Cost to my patient? $150 for test plus $50 collection fee
*Consult fee will apply if advise and treatment is given depending on results – OFFERING 40 % DISCOUNT on all consults from this test
Cost to my patient? $150 for test plus $50 collection fee
*Consult fee will apply if advise and treatment is given depending on results – OFFERING 40 % DISCOUNT on all consults from this test
What a wonderful way to boost your immune system with good nutritious food. What you put into your body is in your control!!! You may feel that you have no control of our current situation but you can take control of your health!!! Start with a simple immune booster to feed your Family , your Gut and Immune health 💕
If you have a cast iron pot in your cupboards then its time to bring it out – Why ? Well its a great way to take in some iron through these yummy delicious , nutritious ingredients while it cooks. Great way to increase your iron especially if your iron deficient🤗 You can make a big batch and freeze or you can keep in the fridge for at least 4-5 days . Crack some eggs in it while warming it up and you can have for breakfast or add some rice or quinoa to make it into a completely new meal.👌
Quantity will depend on how many mouths you want to feed or how any meals you want to make out of it . I like to make up a big 5L pot🤦♀️
Now lets get started 👍🏻
All vegetables should be washed and pulses should be soaked for at least 24 hours , alternatively you can use tin pulses but you must rinse thoroughly.
1-3 Turnips depending on size
1-3 Swedes depending on size
2-4 Potatoes depending on size
Bunch kale or silverbeet or both
3-6 Celery Stalks and leaves
1-2 sweet potaotes
1/2 – 1 Leek
1 large onion Or Three sticks of spring onion
Bunch of fresh sage and basil and nice handful of fresh rosemary
1 chopped up chilli – deseeded if you dont want it too hot
100-200g Mushrooms – if you can use reiki or shiitake or both
Bone broth- 1 Tablespoon of Nutri Organics Mushroom or vegetable broth powder if you cant get hold of this then use collagen or gelatin or eliminate if you cant get hold of it.
Cup or 2 of homemade stock or bought stock use vegetable or use dried vegetable stock like vegetables or Massals
2 – 4 Cloves of fresh Garlic – depends on size or how much you like garlic
Chop everything up chunky or small its up to you how you like it add to Pot and fill with water add a nice pinch of himillyan Salt or Celtic salt, nice pinch coursely ground pepper.
Bring to boil and simmer for about 30 mins then add: Pulses
1 cup of soaked split peas or Dahl 1 cup or can of lentils or Mung beans
Cook slowly for about an hour ensuring all the nutrients from all these lovely vegetables are released. It is ready when pulses are soft and no longer hard .
Serve with a nice drizzle or Extra virgin Olive oil or Truffle oil or Black sesame or combination of all three.
Finish of with some toasted pan fried sesame and Hemp seeds.
Enjoy with toasted Sour dough bread and Butter ( butyrate ) great for the gut and immunity !!!!! 😊😊😊😊😊😊
ENJOY Stay tuned for Number Three for stay at home tips 🦋🦋🦋
GOOD – Arachidonic acid is not one of the essential fatty acids. However it does become essential if there is a deficiency in linoleic acid or if there is an inability to convert linoleic acid to arachidonic acid which is required by most mammals.
BAD – Scientists believe omega-6s are pro-inflammatory, while omega-3s are anti-inflammatory ( 1 ). Of course, inflammation is essential for your survival. It helps protect your body from infection and injury, but it can also cause severe damage and contribute to disease when it’s chronic or excessive. Pro-inflammatory eicosanoids are important chemicals in the immune system. However, when too many of them are produced, they can increase inflammation and inflammatory disease ( 36 ). Although omega–6 fats are essential, the modern Western diet contains far more omega–6 fatty acids than necessary
Arachidonic Acid: The Good and Bad
Arachidonic acid is an essential fatty acid, which is consumed in small amounts in our regular diets. It is considered an “essential” fatty acid because it is an absolute requirement for the proper functioning for the human body. Essential fatty acids (EFA’s) are polyunsaturated fatty acids that the body cannot synthesize and therefore must obtain from the diet. There are two families of EFAs: omega-6 and omega-3. The most important omega-6 fatty acids are linoleic Acid (LA), gamma-linolenic acid (GLA), dihomogamma-linolenic acid (DGLA), and Arachidonic acid (AA). The most important omega-3 fatty acids are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Omega-3 fatty acids can be found in fish and certain plant oils. Linoleic acid, an omega-6 fatty acid, can be found primarily in seeds, nuts, grains and legumes. Linoleic acid can be converted into arachidonic acid. Arachidonic acid can be found mainly in the fatty parts of meats and fish (largely red meat), so vegetarians usually have lower levels of arachidonic acid in the body than those with omnivorous diets.
