{"id":325,"date":"2024-07-08T03:38:53","date_gmt":"2024-07-07T16:38:53","guid":{"rendered":"https:\/\/bornfree.life\/2024\/?p=325"},"modified":"2026-02-11T22:28:49","modified_gmt":"2026-02-11T11:28:49","slug":"2-2-1-diet","status":"publish","type":"post","link":"https:\/\/bornfree.life\/dev\/2-2-1-diet\/","title":{"rendered":"2.2.1 Diet"},"content":{"rendered":"\n\n\n

\n 2.2.1 Diet <\/h1><\/a>\n\n <\/div>\n\n

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Planning and consuming an appropriate \/ strategic diet are complex topics for most people, even without a chronic disease. 

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A new Meal Planner tool<\/a> has been added to help you reach targets safely.

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For those with a chronic disease, it’s significantly more complex. One common challenge is selectivity – trying to ensure that your cells \nare receiving these dietary nutrients, while avoiding feeding them to certain \nmicroorganisms residing in your GI tract – which then produce endotoxins\n \/ mycotoxins that poison your energy metabolism and neurotransmitter \npathways. Acetaldehyde is one of the toxins discussed heavily in the disease model, as part of Gut Fermentation Syndrome (GFS).

Failure to adapt your diet around your personalised microbiome dysbiosis and chronic disease metabolism will invariably lead to “getting stuck” or even back-sliding. Unlike minerals deficiencies, which are normally slow to develop and slow to resolve, microbiome dysbiosis can rapidly shift during immune activity or by feeding the wrong microorganisms over a number of weeks. What you eat determines which microorganisms get promoted or inhibited.
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Diet plays a pivotal role in chronic disease by influencing\nsubstrate availability for fermenting microbes and shaping the gut microbiota\ncomposition. High-carbohydrate diets provide ample fuel for microbial\nfermentation, exacerbating acetaldehyde production and metabolic disruptions.\nConversely, low-carbohydrate diets<\/strong> can reduce substrate availability,\npotentially decreasing microbial fermentation and acetaldehyde levels, however these\ncan also exacerbate glycogen storage issues and contribute to various symptoms\nlike POTS, fatigue, depression and other neurological symptoms<\/strong>. This has\nbeen labelled by some as \u201clow carb limbo\u201d.<\/p>\n\n

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Depending on the functionality of different energy pathways, while first starting this protocol, you may also find you respond better to certain type of macronutrients, ie. carbohydrates, fats and proteins than others.

The performance of your diet can be predicted in the Organic Acids Test (OAT) results, by looking at the relevant pathways for metabolites of each macronutrient, eg. glycolysis, fatty acids, amino acids. Some of the adjacent pathway markers, such as ketogenesis, lactic acid and oxalate metabolism are also helpful in identifying impaired pathways, indirectly. <\/strong>

Therefore, before we go into detailing specific foods and their attributes, it helps to understand a little more about the different energy pathways and how dietary macronutrients can be turned into energy.

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Feeding energy pathways<\/a><\/h4>\n

You need different energy substrates for different purposes and loads. Those pathways need fuels, cofactors and signalling to work correctly. Let’s review them:<\/p>\n

Instant \/ burst energy (muscle tissue)<\/u><\/strong>

ATP-PC (Phosphocreatine) System<\/strong>
Where:<\/strong> Not used in liver and adipose tissue.
Substrates:<\/strong> Phosphocreatine (PC) stored in muscles.
Requirements:<\/strong> Dietary creatine. Creatine produced from the urea cycle, using dietary protein. Dietary phosphorus intake. Promoted by sex and thyroid hormones.
Uses: <\/strong>High-intensity, short-duration activities (e.g., sprinting, weightlifting).
Availability \/ Duration: <\/strong>10-15 second bursts.
Trigger\/Signaling:<\/strong> Immediate energy demand; catecholamines increase utilization.
<\/strong><\/p>\n

High intensity energy demands<\/u><\/strong>

Glycolysis<\/strong>
Where:<\/strong> Not used in red blood cells (RBCs), as they rely entirely on anaerobic glycolysis, and white adipose tissue prefers fatty acid metabolism.
Substrates:<\/strong> Glucose or glycogen.
Requirements:<\/strong> Dietary carbohydrate intake or gluconeogenesis. <\/strong>Phosphorus. Biotin. Vitamin B3 (as NAD+). Zinc. Magnesium \/ Manganese. Potassium. Chromium. Vanadium. Thyroxine (calcium, iodine, selenium, heme, tyrosine). Vitamin B1 (as TPP). Lipoamide. Promoted by sex and thyroid hormones.
Uses:<\/strong> Brain activity. Moderate to high-intensity activities (eg., walking \/ running upstairs, thinking).
Availability \/ Duration:<\/strong> Muscles – up to 2-3 minute bursts, subject to glycogen reserves.
Trigger\/Signaling: <\/strong>Increased ADP levels; catecholamines enhance glucose availability via cAMP-PKA signaling, inhibiting glycogen synthase and activating glycogen phosphorylase.

Glutaminolysis (anaplerosis)<\/strong>
Where:<\/strong> Not used in red blood cells due to lack of mitochondria and adipose tissue due to limited metabolic flexibility.
Substrates:<\/strong> Glutamine.
Requirements:<\/strong> Dietary glutamine, or glutamine created from citric acid cycle activity. <\/strong>Vitamin B3 (as NAD+). Zinc. Magnesium \/ Manganese. <\/strong>Promoted by sex hormones.
Uses:<\/strong> Rapid cellular proliferation (eg., immune response) and intense brain activity.
Duration:<\/strong> Continuous during demand.
Trigger\/Signaling: <\/strong>Stress-induced catecholamine elevation may indirectly upregulate this pathway.
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Sustained energy demands<\/u><\/strong>

Fatty Acid Oxidation<\/strong>
Where: <\/strong>Not used in brain cells due to fatty acids not crossing the blood-brain barrier, nor red blood cells due to lack of mitochondria.
Substrates:<\/strong> Fatty acids
Requirements: <\/strong>Dietary fats or lipolysis. <\/strong>Carnitine for the carnitine shuttle. Vitamin B2 (as FAD). Vitamin B3 (as NAD+). Vitamin B5 + cysteine (as Coenzyme-A). CoQ10. Lymphatic system is used to transport dietary fats. 
Uses:<\/strong> Basal daily metabolism. Low to moderate-intensity activities (eg., walking, endurance sports).
Duration:<\/strong> Indefinite.
Trigger\/Signaling:<\/strong> Prolonged energy demand; catecholamines promote lipolysis, increasing free fatty acids for oxidation.

