The Travis Corner

[Travis]

Cool. Maybe that's one of the reasons I haven't had the trouble I used to have with something like thrush - cutting way back on PUFAs and adding a little coconut oil to food regularly.

Estrogen is also increased along with the more virulent form of Candida. According to @haidut estrogen is responsible for the more virulent form. Sounds like Estrogen and Prostaglandin E2 have things in common...

These are real effects, and surprisingly consistent; I've read a few studies on this. Cyclooxygenase inhibitors stop the Candida hyphal transformation, which grows only slightly in response other eicosanoids besides prostaglandin E₂ (thromboxane B₂ comes in second place):

Guess which one of the images above had indomethacin added? and which one had aspirin? The fact that prostaglandin E₂ is a Candida hormone means that cyclooxygenase inhibitors are actually antifungal. Candida albicans both makes prostaglandin E₂ and responds to the prostaglandin E₂ we produce.

But lauric and caprylic acids have antifungal effects besides, which appear unrelated to prostaglandin E₂. This would make coconuts and goat cheese actually antifungal, besides being somewhat safe non‐immunogenic foods. Candida albicans is naturally present on the skin, making the term 'Candida infection' somewhat of a misnomer. I think the ingestion of ω−6 fatty acids could go a long way in explaining why only some people have 'Candida infections' some of the time.

Alem, M. "Effects of aspirin and other nonsteroidal anti-inflammatory drugs on biofilms and planktonic cells of Candida albicans." Antimicrobial agents and chemotherapy(2004)
Noverr, M. "Regulation of Candida albicans morphogenesis by fatty acid metabolites." Infection and immunity (2004)​

 

[raypeatclips]

@Travis What are your thoughts on eating seafood such as mussels, prawns semi-regularly for the purpose of getting some minerals that are tough to find in other foods?

 

[tara]

I think the ingestion of ω−6 fatty acids could go a long way in explaining why only some people have 'Candida infections' some of the time.

And maybe why 'anti-candida' diets that emphasise restricting carbs and especially simpler sugars, etc, may be missing the point if they ignore or encourage seed-eating and don't always work so well.

 

[tara]

Hi Travis,
A few years ago I was taken with the idea of green smoothies as a way to increase mineral and vitamin intake. I'm a slow eater, have poor teeth, and even if I enjoyed chomping through lots of leaves (I used to try to eat at least a little each day), I don't have time for it.
Reading about it, I found that proponents of making green smoothies a large part of the diet emphasised the importance of vary/cycling different greens to vary the alkaloids (and maybe other toxins?) in all or most leaves that the system would have to dispose of, so it wouldn't get overwhelmed with excesses of particular ones.
They'd have been all for kale smoothies, but not for every meal every day.

I've read Peat's cautions about problems of toxins if one had to get all ones calories from leaves, and I'm not aiming to do that. He seems to favour cooking greens well to deal with some of the toxins.
I want to eat more leaves on a regular basis for minerals, and I can enjoy them cooked with other food. I occasionally have and enjoy a green juice or a smoothie that includes leaves and fruit, and I think I could enjoy having a few more.

I think at least one of the anti-cancer specialists quoted in this forum (Koch? Gerson?) mentioned issues with oxidation of nutrients by blending.
Personally, I'm not making a choice between juicing/blending or chewing the same quantities of leaves, because I wouldn't have that much at all if I had to chew them.

Blending keeps the fibre; juicing discards it. Peat might might consider those leafy fibres to be more of a liability (I'm not entirely sure - I guess it depends on how fermentable they are in the particular gut bacteria/how much they irritate the gut, what transit is like, how much they contribute to carrying out bile, etc), some others would count them a benefit.

Q1. What are your thoughts on the risks of excessive alkaloids or other toxins from large quantities of commonly eaten leaves? Do you make a point of varying yours at all for this reason?

Q2. Do you see any significant downsides from juicing or blending leaves, compared with not having them at all or compared with boiling them (and drinking the broth), and do you see significant advantages of one over the other?

 

[Travis]

And maybe why 'anti-candida' diets that emphasise restricting carbs and especially simpler sugars, etc, may be missing the point if they ignore or encourage seed-eating and don't always work so well.