There is a great deal of controversy about arachidonic acid. Some information says that arachidonic acid can cause health problems and other sources say it is needed to aid in muscle growth. Arachidonic acid is vital to the operation of the prostaglandin system. Prostaglandins are part of a class of substances called eicosanoids. Eicosanoids influence numerous metabolic activities including platelet aggregation (blood clotting), inflammation, hemorrhages, vasoconstriction and vasodilation, blood pressure, and immune function. The eicosanoids contain twenty carbons and include the prostaglandins (PG), prostacyclins (PGI2), thromboxanes (TX), leukotrienes (LT), and hydroxy acids. There are bad (pro-inflammatory) and good eicosanoids (anti-inflammatory) and they compete with each other. Two prostaglandins arachidonic acid is the substrate to are PGE2 and PGF2a. The first one is generally thought to be bad while the second is thought to be good. Studies point to PGF2a, specifically, as being the prostaglandin most closely tied to increase skeletal muscle protein synthesis. Skeletal muscle tissue has no capacity to actually store prostaglandins, so the only local source for PGF2a is the arachidonic acid that is retained in the outer phospholipids layer of each cell. It is the stretching of muscle fibers during intense physical exercise that causes arachidonic acid to be released and metabolized to active prostaglandins. Arachidonic acid is actually the chemical messenger first released by your muscles during intense weight training, controlling the core physiological response to exercise and regulating the intensity of all growth signals to follow. Also, anytime you have tissue injury, inflammation is involved in healing the wound. Some prostaglandins have pro-inflammatory affects. The fact is, if you work out, you have tissue injury – micro trauma to the muscle tissue. As your delayed onset muscle soreness will tell you, inflammation is involved in the healing of this micro trauma. Furthermore, in both animal and human studies it has been shown that exercise lowers the content of arachidnoic acid in skeletal muscle tissue. Therefore, there has been talk of arachidonic acid supplementation.
The omega-6 and omega-3 fatty acid families form different eicosanoids with different activities. They compete with one another for the enzyme (PLA2) that catalyzes the release of the essential fatty acids from the cell membrane. Also, they compete for cyclooxygenase and lipoxygenase, the enzymes necessary for eicosanoid synthesis. A proper balance of these fatty acids in the diet is therefore important for the maintenance of good health. An increase in the consumption of one family will reduce the synthesis of eicosanoids derived from the other family, which will ultimately have an effect on overall health. According to many sources, humans evolved on a 1:1 dietary ratio of omega-6 to omega-3. With today’s typical “Western” dietary habits the average person consumes a dietary ratio of between 25 and 40 to 1 omega-6 to omega-3. This highly imbalanced ratio is due to the dramatic increase in consumption of omega-6 fatty acids in vegetable oils, which contain linoleic acid, and meat and shellfish, which contain arachidonic acid. At the same time, we are consuming less of the omega-3 fatty acids. Since the omega-6 compete with the omega-3 fatty acids for incorporation into cell membranes and subsequent metabolism, high intake of the omega-6 fatty acids will result in an increased production of unhealthy eicosanoids derived from arachidonic acid. Omega-3 fatty acids produce eicosanoids that are anti-inflammatory. These eicosanoids help support normal blood pressure by relaxing the arteries and blood vessels and decreasing blood lipids. They also decrease blood-clotting factors. Omega-6 fatty acids can produce both anti-inflammatory and/or inflammatory and vasoconstricting eicosanoids. Omega-6 can be good for you if you take them in the right amount with omega-3. Omega-3 can counteract the pro-inflammatory effects of omega-6 fatty acids. When omega-3 and omega-6 are in balance, they are both very good but when omega-6 is in excess, they become bad. For that reason, it is essential to have a proper balance of omega-6 and omega-3 fatty acids. A healthy ratio of omega-6 to omega-3 ranges from 1:1 to 1:3.