Branched Chain Amino Acid (BCAA) Catabolism<\/strong>
Where:<\/strong> Low activity in the smooth muscle, brain and liver. Primarily used in skeletal muscle, heart, and kidney tissues.
Substrates:<\/strong> Leucine, isoleucine, valine.
Requirements:<\/strong> Dietary protein intake. Vitamin B1 (as TPP). Vitamin B2 (as FAD). Vitamin B3 (as NAD+). Lipoic acid (as lipoamide). Biotin. Vitamin B12 (as adenosylcobalamin). Vitamin B6 (as P5P). <\/strong>Vitamin B5 + cysteine (as Coenzyme-A). CoQ10. Potassium. Magnesium.<\/strong>
Uses:<\/strong> Prolonged exertion, especially with low glycogen.
Duration:<\/strong> Sustained.
Trigger\/Signaling: <\/strong>Catecholamines promote protein breakdown, increasing BCAA availability.
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Backup energy pathways for excessive load and various mitochondrial dysfunction<\/u><\/strong>

Anaerobic Glycolysis \/ Lactic Acid Metabolism<\/strong>
Where: <\/strong>Not used in liver (under normal conditions) and heart (prefers aerobic metabolism). Promotes neurogenesis and myogenesis.
Substrates:<\/strong> Glucose.
Requirements:<\/strong> Dietary carbohydrate intake or gluconeogenesis, NAD+, Zn, Mg, Biotin.
Uses:<\/strong> High-intensity activities with limited oxygen.
Duration:<\/strong> Short bursts, up to 2-3 minutes.
Trigger\/Signaling: <\/strong>High ADP\/ATP ratio, catecholamines enhance lactate production through glycogenolysis.

Astrocyte-Neuron Lactate Shuttle (ANLS)<\/strong>
Where: <\/strong>Found in the brain. Lactate can also circulate and participate in the Cori Cycle.
Substrates:<\/strong> Glucose (astrocytes), lactate (neurons).
Requirements:<\/strong> Dietary carbohydrate intake or gluconeogenesis.TBC.<\/strong>
Uses:<\/strong> Neural activity, intense cognitive tasks where glycolysis is insufficient.
Duration:<\/strong> Continuous during brain function.
Trigger\/Signaling:<\/strong> IFN-gamma, others. Norepinephrine enhances glucose uptake in astrocytes, promoting lactate production for neurons, similar to an intra-brain Cori cycle.

Cori Cycle<\/strong> \/ Lactic Acid Cycle
Where:<\/strong> Systemic  
Substrates:<\/strong> Lactate (from muscles, brain).
Requirements: <\/strong>Dietary carbohydrate intake or gluconeogenesis. <\/strong>TBC.<\/strong>
Uses: <\/strong>High-intensity exertion \/ mitochondrial dysfunction.
Duration:<\/strong> Normally short-term, during recovery.
Trigger\/Signaling: <\/strong>Epinephrine increases lactate production, fueling the Cori cycle.<\/strong>

Ketogenesis + Ketosis<\/strong>
Where: <\/strong>Ketones are generated in the liver, but not used by it. Red blood cells cannot use ketones due to lack of mitochondria.
Substrates:<\/strong> Fatty acids.
Requirements:<\/strong> Dietary fats and\/or lipolysis. TBC.
Uses: <\/strong>Prolonged fasting, low carbohydrate intake \/ impaired glycolysis, or low liver glycogen.
Duration:<\/strong> Sustained during glycogen depletion.
Trigger\/Signaling:<\/strong> Catecholamines promote lipolysis, increasing fatty acids for ketone body production.
<\/strong><\/p>\n

Examples of some less utilised pathways<\/strong><\/u>, which may be promoted \/ abused when primary pathways fail<\/u>

Tyrosine Catabolism<\/strong>
Where: <\/strong>Not used in red blood cells and adipose tissue due to limited enzymatic activity for this pathway.
Substrates:<\/strong> Tyrosine.
Requirements:<\/strong> Dietary intake of tyrosine and\/or microbiome synthesis. P5P. Ferritin. Calcium. Magnesium.
Uses:<\/strong> Various, including stress, mitochondrial dysfunction.
Duration:<\/strong> Continuous, where tyrosine exists.
Trigger\/Signaling:<\/strong> Catecholamines do not directly regulate but are derived from tyrosine.

GABA Shunt<\/strong>
Where:<\/strong> Not used in liver and skeletal muscle as they are not involved in neurotransmitter metabolism.
Substrates: <\/strong>GABA via glutamate or polyamine metabolism.
Requirements: <\/strong>P5P, magnesium.
Uses:<\/strong> Neural activity, especially during TCA cycle impairment and oxidative stress.
Duration:<\/strong> Continuous.
Trigger\/Signaling: <\/strong>Catecholamines influence neurotransmitter release but do not directly regulate GABA metabolism.

<\/strong>Urea Cycle (Argininosuccinate)<\/strong><\/strong>
Where:<\/strong> Not used in brain and muscle tissue since the urea cycle is primarily hepatic.
Substrates:<\/strong> Amino acids (arginine).
Requirements:<\/strong> Dietary protein intake. Aspartate.
Uses: <\/strong>Ammonia elevation, protein metabolism \/ high protein intake.
Duration:<\/strong> Continuous.
Trigger\/Signaling:<\/strong> Catecholamines indirectly increase ammonia load, requiring urea cycle activity.
<\/strong><\/p>\n


Food Intolerances<\/strong>
You also may have already developed a number of food intolerances.

Some of these intolerances are “simply” endotoxins being produced by overgrowth of unwanted microbial species living in biofilms inside your GI tract, consequently being sustained by your intake of various dietary carbohydrates and\/or other nutrients, such as sulfur-rich compounds These endotoxins can inhibit energy metabolism, neurotransmitter homeostasis, histamine degradation and various other pathways. <\/strong>
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Standard mixed diets vs ketogenic diets<\/a><\/h4>\n


“Sometimes the easiest way to solve a problem is to stop participating in the problem.” <\/strong><\/span><\/span>– Unknown
(In this context, “You cannot efficiently eliminate or reduce overgrown species while you’re also feeding them.”)