Yeah, and you can have perfect toenails on a basically all‐fruit and all‐leaf diet.

The popular alternative press will usually say that 'fat' and 'sugar' together feed candida as an explanation, but they will also say that 'coconut oil kills Candida.' I suppose they are right in both accounts, or close to it, but I think if we elaborate a bit we can gain a fuller understanding. We all have Candida naturally on our skin, and it's only the ω−6 fatty acids which seem to transform it; this explains why people who eat dairy and coconuts are practically exempt from the 'sugar + fat' rule (and also explains some of my symptoms after eating eggs; the tryptophan and androgens can explain the rest).

Hi Travis,
Q1. What are your thoughts on the risks of excessive alkaloids or other toxins from large quantities of commonly eaten leaves? Do you make a point of varying yours at all for this reason?

I just stay away from purple stem kale, which has high isothiocyanate potential; over generations, these have been largely bred‐out of most kale and broccoli. Most of the goitrogen research appears to have been done on cassava and CANOLA, with kale implicated only by extrapolation (it also contains isothiocyanate). The isothiocyanate ion has about the same affinity for the thyroid as does iodide (I⁻ ), and kale's antithyroid effects are usually understood simply in terms of competitive displacement. This means that it inhibits thyroid hormone synthesis to the extent that a person is deficient in iodide, but even massive amounts of Lacinato kale wouldn't do much with amounts so low. Nonetheless: acknowledging the isothiocyanates in foods makes a person realize that they need to consume iodide, which is found in kelp in relatively high concentrations.

Oxalic acid is found in spinach in high amounts. Here, it inhibits calcium absorption being a strong dicarboxylic acid chelator. However, this isn't particular toxic besides and it's a normal metabolite of glucose and appears in the Kreb's cycle. Kidney stones are more commonly caused by high uric acid than by oxalic acid.

Calcium is found in the oxygen‐evolving complex of photosystem II, a very elaborate enzyme system which converts water into oxygen. So wherever you have leaves doing photosynthesis, you have calcium. Also necessary for photosynthesis is magnesium, which of course forms the center of chlorophyll.

Q2. Do you see any significant downsides from juicing or blending leaves, compared with not having them at all or compared with boiling them (and drinking the broth), and do you see significant advantages of one over the other?

I like to eat them plain, but they are really good steamed with either shredded goat cheese or shredded coconut. I think the fiber is actually a good thing because it prevents that cooked food amino acid spike. Raw foods seem to release amino acids and sugars more slowly, a fact which can be easily verified by looking at their glycemic indices. Millions of animals eat leaves every day and few of them are overweight or have cancer. Of course some leaves try to stay alive by synthesizing toxins but the more prolific ones don't seem to bother with that particular metabolic strain, tending more towards faster growth. I think lettuce is a good example of a leaf with very few toxins, and perhaps bay leaf so concentrated with phyto‐detractants as to be completely inedible. Things like dill, arugula, and anise appear to be somewhere between 'too strong' and 'nearly edible'—not as strong as spices and usually relegated to the 'minor salad component' category. I think in nature animals try to eat immature plant parts before the defensive molecules start to be synthesized, but some of these phytomolecules can actually be good (i.e.those in dill).

 

[Travis]

@Travis What are your thoughts on eating seafood such as mussels, prawns semi-regularly for the purpose of getting some minerals that are tough to find in other foods?

It could be better than eating seeds, which are also high in zinc. But with shellfish, you have peculiar toxins which need to be considered; some religions avoid these entirely. I think we need to search for the best zinc food, because when I do the cronometer I get over 100% on essentially everything besides zinc and selenium. But after reading about selenomethionine and selenocysteine, I'm starting to wonder how selenium in foods is measured. Perhaps it is underestimated in plants due to them measuring only the free, inorganic form?

But I remember seeing some seeds high in zinc, yet these are too high in linoleic acid for rational consumption. I bet there's some seafood out there which has zinc yet doesn't have anything shellfish toxins.. .

 

[Mito]

Candida albicans is actually responsive to prostaglandin E₂, and it actually makes it.

