as the average Asian person consumes about 6-8 grams of RS per day. Most people therefore do not consume enough resistant starch from food alone and thus need to add a supplement. That said if you start making your primary carb sources cold rice, potatoes & properly prepared beans it can help create a good foundation.

Resistant Starch foods 

Tim Steele has done a lot of research and compiled a master list of resistant starch content from major foods. Click here to download the PDF to get a good idea of how much is in various foods

Your mileage may vary

If you have lived your life and never or perhaps rarely taken antibiotics and you typically eat fermented food on a routine basis, chances are RS may not benefit you as much as someone else. If however you have been exposed to repeated rounds of antibiotics and don’t eat much fermented food, chances are RS can offer you great improvements in terms of health. The people it helps most notably are people who are struggling with Intestinal issues such as IBS, Chron’s, diabetes, metabolism issues and people struggling with immune system related issues. It also offers considerable benefit to those struggling with hormonal and neurotransmitter issues as well as things like anxiety, depression and OCD.

It’s ironic that those most compulsively concerned about “germs” are likely people who have suffered from immune system related problems in early childhood causing health ailments where dysbiosis has been at the root, often unbeknownst to them. It has been said the best offense is a great defense. And this couldn’t be anymore true here.

It’s not that all “germs” are bad and should be eradicated, the fact is RS works precisely because it feeds and supports “germs” namely the “good” ones rather than the “bad” ones. The old wives tale of living in too clean of an environment leads to immunity issues such as allergies down the road such as in the hygiene hypothesis therefore is only partially true. It’s not lack of exposure that is the issue rather it is that many people carpet bombed their immune system/bacterial support system to the point where it was so compromised it has never fully recovered.

Serotonin & the Gut-Brain connection

95% of the bodies serotonin is produced in the gut by bacteria. One of the main bacteria implicated in the serotonin production pathway is Bifidobacerium Infantis. If you remember Tim Steele’s most enriched bacteria was the bifidobacterium at an eleven fold increase above normal levels. This means that taking appropriate prebiotics and ensuring that you are also taking the right bacterial strains could lead to dramatic shifts in neurotransmitter and hormone production capability.

There has been a lot of research lately showing how various bacteria can reduce anxiety and depression and alter mood and behavior. One of the root causes of depression and anxiety is a gut imbalance which then leads to a neurotransmitter imbalance.

What else is interesting is the reverse is also true. Negative thoughts, feelings and stress also influence bacteria and can raise levels of “bad” bacteria and lower levels of beneficial bacteria through stress hormonal activation.

It seems resistant starch may have powerful effects on serotonin and therefore melatonin as well. I have personally found that that taking RS 4-5 hours before bedtime to be important. If I take it right before bed I wake up feeling exhausted. I believe the reason is that transit time from mouth to colon is roughly about 4-5 hours and it is ideal to have the RS arriving in your colon as you sleep. It seems to promote more rejuvenating sleep and perhaps assist with critical liver detox that occurs in the early morning hours.

Diversity is key

A brief map showing species variation depending on location as well as average number of organisms. The lactobacilli tend to occupy the upper intestines while the bifido dominate the lower intestine.

Intestinal Microflora Resistant Starch


It is possible to get you gut biome tested via a stool sample. In fact if this is you first time reading about resistant starch and you are interested in trying it out, consider getting yourself tested first so you can do a before and after comparison and then post your results online somewhere. It would be of an immense benefit to helping us collectively understand better what is going on in peoples guts. Good tests to do are as follows:

Both the above tests are genetics based in that they are sequencing the DNA of the micrboes in your stool. This is quite different than then standard practice of using a microscope and eyeball-estimating or culturing.

Bifido bacteria are your friends

On of the primary organism that RS appears to increase is bifidobacteria. It is these bacteria that confer many benefits to you their host. Bifido constitute 90% of the gut microflora in infants that are breast fed. Bifido do things like:

  • Improve digestion
  • Production of Vitamins
  • Bioconversion of many compounds such as folate
  • Inhibit Candida and E.coli by lowering pH in the gut
  • Reduce gas
  • Enhance the immune system

In many cases supplemental bifido can also completely eliminate IBS and diarrhea.

But perhaps one of it’s most beneficial aspect is that  bifido cross-feed other beneficial bacteria species. Specifically Clostrida being one which then produce SCFAs.

SCFA are an energy source for your intestinal cells. They also help tighten the junctures in the intestinal cell lining preventing conditions such as leaky gut.

While there is still a lot that is unknown about how Resistant Starch works and what it feeds specifically it appears that:

“Leitch et al. [24] found relatives Eubacterium rectale, Ruminococcus bromii and Bifidobacterium adolescentis to be the main colonisers of resistant starch particles, and these same species were detected using stable isotope probing with labelled starch by Kovatcheva-Datchary et al. [25]” (source)

The online community that is currently experimenting with RS is trying different bacteria and combinations of bacteria to see what works best. There is likely to be a lot of individual variance. So far the following stand out.

Other beneficial bacteria

While there are many bacteria that have benefits for one reason or another these ones specifically are singled out for their remarkable properties in conjunction with RS. B.Infantis which is likely the primary bacteria responsible for Serotonin production is not found in 90% of probiotics on the market. This is why doing your research is important before buying probiotics.