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Standard mixed diet<\/strong><\/h4>\n\n

A standard mixed diet typically includes a balanced intake\nof carbohydrates, proteins, and fats. In the context of the disease model, this diet may\ninadvertently contribute to increased fermentation and unwanted biofilm development. The high carbohydrate\ncontent fuels microbial ethanol and acetaldehyde production, leading to\ncontinued impairment of energy pathways due to elevated acetaldehyde. Symptoms\nsuch as fatigue, cognitive impairment, and metabolic abnormalities may persist\nor worsen under this dietary regimen.

Depending on the species and locations of the biofilms \ncontaining these microbial species, you may have more success avoiding \nsymptoms by consuming different types of carbohydrates. <\/strong>
eg.
a.\n Simple carbohydrates \/ sugars may feed any existing microbial \novergrowth in the mouth \/ throat \/ oesophagus \/ stomach \/ small \nintestine. In the absence of dysbiosis in those tissues, simple \ncarbohydrates can also be readily absorbed in the small intestine, \nbefore reaching any dysbiosis in the large intestine, should it exist.
b.\n Complex carbohydrates may not be broken down until further along the GI\n tract and may skip feeding some of the populations residing in biofilms\n in the small intestine.
c. Different types of dietary fibres and starches may selectively feed some species and not others. (see “2.2.3 — Prebiotics<\/a>“”)
d.\n Gliadin in gluten may generate an immune response due to molecular \nmimicry of the protein in the “hook” of Candida’s hyphae form. Gliadin \nis also used by a particular pathogenic strain of Streptococcus \nsalivarus to produce an antigen that punches holes in enterocytes, \nleading to gut barrier degradation, immune response and inflammation. Giardia infections are also known to create gluten intolerance.
https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4368562\/<\/a>
<\/a>https:\/\/pubmed.ncbi.nlm.nih.gov\/22617359\/<\/a>

In some types of more severe dysbiosis (and where your B vitamin and mineral status also supports this), you may find swapping more carbohydrates for \nprotein can be helpful in avoiding endotoxemia symptoms<\/strong> such as\n nausea, bloating, diarrhoea, histamine reactions, tachycardia, \nheadaches, etc. These will resemble die-off symptoms, as the same toxins\n are involved (see: 2.3.1-Herxheimer \/ die-off \/ acetaldehyde-support<\/a>).
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Here is an example 2000kcal mixed-diet, visualised in Cronometer:<\/strong>
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Ketogenic diet<\/strong><\/h4>\n\n

The ketogenic diet, characterized by high fat, moderate\nprotein, and very low carbohydrate intake, offers a contrasting approach to\na standard mixed diet or a low carbohydrate diet<\/strong>.It also avoids “low carb limbo” by promoting generation of ketone bodies in the liver.

In extreme gut microbiome dysbiosis cases, changing to a \nketogenic diet for a period of time can also be very helpful in reducing\n fermenting species, however will require commitment to endure an often \nunpleasant induction (1 week) and then adaptation phase (2 weeks). If \nyour OAT results already show elevated ketone markers, this is much \neasier. Studies suggest the acute effects of a ketogenic diet on your \ngut microbiome will last around 12 weeks, before the microbiome adapts. \nCombining this window of opportunity with other interventions in this protocol can allow \nyou to break the existing cycle with lasting results. <\/strong>
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\nBy significantly reducing carbohydrate consumption, this diet limits the\nsubstrates available for microbial fermentation. As a result, endogenous\nethanol and acetaldehyde production may decrease significantly in response to food\nintake, alleviating some of the metabolic disruptions caused by GFS.
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\nHowever, circulating acetaldehyde and other endotoxins will still be\nexperienced, making the first 1-2 weeks of a ketogenic (the induction phase)\nmore unpleasant than it would be for someone without GFS.

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A key point of difference is that the ketogenic diet\npromotes fatty acid oxidation and ketone body production as alternative energy\nsources. Ketone bodies can cross the blood-brain barrier and provide energy to\nthe brain (much more efficiently after weeks of being on a ketogenic diet),\npotentially improving cognitive function and reducing fatigue. Additionally,\nthis diet may alter the gut microbiota significantly, reducing fermenting\nmicrobial populations and promoting a healthier balance.<\/p>\n\n


Mechanisms of Ketogenic Diet’s Impact on GFS<\/strong><\/p>\n\n


Carbohydrate Restriction<\/strong><\/p>\n\n

Limiting carbohydrate intake directly reduces the amount of\nglucose and other fermentable sugars in the gut. This reduction in substrates\ncan lead to decreased microbial fermentation activity, resulting in lower\nethanol and acetaldehyde production. With less acetaldehyde burden, the\ninhibitory effects on metabolic enzymes are alleviated, helping to restore the\ncellular redox balance and improve the function of gluconeogenesis and fatty\nacid oxidation pathways.<\/p>\n\n


Fatty Acid Oxidation and Ketogenesis<\/strong><\/p>\n\n

The ketogenic diet’s high-fat composition encourages the\nbody to utilize fats as the primary energy source. This shift promotes the\nproduction of ketone bodies in the liver through a process called ketogenesis.\nKetone bodies serve as an efficient alternative energy source for various\ntissues, including the brain and muscles. By providing a consistent energy\nsupply, the diet addresses the energy deficits caused by acetaldehyde-induced\nmetabolic disruptions. Additionally, relying less on impaired glucose production\npathways reduces the risk of hypoglycaemia.<\/p>\n\n\n\n


Benefits of a Ketogenic Diet in GFS<\/strong><\/p>\n\n

Implementing a ketogenic diet in GFS management offers\nseveral potential benefits. By reducing acetaldehyde levels, the diet can help\nrestore normal metabolic functions, improving energy production and overall\nwell-being. The provision of ketone bodies as an alternative energy source may\nalleviate symptoms such as fatigue and cognitive impairments. Furthermore, the\nreduction in carbohydrate intake may lead to favourable shifts in gut\nmicrobiota composition, decreasing the population of fermenting microbes\nresponsible for excessive acetaldehyde production.