Organic acid tests measure urinary arabinose. They claim a high measurement indicates Candida albicans overgrowth.

 

[Ulysses]

Travis, do you have any advice on how to treat varicocele?

 

[tara]

But with shellfish, you have peculiar toxins which need to be considered; some religions avoid these entirely.

Are you talking about toxins that are inevitable in all shellfish consumption, whatever the source and freshness, or ones that develop if they are contaminated with algal blooms or microbial infections or in high-toxic metal zones or hanging around too long after harvest or something?

[eta:]
I'm wonderig how significant the toxins/risks are from oysters from clean waters that may be transported and stored chilled for a few days before being cooked and eaten - which I consider an occasional nutritious and delicious treat.

I'm also wondering if there is any toxin problem with other shellfish harvested fresh below low tide level in clean waters without algal blooms, cooked immediately (within 10-20 mins) and eaten straight away? As I occasionally have the opportunity to enjoy.

 

[Travis]

Organic acid tests measure urinary arabinose. They claim a high measurement indicates Candida albicans overgrowth.

View attachment 8411

Interesting. I think this could mean that Candida albicans breaks‐down cellulose in the intestines.. .

'From the normal subjects 22.4% of the ingested cellulose was excreted, indicating approximately 80% of the cellulose was digested in the normal subjects. From the water insoluble ingested hemicelluloses 27.5% were excreted from the small bowel, 4.0% from normal subjects. That is approximately 96% digestion of the hemicelluloses in normal subjects. Lignin was found to be undigested in both the small and large bowel. This has important implications in future fiber research.' ―Holloway​

Yet lignan appears resistant to degradation. Nonetheless, many people seem to be under the wrong impression that cellulose is not digested by humans.

Holloway, W. D. "Digestion of certain fractions of dietary fiber in humans." The American journal of clinical nutrition (1978)​

 

[Travis]

Are you talking about toxins that are inevitable in all shellfish consumption, whatever the source and freshness, or ones that develop if they are contaminated with algal blooms or microbial infections or in high-toxic metal zones or hanging around too long after harvest or something?

I think it could be a mix: both constitutional proteins being allergens and contaminants also playing a role. This should be pretty easy to find out, since their are many ocean biologists out there with little else to do.. .

Fujiki, H. "Diarrhetic shellfish toxin, dinophysistoxin‐1, is a potent tumor promoter on mouse skin." Cancer Science (1988)​

This shellfish toxin induces ornithine decarboxylase; interesting to know and also another example of how polyamines are central to the process of carcinogenesis.

This is an unusual looking molecule; here is some info:

'Dinophysistoxin-1 belongs, together with okadaic acid and the dinophysistoxins-2 and 3, to a class of toxins responsible for a red tide phenomenon known as Diarrhetic Shellfish Poisoning. These toxins are produced by the dinoflagellates Prorocentnrm lima, Dinophysis fortii and Dinophysis acuminata, and it has been established that they are potent tumour-promoting agents and protein phosphatase inhibitors. The structure of this group of toxins somewhat resembles the polyether ionophores from terrestrial microorganisms, which are characterized by possessing oxolane and oxane rings. Conversely, other groups of polyether marine toxins isolated from red tide dinoflagellates, the brevetoxins produced by Phtytochodiscus brevi, maitotoxin and ciguatoxins isolated from Gambierdiscus toxicus are charactekzd by the presence of 6/7/8/g ether rings trans‐fused in a ladder‐like manner.' ―Norte​

This molecule appears to be constructed out of succinate after two rounds through the TCA cycle, hydroxyl‐3‐methyl‐glutarate, and perhaps even isobutyrate derived from L‐valine. Even with NMR studies using radio‐labeled carbons, the chemists couldn't be 100% sure how it's normally made.

So it seems as though I've found a major class of shellfish toxins, but I'm pretty sure there are some protein allergens as well.. .

This appears to be the case, the shellfish muscle protein tropomyosin has an antigenic sequence. But like any immunogenic protein, this would depend on stomach pH and preparation techniques. I has a very stable alpha helical core which allows its immunogenicity to persist after cooking—or even increase!