  • Bifidobacterium infantis – implicated in the serotonin production pathway, has anti-depressant like effects and improves motivation. Also rated the top bacteria in a comparison study with 9 others from VSL#3 in terms of reducing gut permeability.
  • Lactobacillus brevis and Bifidobacterium dentium – best GABA producers (reference) B.Brevis is rated 2nd in terms of reducing gut permeability in a 9-species comparison.
  • Lactobacillus Plantarum – strong imuno-modulation tendencies; may also cure eczema (reference) Rated 3rd in reducing gut permeability compared to 9 other species. 1st in reducing soy allergy in this study.
  • Bifidobacterium bifidus – known to be good at displacing the bad guys
  • Lactobacillus rhamnosus – reduces anxiety and OCD; also makes GABA
  • “Roseburia intestinalis” and “Eubacterium rectale” –  primary producers of SCFAs
  • Clostridium cluster XIVa [Roseburia] and F. prausnitzii
  • Bifidobacterium adolescentis – cross-feeders of SCFA producers (reference)
  • B. subtilis – makes Vitamin K2 and digests gluten, casein & sourdough. Also 2nd in reducing soy allergy. Jenny McCarthy attributes curing her son of autism partly through the use of Threelac which contains this bacteria. Anecdotally other people have cured their allergies and eczema as well.

Recommended Probiotics for purchase:

According to the evidence collected so far it will not. In fact the opposite seems to be the case, in that it feeds primarily the beneficial bacteria and crowds out/inhibits the more dangerous Proteobacteria such as E.coli, Salmonella, Vibrio and Helicobactera. If you look above at Tim Steels n=1 report you will see he has less pathogenic Proteobacteria than anyone else! This has seemingly been one of the most profound discoveries when it comes to RS.

In fact resistant starch has been used as an effective treatment to treat cholera. It has been shown in a lab that 98% of cholera bacteria will detach from an agar substrate and bind to the resistant starch for elimination. (reference)  Dr. B G uses resistant starch as part of her Small Intestinal Bacteria Over-growth (SIBO) protocol to flush out excess microbes from the small intestine.

The increase in beneficial bifido populations which is on of the primary functions of RS helps create a more acidic environment through enhanced SCFA production in the colon which is considered a good thing. This environment inhibits the virulent hyphal from of the fungus Candida reverting it to its non-pathogenic unicellular form. (references) Anecdotally for me personally RS was the key that helped me get over a pervasive candida infection.

Other prebiotics:

  • Galacto-oligosaccharides (GOS) – known for it’s bifido specificity; sold as Bimuno
  • Short-chain fructooligosaccharides (FOS)
  • Inulin
  • Mannan-oligosaccharides (MOS)
  • Lactulose
  • Glucomannan – from konjac root
  • Galactomannan aka. Guar Gum from guar beans
  • Larch Arabinogalactan
  • Beta-glucan
  • Various Pectins
  • Flavonols – from greens and cocoa (reference)

All prebiotics are in the form of molecules called glycans. There are over 2,000,000,000 glycans the constitute the “human glycome”.  Cutting edge research is exploring these glycans and how they relate to various microbiota.

Your body produces mucin (as in mucous a type of glycan) in the gut and this is also there for the purposes to help nourish your microbiome.

So how do all these other prebiotics/glycans compare to resistant starch?  Not all glycans are equal. No one really knows and studies are mixed in terms of results. In vitro vs in vivo can make a difference and cross-feeding among bacteria and individual biome uniqueness can create hundreds of confounding variables further complicating the matter. Ultimately a mix of the various prebiotics is probably best to cover most of your basis. However using RS as a foundation is probably wise because anecdotally we know it works for many people.

GOS is another well known prebiotic that has been empirically shown to have good bifidogenic properties. GOS is a substrate similar to those secreted in breast milk that fuels the 90% bifido as a ratio of gut population in infants.

Prebiotics is something that needs to be researched further and experimented with. It could be a serious contender to RS, but for the time being RS is much more accessible found in most local grocery stores. Plus it’s cheap.

Supper Booster recipe – Mix it up:

Diversity is a good thing especially when it comes to prebiotics and probiotics. What I do personally is mix a bunch of things together into a super booster style drink and rotate various probiotics. I drink this once a day on an empty stomach 4-5 hours before bedtime. Mixing the probitoics with RS in water is ideal because it will enhance survivability and should increase transit length through the GI tract as well.

Then I drink that and swallow the following:

Benefits of Resistant Starch: (long list)

— decreased glycemic response (in both healthy subjects and diabetics)
— increased insulin sensitivity
— improved fasting blood sugar (10 or 15 point drops in many individuals, sometimes even greater)
— increased satiety
— improved metabolism
— improved fat burning
— improvement of adipose tissue patterning (body fat)
— improved sleep (deep and “movie-like” vivid dreams)
— improved digestion
— improved regularity
— improved blood/lipid profiles
— improved chelation/elimination of heavy metals
— improved colon pH (acidic is better)
— improved uptake/absorption of vitamins and minerals
— improved neurotransmitters (like serotonin)
— improved butyrate and Short-Chain Fatty Acid production (by feeding butyrate producing bacteria)
— improved colon health (by the production of Short-Chain Fatty Acids)
— improved previous damage to colonocytes
— improved mucosal integrity (gut barrier)
— protection against (experimental) colorectal cancer
— increased nitrogen disposal and reduced blood urea concentrations
— improved eye health
— improved body temperature
— reduced stress and improved well being (anecdotal)
— potential treatment for ulcerative colitis
— does not affect one’s ability to maintain ketosis (if that’s desired)



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