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Potential Challenges<\/strong><\/p>\n\n

Despite its potential advantages, the ketogenic diet\npresents challenges that must be carefully considered. The restrictive nature\nof the diet can make long-term adherence difficult for some people. There is\nalso a risk of nutrient deficiencies, particularly in electrolytes, fibre,\nvitamins, and minerals, if the diet is not properly managed. Monitoring thyroid\nfunction is also helpful, as very low carbohydrate intake can sometimes reduce\nT3 levels, potentially affecting metabolic rate. Additionally, high-fat diets\ncan impact beneficial gut bacteria, necessitating careful planning to maintain\ngut health.

<\/strong>A manganese deficiency will significantly impact hepatic gluconeogenesis, as will zinc and magnesium deficiencies.\nThese should be somewhat addressed before attempting keto induction.<\/strong>

NB. The reduction in glucose availability may affect cognitive function where neural hypoxia exists – due to eg. structural issues<\/a>, coagulation and\/or transport issues<\/a>, severe iron deficiency<\/a>, and also blocked lymph nodes in the neck and\/or nasopharynx<\/a> (usually relating to localised infection). The reduced glucose affects lactic acid metabolism involved in the Astrocyte-Neuron Lactate Shuttle and ultimately energy availability in neurons. This can also be a cell danger response trigger.<\/strong>

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Strategic Implementation<\/strong><\/p>\n\n

Successful implementation of a ketogenic diet for GFS\nrequires proper planning to ensure safety and efficacy. A personalised\nnutritional plan tailored to individual needs and tolerances can enhance\nadherence and effectiveness. Cronometer\nis very helpful in planning and visualising a successful day. Setting expectations ahead of time will help allow you to “keep calm and keto on” during unpleasantness.
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\nSupplementation with essential electrolytes, vitamins, minerals, and probiotics\nlike the ones in this protocol may be necessary to address deficiencies and\nsupport gut health.
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\nA gradual transition into the diet, by slowly reducing carbohydrate intake, prolongs\nketo adaptation and exacerbates energy crisis symptoms. It is not recommended. <\/strong>
 
\nA rapid transition normally creates temporary symptoms of “keto flu”,\nwhich can be managed by using GoBHB exogenous ketone supplements and essential\namino acids (EAAs) during the dietary transition.

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Strictly restricting carbohydrate intake is paramount to the\ndiet, which involves eliminating sugars and refined carbohydrates like\nsweets, sugary drinks, white bread, and pastries<\/strong>. Removing starchy foods\nsuch as potatoes, rice, pasta, and grains is also necessary. Instead, consuming\nnon-starchy vegetables like broccoli, cauliflower, kale, and bell peppers (capsicum)\nprovides essential nutrients with minimal carbohydrates. The target daily net\ncarbohydrate (total carbohydrates, minus fibre) upper limit is 25g.

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Increasing the intake of healthy fats supports the\nketogenic approach. This includes consuming monounsaturated fats found in olive\noil, avocados, and nuts, as well as omega-3 fatty acids from fatty fish such as\nsalmon and mackerel. Saturated fats from sources like coconut oil and butter\ncan be included. Butter is also a good source of butyrate, which may trigger rapid,\nbeneficial changes to the microbiome and energy metabolism, however, this will also trigger die-off\nsymptoms and potentially induce rapid alcohol withdrawal symptoms<\/a>.

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Protein intake is important for essential amino acids and to\nallow the liver to perform hepatic gluconeogenesis for brain and other tissues.\nBalancing protein intake is important because excessive protein can be\nconverted into glucose, potentially triggering an insulin response that\ninhibits keto induction \/ adaptation, while also fuelling microbial fermentation,\ndepending on the location of the biofilms. The longer the protein take to\ndigest, the further along the GI tract it will be before potentially feeding\nthe microbiome.

Keto induction is easier with more fats than protein, initially.\nFor example,

During keto induction, you could consume: <\/strong>
170g fat @ 1530 kcal +
100g protein @ 400 kcal
= 1930kcal

After keto induction, you can transition to consuming roughly 1:1 of fat:protein, on a per-gram\nbasis:<\/strong>
150g fat x9 = 1350kcal
150g protein x4 = 600kcal.
= 1950kcal.

(Scale this by your calorific needs.)
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\nHigh-quality protein sources such as lean meats, poultry, eggs (a great source of\nlecithin for phosphatidylcholine), and plant-based proteins like nuts (good\nmineral sources) and tofu (some people may have tolerance issues) are\nrecommended.

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Maintaining proper hydration and electrolyte balance is\nessential. Adequate water intake supports detoxification and metabolic\nprocesses, while sufficient electrolytes help prevent imbalances that will\nreliably occur during the initial stages of a ketogenic diet, as glycogen\nstores are intentionally depleted.
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Here is an example 2000kcal ketogenic diet, visualised in Cronometer:<\/strong>
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<\/span><\/span>Inflammation and\/or gut membrane permeability issues due to microbiome dysbiosis and related immune activity often leads to further histamine elevation and temporary IgG antibodies being produced. This is normal behaviour in response to complete foreign proteins getting through the barrier and triggering an immune response. In this state, foods which trigger mast cell activation and histamine release should be avoided for 6-8 weeks before reintroducing them, preferably after the barrier dysfunction has been sufficiently improved \/ resolved.<\/span> <\/strong><\/span><\/strong><\/span>

Due to metabolic impairments being described in this disease model, other food intolerance issues are entirely expected<\/strong>. The disease model and collected data shows that aldehyde toxicity \/ impaired aldehyde metabolism leads to elevations of serum Vitamin B6, creates issues metabolising “inactive” forms of Vitamin A into the active forms, creates issues degrading histamine and separately, other issues promoting lactic acid metabolism also elevate endogenous biosynthesis of oxalate.

In this state, additional intakes of these nutrients \/ compounds may exacerbate existing symptoms. These issues are targeted in Stage 1 of the protocol and allows dietary intakes to become more flexible. Overall, foods need to be carefully managed and reintroduced as the related \nmetabolic impairments and barrier function issues are resolved.