Now that arachidonic acid supplements are on the market, athletes need to be aware that there needs to be a balance of omega-6 and omega-3 fatty acids in their diet. Supplementation is acceptable only if you are consuming enough omega-3 fatty acids to balance with the added omega-6 fatty acid (arachidonic acid) from the supplement. You have a choice to make. If your primary concern is muscular gain supplementing arachidonic acid could help as long as you are consuming enough omega-3 to balance your diet. However, if you suffer from one of the many inflammatory conditions that plague many people who exercise (tendonitis, bursitis, arthritis, etc.) then you should probably stay away from it since it can be pro-inflammatory. Furthermore, if you suffer from diabetes, asthma, high blood pressure, high cholesterol, heart disease, are pregnant, or are suffering from any inflammatory disease you should not supplement arachidonic acid in your diet. Just remember if you are going to take arachidonic acid supplements you should have a healthy ratio of omega-6 to omega 3.
The acute inflammatory process, arachidonic acid metabolism and the mode of action of anti-inflammatory drugs.- Arachidonic acid is a polyunsaturated fatty acid covalently bound in esterified form in the cell membranes of most body cells. Following irritation or injury, arachidonic acid is released and oxygenated by enzyme systems leading to the formation of an important group of inflammatory mediators, the eicosanoids. It is now recognised that eicosanoid release is fundamental to the inflammatory process. For example, the prostaglandins and other prostanoids, products of the cyclooxygenase enzyme pathway, have potent inflammatory properties and prostaglandin E2 is readily detectable in equine acute inflammatory exudates. The administration of nonsteroidal anti-inflammatory drugs results in inhibition of prostaglandin synthesis and this explains the mode of action of agents such as phenylbutazone and flunixin. Lipoxygenase enzymes metabolise arachidonic acid to a group of noncyclised eicosanoids, the leukotrienes, some of which are also important inflammatory mediators. They are probably of particular importance in leucocyte-mediated aspects of chronic inflammation. Currently available non-steroidal anti-inflammatory drugs, however, do not inhibit lipoxygenase activity. In the light of recent evidence, the inflammatory process is re-examined and the important emerging roles of both cyclo-oxygenase and lipoxygenase derived eicosanoids are explored. The mode of action of current and future anti-inflammatory drugs offered to the equine clinician can be explained by their interference with arachidonic acid metabolism. For full article : https://onlinelibrary.wiley.com/doi/abs/10.1111/j.2042-3306.1984.tb01893.x?sid=nlm%3Apubmed
1. Galli, C., Simopoulos, A.P., Tremoli. Fatty Acids and Lipids: Biological Aspects. World Rev Nutr Diet 1994, 75: 1-196.
2. Mann and Sinclair. Contribution of Meat Fat to Dietary Arachidonic Acid. Lipids 1998, 33: 437-40
3. Phinney et al. Reduced Arachidonate in Serum Phospholipids and Cholesterol Esters Associated with Vegetarian Diets in Humans. Am. J. Clin. Nutr. 51: 385-92.
4. Rodemann, Peter and Alfred Goldberg. Arachidonic Acid, Prostaglandin E2 and F2a Influence Rates of Protein Turnover in Skeletal and Cardiac Muscle. J Biol Chem
5. Simopoulos, A.P., Leaf, A., Salem, N. Jr. Essentiality of and Recommended Dietary Intakes for Omega-6 and Omega-3 Fatty Acids. Ann Nutr Metab 1999, 43: 127-130.
6. Smith, WL. The Eicosanoids and Their Biochemical Mechanisms of Action. Biochem J 1989, 259:315-324.
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)
Serve with Fresh Cos lettuce with squeeze of lemon and dash of Truffle oil.
YUMMOOOOO 😋 😋 😋
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.
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.
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.
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.
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|
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.
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.