―Kamath

So you have a muscle protein allergen, which in unavoidable, but also a toxin which could potentially existing in varying amounts. But most people do seem to eat lobster without too much discomfort, and the true shellfish allergy seems somewhat rare. But it's still probably good to know about these things and also the difference between tropomyosin anaphylaxis and dinophysistoxin poisoning, should they occur.

Norte, M. "Studies on the biosynthesis of the polyether marine toxin dinophysistoxin-1 (DTX-1)." Tetrahedron letters (1994)
Kamath, S. "Impact of heat processing on the detection of the major shellfish allergen tropomyosin in crustaceans and molluscs using specific monoclonal antibodies." Food chemistry (2013)​

 

[CarbAppreciator]

I've been exploring the mechanisms behind cholinergic modulation, and polyamines appear to play a critical role. This understanding better framed my ideas on cancer metabolism regarding chronic adaptations to stressful states. I wondered about polyamine levels in the brains of people with Alzheimer's, and indeed there were significant differences.

-Brain polyamine levels are altered in Alzheimer's disease.
-Beta-amyloid induces neuronal death through disrupting polyamine homeostasis
​

Similar disruptions are seen in cases of dementia and Parkinson's, probably MS and other nervous diseases.



The enzyme responsible for regulating polyamine levels in this cocktail blend is Ornithine Decarboxylase (ODC.) ODC is a pretty big deal, disruption of its activity during development led to changes in nicotinic acetylcholine receptors. These receptors are critical for modulating inflammatory states throughout the body (see reference below.) So the activity of ODC can be a very important marker showing the state of nervous activity in tissue.

-Long-lasting CNS effects of a short-term chemical knockout of ornithine decarboxylase during development: nicotinic cholinergic receptor upregulation and subtle macromolecular changes in adulthood.
-Spermidine, a polyamine site agonist, attenuates working memory deficits caused by blockade of hippocampal muscarinic receptors and mGluRs in rats
-Polyamine treatment in early development leads to increased numbers of rat sympathetic neurons
​

There is also some evidence for a direct effect of polyamines on synaptic cholinesterase.

-Regulatory effects of polyamines on membrane-bound acetylcholinesterase




​

I thought the polyamine treatment causing increased sympathetic neurons was very interesting, and found that the correlation between sympathetic nervous activation and ODC expression and polyamine synthesis was so great that changes in ODC levels were used for a measurement. So the correct regulation of polyamine synthesis was critical for proper sensitivity to catecholamines and sympathetic nervous drive.

-Sympathetic nervous system development in hypertensive rats.
​

One of the fundamental effects of thyroid is to increase cholinergic signalling and turnover, and one of the ways it does this is through altering polyamine synthesis.

-Accelerated Development of Rat Sympathetic Neurotransmission Caused by Neonatal Triiodothyronine Administration



​

So polyamine synthesis is tied into cholinergic nerve signalling, and cholinergic nerve signalling is critical to being alive. I think that fatigue of the sympathetic nervous system induces persistent induction of ODC and generally increased polyamine levels, and this is one major cause of reduced nervous sensitivity and movement towards cancer metabolism and heart and vascular disease.

-Effects of various kinds of stimulation on ornithine decarboxylase activity in superior cervical sympathetic and nodose ganglia of rats.
​

__________________________________________________________________

-Nicotinic acetylcholine receptor α7 subunit is an essential regulator of inflammation

-Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

-The sympathetic nervous response in inflammation

-The Involvement of Parasympathetic and Sympathetic Nerve in the Inflammatory Reflex

-Autonomic nervous system activity and inflammation: good ideas, good treatments, or both?

-Toll-Like Receptor 4 Promotes Autonomic Dysfunction, Inflammation and Microglia Activation in the Hypothalamic Paraventricular Nucleus: Role of Endoplasmic Reticulum Stress

-The Role of the Autonomic Nervous System in Atherosclerosis - Targeting the Cholinergic Anti-inflammatory Pathway in Humans and Mice

​

Autophagy seems to be central in AD prevention, nicotine promotes autophagy:
https://www.researchgate.net/public...y_protects_neuron_from_A-induced_cytotoxicity
On autophagy generally as relating to AD:
Cell “Self-Eating” (Autophagy) Mechanism in Alzheimer’s Disease

 

[CarbAppreciator]

Androgens upregulate ornithine decarboxylase and so does prostaglandin E₂. I think these facts alone could go a long way in explaining their anabolic effects. I see polyamines as forming the link between cell biology and physical chemistry, unfurling the dNA of housekeeping genes which translate for basic enzymes and structural proteins at rates determined by dietary methionine and ornithine decarboxylase activity.