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Active Vitamin A deficiency<\/a><\/h4>
Vitamin A isn’t a single molecule, but rather a chain of metabolic conversions that transform dietary precursors into active signalling compounds. The story begins with retinyl esters, the storage form found in the liver and other tissues. When needed, these are converted into retinol, a transportable alcohol that circulates through the bloodstream and enters cells as required. (see Figure 8<\/a>)

Inside the cell, retinol takes on a more active role. It’s oxidised into retinaldehyde (often shortened to retinal) and then further into retinoic acid, the bioactive form that influences gene expression. These transformations are not spontaneous. They are mediated by specific enzymes, and each one depends on particular cofactors and cellular conditions.

There are several isomers involved in this process. The most common is all-trans-retinol, which feeds into the production of all-trans-retinoic acid (atRA). But there are also 9-cis and 11-cis forms of both retinol and retinal, each with their own signalling roles. The final step – the irreversible conversion of retinal into retinoic acid – is catalysed by the aldehyde dehydrogenase enzymes: primarily ALDH1A1, with ALDH1A2 and ALDH1A3 playing secondary roles depending on the tissue. This is the same enzyme responsible for degrading neurotransmitters.

This is where problems begin to surface. ALDH1A1 is a fragile enzyme. It requires NAD\u207a to function, which makes it vulnerable in states of redox imbalance. Conditions that lower NAD\u207a, such as mitochondrial dysfunction, acetaldehyde excess, inflammation, or chronic infection-can slow the enzyme down. Worse, acetaldehyde, a byproduct of both alcohol metabolism and microbial fermentation, also directly inhibits ALDH1A1. Add in common deficiencies of zinc and magnesium, or a cellular environment overloaded with oxidative stress, and the enzyme\u2019s activity may be effectively crippled.

When ALDH1A1 fails, the metabolic pathway clogs. Retinal cannot be converted into retinoic acid. As this step is irreversible, there\u2019s no workaround within the body. Retinol supplements won’t help – in fact, retinol can build up to apparently toxic levels. Carotenoids won’t help. The machinery is blocked downstream, and the most critical signals simply don\u2019t arrive.

Retinoic acid itself exists in several forms. All-trans-retinoic acid activates retinoic acid receptors (RARs) that regulate genes responsible for epithelial integrity, preventing hyperkeratosis (KLK pathway), immune regulation, detoxification, and neurodevelopment. Meanwhile, 9-cis-retinoic acid is required to activate retinoid X receptors (RXRs). RXRs are the central dimerisation partners for many other nuclear receptors, including PPARs, LXR, FXR, VDR, TR, and others. Without 9-cis-retinoic acid, these systems cannot operate at full capacity.

The consequences of low 9-cis-RA reach far beyond vitamin A metabolism. RXR-PPAR dimers, which govern fatty acid oxidation, ketogenesis, lipoprotein metabolism, adipogenesis, insulin sensitivity, inflammation resolution, energy expenditure, muscle metabolism and neuroprotection become hypoactive.

RXR-LXR dimers, essential for cholesterol transport and immune homeostasis, stall. Even RXR-VDR complexes, which modulate calcium and vitamin D responses, lose efficacy. FXR heterodimers regulating bile acid synthesis inhibition, plus lipid & glucose metabolism start fail to perform.

The deficiency of this one vitamin’s  metabolites sends a ripple through every metabolic and endocrine axis it touches.

When this problem is recognised, the logical therapeutic step, while correcting the upstream influences, would be to provide retinoic acid directly, bypassing the broken ALDH enzymatic activity. However, rather than being available as a dietary supplement, all-trans-retinoic acid is sold as a drug under the name Tretinoin. It\u2019s used clinically for certain types of acne, photoaging, and acute promyelocytic leukaemia. But it is also a prescription-only, regulated substance, patented and restricted, despite being identical to a molecule the body produces endogenously.. when it can.

Your doctor may provide a prescription for off-label use of a tretinoin cream<\/a> (not to be mistake for isotretinoin \/ 13-cis retinoic acid<\/em>), which can be used inside a mucosal tissue targeting a daily dose of around 1mg, which might be an amount of cream resembling something like the “size of a pea”, twice per day, depending on the concentration of the cream (typically 0.05 – 0.1%). For 0.1% concentration, 1g of cream = 1mg of all-trans retinoic acid. 

It would be best to implement tretinoin after any pre-protocol support \/ basic stage 1 onboarding has completed.<\/strong>

Unlike other forms of vitamin A, all-trans retinoic acid does NOT accumulate \/ store and has a very short half-life of under 1 hour<\/a>.

Very large (non-nutritional, eg. 700x) doses of all-trans retinoic acid inhibits Hypoxia Inducible Factors (HIF)<\/a> and are therefore being explored in early cancer research. In (often infected) tissues relying Warburg metabolism, this can trigger cellular apoptosis \/ necrosis, by inhibiting the metabolic sensor downstream of prolyl hydroxylase activity, that signals for cells to switch to lactic acid metabolism \/ anaerobic glycolysis for survival.

There\u2019s something quite peculiar about how a key developmental and repair vitamin which determines the behaviour of epithelial cells, immune tolerance, and even neural differentiation is, for most people, functionally inaccessible unless they’re being treated for a specific, medically recognised condition. Its dietary replacement has been patented, monetised, and regulated as acne medication or an ingredient for therapeutic skin care products<\/a>.

In situations where ALDH1A1 is impaired-through eg. chronic alcohol exposure, microbial fermentation, or long-term metabolic damage-this silent blockade may contribute to a breakdown in tissue maintenance, mucosal immunity, and metabolic feedback. It is a central mechanism, rarely measured, yet fundamental to the organism’s capacity to respond to stress, repair damage, and regulate its own biochemistry.


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Meal composition and timing is also important when energy metabolism is impaired. Part of the metabolic cascade includes type-2 diabetes and metabolic syndrome, so the dietary strategies will look very similar.

In the context of the disease model including glucose uptake and glycogen storage issues, the BCAA content of dietary protein intake may be very helpful in refilling glycogen stores via an alternate route, depending on your manganese, zinc, magnesium, biotin, B1, B2, B3, P5P and B12 status. In addition to general energy availability improvements, the model shows this is helpful for preventing PEM and crashes, providing oxidative stress and coagulation is being managed.
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Vitamin Q deficiency<\/a><\/h4>\n
A healthy microbiome normally produces queuine or “Vitamin Q”<\/a>, which has been identified as an essential nutrient (our bodies can’t make it). Vitamin Q is needed for \nmaintaining BH4, aspartic acid, asparagine, histidine, and tyrosine<\/a>. It’s required for mitochondrial metabolism, blood-flow and neurotransmitter homeostasis. Vitamin Q also promotes \nlactobacillus species. RAW coconut water is a surprisingly rich source (heat treating destroys it, so choose carefully). Milk and particularly wheat germ (gluten source) are also rich sources.<\/strong><\/a>

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Strategic foods<\/a><\/h4>\n


A table of microbiome transforming foods is provided in 2.2.3 — Prebiotics<\/a> and should be considered a required part of the protocol and any strategic diet.

The concept of “roughage” and its role in helping to disrupt and remove mucous + biofilms<\/a>, especially when combined with additional biofilm breaking food items \/ compounds is often underappreciated in meal planning.

Foods to generally consume as part of the protocol (as tolerance allows \/ increases):<\/strong><\/p>\n\n\nOat bran\n40g+\/day. 100g contains 143mg of silicon. Contains inulin + FOS, beta glucans which \nincreases sIgA, NK cells, inhibits glyoxylate shunt \/ isocitrate lyase. Removes PFAS (studied in mice).\n\n\nBlack pepper\n500mg contains 35mg beta-caryophyllene. Nice with salt and lime as dipping sauce.\n\n\nCodonopsis tea\n5\u201310g\/day. Promotes bifidobacteria, inhibits sulphur reducing bacteria.\n\n\nCoconut water\n1\/4 -1\/2 glass \/ day is keto-friendly. Ensure it’s not heat-treated. Ideally should be low sugar, organic. Rich source of dietary queuine.\n\n\nSeeds\nMinerals sources, “roughage” to help promote biofilm removal.
\n\n\nBrazil and other nuts\nContains silica, rubidium, strontium, cobalt. Warning, high selenium. Walnuts assist dysbiosis interventions. “Roughage” to promote biofilm removal.\n\n\nLiver, organ meats\nVery nutrient dense. Not every day.\n\n\nBroccoli + radish \/ mustard seed\nAdditional sulforaphane \/ NRF2, trace elements.\n\n\nSeaweed \/ kelp \/ wakame\nContains bromine, trace elements, minerals, and supports cortisol metabolism. Supplement added for kelp.
\n\n\nCheese\nProtein and fat source. Contains pentadecanoic acid. https:\/\/www.nature.com\/articles\/s41598-020-64960-y<\/a>\n\n\nButter\nFat source. Contains butyrate.\n\n\nMilk*
\nIn nature, (raw) milk serves as an exogenous immune system to protect the newborn’s GI tract and acts as a source of macro\/micronutrients. Milk contains xanthine oxidase for (pro-inflammatory) IFN-gamma related reactive oxygen species generation, colostrum, lactoferrin and IgG. It also provides a pH buffering carrier \/ vehicle, allowing probiotic microrganisms like Bifidobacterium and Lactobacillus species to survive stomach acid. It further contains the prebiotics which feed these species and support colonisation, such as lactose and (human) milk oligosaccharides. Many of these features are missing in pasteurised milk.<\/strong> *Reactions to milk consumption may relate to induced immune activity and die-off, however lactose is also a prebiotic enjoyed broadly by many microorganisms.
\n\n\nCabbage\nContains zirconium, rubidium and “Vitamin U” (S-methylmethionine). Homemade “cabbage juice” may be especially helpful for H. pylori, gastritis, reflux \/ GERD and peptic ulcers. As a juice, it delivers S-methylmethionine in an available form to the upper GI.
\n\n\nGreen beans\nContains silica.\n\n\nInulin + FOS sources
\nChicory Root, Dandelion Greens, Jerusalem Artichoke, Yucon Root, Garlic, Onion, Leeks, Asparagus, others (see tables below).
\n\n\nGOS sources
\nAsparagus, Chickpeas, Lentils, Black Beans, Beans, Kidney Beans, Beetroot.
\n\n\nResistant starch sources
\nCooked + cooled potatoes \/ potato starch, rice.
\n\n\nPurple foods\nContains anthocyanins. Purple berries. Pomegranate<\/strong> or low sugar pomegranate juice (start at 1\/4 serving, promotes Akkermansia spp., bifidobacterium spp.). Purple sweet potato, etc.\n\n\nEggs\nContains iron, iodine, choline, lecithin, biotin, etc.\n\n\nPumpkin seeds\/oil\nContains phosphorus, omega fatty acids.\n\n\nBeetroot\nContains nitrates for blood volume, nitric oxide and dopamine synthesis.\n\n\nGinger\n2.5\u20135g\/day. Raw, teas, powders, etc. To help resolve microbiome dysbiosis and itaconate \/ isocitrate lyase inhibition.\n\n\nPineapple\n100\u2013200g for silicon, bromelain (which also degrades histamine), fibrin. Warning, increases IFN-\u03b3.\n\n\nHigh protein diet\n2.5-3g per kg of body weight, per day.<\/strong> Provides \nessential amino acids, and often good phosphorus sources. Provides \npotentially dysbiosis-friendly energy. Your mileage may vary – some \novergrowth benefits from animal proteins.\n\n\nCarbohydrates\n>1.5\u20132g per kg body weight per day spread across multiple 20\u201340g \nnet carb meals, just like in diabetes, unless employing a ketogenic \ndiet.<\/strong> Glycogen storage is also impaired when cortisol is \nelevated. Shakiness, tinnitus, nausea, drowsiness, elevated cortisol \/ \nanxiety can be triggered by insufficient glycogen \/ carbohydrate intake.\n See \u201c2.2.9 PEM prevention and recovery<\/a>\u201d.\n\n\nWater\n2.5\u20133L of water per day to assist detoxification and help prevent red blood cell \u201crouleaux\u201d formation.\n\n\n


Foods to consume cautiously (or in some cases, avoid) as your aldehyde metabolism, etc normalises (monitor serum cholesterols, B6, beta-carotene):<\/strong><\/p>\n\n\nAlcohol\nIs metabolised to acetaldehyde which will exacerbate all symptoms, e.g. \nhistamine intolerance, tachycardia, etc. Conversely, can sometimes be a \nuseful patch, when used carefully, for tapering off and avoiding \nacetaldehyde withdrawal symptoms, if rapid changes to the microbiome \ncomposition are made.\n\n\nGluten\nMay be poorly tolerated, inhibits glucose uptake and damages celia, \nincreasing severity of symptoms. This can be found in many processed \nfoods, soy sauce, wheat products. Oats are often processed on the same \nmachinery as wheat and can have traces of gluten. https:\/\/celiac.org\/gluten-free-living\/what-is-gluten\/sources-of-gluten\/<\/a>\n\n\nHigh Vitamin B6 foods\nYou need some <\/em>vitamin B6<\/strong> to maintain P5P stores, however will have issues degrading excess pyridoxal , at first<\/strong>. This normally improves with remineralisation and allows the diet to become much more flexible. B6 degradation is also affected by hypoxia. https:\/\/ods.od.nih.gov\/factsheets\/VitaminB6-HealthProfessional\/<\/a>\n\n\nHigh Vitamin A foods\nYou need some<\/em> (inactive) vitamin A<\/strong> for immune function, neurotransmitter homeostasis, glucose metabolism and other important pathways, however, you will also have issues metabolising excess retinol -> retinal<\/strong> (aldehyde) -> retinoic acid (most active form), at first<\/strong>. The Daily Value for Vitamin A is 3000IU \/ 900 mcg RAE for adults and children age 4 years and older, where 1 mcg RAE = 1 mcg retinol, 2 mcg beta-carotene from supplements, 12 mcg beta-carotene from foods, 24 mcg alpha-carotene, or 24 mcg beta-cryptoxanthin. This intake level is normally well-tolerated. Vitamin A metabolism normally improves over Stages 1 & 2 to allow the dietary intakes to become significantly more flexible. Spirulina (variable content, depending on source) and chlorella (potent source) contain Vitamin A. https:\/\/www.healthline.com\/nutrition\/foods-high-in-vitamin-a<\/a>\n\n\nHigh histamine foods\nWhile histamine degradation is inhibited, these foods may be unpleasant. Remineralisation and correcting (gut) microbiome dysbiosis -> acetaldehyde production allows the diet to become more flexible. https:\/\/www.histamineintolerance.org.uk\/about\/the-food-diary\/the-food-list\/<\/a>\n\n\nHigh oxalate foods\nSome oxalates are needed to promote O. formigenes growth. Spinach is highly problematic. https:\/\/www.stjoes.ca\/patients-visitors\/patient-education\/patient-education-k-o\/pd-9447-oxalate-in-food.pdf<\/a>\n\n\nSoy products\nDaidzin and daidzein are soy isoflavones<\/a> which inhibit ALDH2 <\/a>in a similar way to disulfiram.<\/em><\/strong>\n\n\nSimple sugars and fructose\nThese do provide a substrate for maintaining glycogen; however the \nsimple forms may also promote overgrowth of fermenting microbial species in the small intestine \nand acid reflux<\/strong>. Excess fructose may inhibit copper homeostasis to some \nextent, also. If you tolerate simple carbohydrates well, but suffer when\n eating some complex carbohydrates, these may be entirely tolerable and \nappropriate, as small amounts per serving, over the day, just like in \ntype 2 diabetes.
\n\n\n


In the tables below, you’ll find food items and their relevant attributes, which you can use to help you get started building meals.
These tables are best viewed on a computer or tablet. On mobile devices, some columns will be hidden to fit the screen.
<\/strong>
The columns can be sorted and cautions or elevations of potentially inappropriate nutrients in foods items when getting started have been highlighted in red.
These tables are not intended to replace https:\/\/cronometer.com<\/a>, which is incredibly helpful in visualising and planning your dietary strategy.<\/span>

Protein sources:<\/strong>
<\/p>\n\n

\n \n \n\n \n \n \n \n\n\n wdt_ID<\/th> Food Item (100g)<\/th> Calories<\/th> Total Carbs (g)<\/th> Total Fructans (Inulin + FOS g)<\/th> GOS (g)<\/th> Fibre (g)<\/th> Net Carbs (g)<\/th> Protein (g)<\/th> Fat (g)<\/th> B6 (mg)<\/th> Histamine (mg)<\/th> Vitamin A (IU)<\/th> Fructose (g)<\/th> Oxalate (mg)<\/th> Grams Per 35g Protein<\/th> <\/tr>\n<\/thead>\n \n\n \n \n\n\n
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221<\/td>\n Brazil nuts<\/td>\n 656<\/td>\n 15.20<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 7.50<\/td>\n 7.70<\/td>\n 14.30<\/td>\n 66.40<\/td>\n 0.10<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 95<\/td>\n 244<\/td>\n <\/tr>\n
222<\/td>\n Almonds<\/td>\n 579<\/td>\n 22.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 12.50<\/td>\n 9.00<\/td>\n 21.00<\/td>\n 49.00<\/td>\n 0.14<\/td>\n Trace<\/td>\n 1<\/td>\n 0.00<\/td>\n 120<\/td>\n 166<\/td>\n <\/tr>\n
223<\/td>\n Pumpkin seeds<\/td>\n 559<\/td>\n 16.70<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 6.00<\/td>\n 10.70<\/td>\n 30.20<\/td>\n 49.10<\/td>\n 0.10<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 26<\/td>\n 115<\/td>\n <\/tr>\n
225<\/td>\n Soybeans<\/td>\n 446<\/td>\n 30.20<\/td>\n 1.20<\/td>\n 1.60<\/td>\n 9.30<\/td>\n 20.90<\/td>\n 36.50<\/td>\n 19.90<\/td>\n 0.38<\/td>\n Releaser<\/td>\n 22<\/td>\n 0.00<\/td>\n 45<\/td>\n 96<\/td>\n <\/tr>\n
226<\/td>\n Oats<\/td>\n 389<\/td>\n 66.00<\/td>\n 0.30<\/td>\n 0.00<\/td>\n 10.00<\/td>\n 56.00<\/td>\n 16.90<\/td>\n 6.90<\/td>\n 0.12<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 19<\/td>\n 207<\/td>\n <\/tr>\n
227<\/td>\n Barley<\/td>\n 354<\/td>\n 31.80<\/td>\n 0.50<\/td>\n 0.00<\/td>\n 3.80<\/td>\n 28.00<\/td>\n 12.50<\/td>\n 2.30<\/td>\n 0.26<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 30<\/td>\n 286<\/td>\n <\/tr>\n
228<\/td>\n Black Beans<\/td>\n 341<\/td>\n 62.40<\/td>\n 0.40<\/td>\n 1.00<\/td>\n 15.50<\/td>\n 46.90<\/td>\n 21.60<\/td>\n 1.40<\/td>\n 0.40<\/td>\n Low<\/td>\n 0<\/td>\n 0.00<\/td>\n 35<\/td>\n 162<\/td>\n <\/tr>\n
229<\/td>\n Rye<\/td>\n 338<\/td>\n 75.90<\/td>\n 3.00<\/td>\n 0.00<\/td>\n 15.10<\/td>\n 60.80<\/td>\n 10.30<\/td>\n 1.60<\/td>\n 0.29<\/td>\n Low<\/td>\n 9<\/td>\n 0.00<\/td>\n 5<\/td>\n 340<\/td>\n <\/tr>\n
230<\/td>\n Kidney Beans<\/td>\n 333<\/td>\n 60.00<\/td>\n 0.50<\/td>\n 0.90<\/td>\n 25.00<\/td>\n 35.00<\/td>\n 24.00<\/td>\n 0.80<\/td>\n 0.14<\/td>\n Low<\/td>\n 0<\/td>\n 0.00<\/td>\n 30<\/td>\n 146<\/td>\n <\/tr>\n
231<\/td>\n Wheat<\/td>\n 327<\/td>\n 71.20<\/td>\n 1.50<\/td>\n 0.00<\/td>\n 12.20<\/td>\n 59.00<\/td>\n 12.60<\/td>\n 1.50<\/td>\n 0.30<\/td>\n Low<\/td>\n 9<\/td>\n 0.00<\/td>\n 5<\/td>\n 278<\/td>\n <\/tr>\n
234<\/td>\n Beef<\/td>\n 250<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 26.00<\/td>\n 15.00<\/td>\n 0.37<\/td>\n Low, Releaser<\/td>\n 0<\/td>\n 0.00<\/td>\n 2<\/td>\n 134<\/td>\n <\/tr>\n
235<\/td>\n Oat bran<\/td>\n 231<\/td>\n 62.30<\/td>\n 0.80<\/td>\n 0.00<\/td>\n 14.50<\/td>\n 47.80<\/td>\n 16.30<\/td>\n 6.60<\/td>\n 1.30<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 58<\/td>\n 214<\/td>\n <\/tr>\n
236<\/td>\n Wheat Bran<\/td>\n 216<\/td>\n 64.50<\/td>\n 6.00<\/td>\n 0.00<\/td>\n 43.00<\/td>\n 21.50<\/td>\n 15.50<\/td>\n 4.20<\/td>\n 0.34<\/td>\n Low<\/td>\n 9<\/td>\n 0.20<\/td>\n 25<\/td>\n 226<\/td>\n <\/tr>\n
237<\/td>\n Fish<\/td>\n 206<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 20.00<\/td>\n 12.00<\/td>\n 0.64<\/td>\n Low, Releaser<\/td>\n 20<\/td>\n 0.00<\/td>\n 1<\/td>\n 175<\/td>\n <\/tr>\n
238<\/td>\n Chicken<\/td>\n 165<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 31.00<\/td>\n 3.60<\/td>\n 0.50<\/td>\n Low, Releaser<\/td>\n 56<\/td>\n 0.00<\/td>\n 2<\/td>\n 112<\/td>\n <\/tr>\n
239<\/td>\n Chickpeas<\/td>\n 164<\/td>\n 35.00<\/td>\n 1.60<\/td>\n 1.20<\/td>\n 8.00<\/td>\n 27.00<\/td>\n 8.90<\/td>\n 2.60<\/td>\n 0.54<\/td>\n Low, Releaser<\/td>\n 67<\/td>\n 0.30<\/td>\n 31<\/td>\n 393<\/td>\n <\/tr>\n
242<\/td>\n Eggs<\/td>\n 155<\/td>\n 1.10<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 1.10<\/td>\n 13.00<\/td>\n 11.00<\/td>\n 0.17<\/td>\n Trace<\/td>\n 520<\/td>\n 0.00<\/td>\n 0<\/td>\n 269<\/td>\n <\/tr>\n
247<\/td>\n Chicken liver<\/td>\n 119<\/td>\n 0.70<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.70<\/td>\n 16.90<\/td>\n 4.80<\/td>\n 0.90<\/td>\n High, Releaser<\/td>\n 14334<\/td>\n 0.00<\/td>\n 2<\/td>\n 206<\/td>\n <\/tr>\n
249<\/td>\n Cottage Cheese<\/td>\n 98<\/td>\n 3.40<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 3.40<\/td>\n 11.00<\/td>\n 4.30<\/td>\n 0.08<\/td>\n Moderate, Releaser<\/td>\n 65<\/td>\n 0.00<\/td>\n 3<\/td>\n 318<\/td>\n <\/tr>\n
254<\/td>\n Tofu<\/td>\n 76<\/td>\n 4.20<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 2.30<\/td>\n 1.90<\/td>\n 8.00<\/td>\n 4.80<\/td>\n 0.05<\/td>\n Trace<\/td>\n 0<\/td>\n 0.00<\/td>\n 13<\/td>\n 437<\/td>\n <\/tr>\n
259<\/td>\n Greek Yogurt<\/td>\n 59<\/td>\n 3.60<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 3.60<\/td>\n 10.00<\/td>\n 0.40<\/td>\n 0.05<\/td>\n Moderate, Releaser<\/td>\n 27<\/td>\n 0.00<\/td>\n 2<\/td>\n 350<\/td>\n <\/tr>\n
270<\/td>\n Cow's Milk<\/td>\n 42<\/td>\n 4.80<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 0.00<\/td>\n 4.80<\/td>\n 3.40<\/td>\n 1.00<\/td>\n 0.04<\/td>\n Releaser<\/td>\n 126<\/td>\n 0.00<\/td>\n 2<\/td>\n 1,029<\/td>\n <\/tr>\n <\/tbody> \n\n \n \n \n <\/table>\n\n<\/div>