For consideration with regards to ornithine decarboxylase:
A Definitive Role of Ornithine Decarboxylase in Photocarcinogenesis
"Under similar UVB-exposure protocol, the nontransgenic littermates or SKH-1 hairless mice did not develop tumors or pigmented cysts for up to 50 weeks."

Another hint at the centrality of the polyamine pathways mentioned in this thread.

 

[Travis]

Autophagy seems to be central in AD prevention, nicotine promotes autophagy:
https://www.researchgate.net/public...y_protects_neuron_from_A-induced_cytotoxicity
On autophagy generally as relating to AD:
Cell “Self-Eating” (Autophagy) Mechanism in Alzheimer’s Disease

Another unbelievable syncronicity; I was just reading about autophagy today. This is super cool and happens all the time. A person's first thought upon hearing the word would perhaps be a macrophage, or a situation in which one cell engulfs another cell. This is not correct: What happens in that proteins are transcriptionally upregualted within the cell with intent of degrading other cellular components. This means during an intermittent fast, cellular lipids will be β-oxidized for fuel. This would mean a relatively rapid depletion of prostaglandin potential.

Intracellular proteins are also degraded for the tryptophan to create niacin, serotonin, and melatonin; they are degraded for the tyrosine to form dopamine, histidine to create histamine, and glutamate to be an exitatory neurotransmitter without modification. Proteins are degraded yet others are formed; this process happens all the time, and in the metabolically‐active liver about 1% of each cell is recycled by phagocytosomes.

Fasting used to be researched; there are a few older studies circa 1910. There are a few newer studies, but it's always been a fringe topic like 'ultra‐weak fluorescence.' But it's clear that fasting will change the mRNA produced, both by sensing—or not sensing—tryptophan . . . and a few other signalling amino acids such as leucine can be sensed by the body (through mTOR). There is enough science behind fasting to feel comfortable and confident in doing so, and it's main opponents appear to be the food industry and that residual primitive folklore in our psyche passed on throughout the generations (think about that stereotypical, slightly overweight aunt who always tries to feed you cookies.)

I had come across p62 in Alzheimer's in the article I was reading, and it probably even references the one you had posted. This makes sense, as the Alzheimer's inclusion bodies are essentially polymerized proteins crosslinked by lipid peroxide dialdehydes and/or the aluminum ion (Al³⁺). You might think that nascent lipofuscin—an inclusion body which increases in postmitotic cells over time—could perhaps be degraded by autophagy before it has a chance to become solidified into a polymerized mass resistant to proteolysis; lipofuscin proper. Of course minimizing iron, excessive unsaturated fatty acids, and aluminum is a good way to avoid lipofuscin formation to begin with.

 

[Travis]

For consideration with regards to ornithine decarboxylase:
A Definitive Role of Ornithine Decarboxylase in Photocarcinogenesis
"Under similar UVB-exposure protocol, the nontransgenic littermates or SKH-1 hairless mice did not develop tumors or pigmented cysts for up to 50 weeks."

Another hint at the centrality of the polyamine pathways mentioned in this thread.

I see polyamines and cancer as nearly the same word, or that the author had made a Freudian slip whenever (s)he'd written cancer instead of polyamines . . . or vice versa.

Just look how synonymous the two words are (from your article):

'Excessive exposure of skin to ultraviolet (UV) light, particularly in the middle wavelength range (UVB; 290 to 320 nm), elicits a variety of adverse effects that include skin aging, cutaneous inflammation, erythema, immunosuppression, cell death, and skin cancer polyamines.' ―Ahmad

'Ornithine decarboxylase (ODC) is the first and the rate-limiting enzyme in the polyamine cancer biosynthetic pathway.' ―Ahmad

'A considerable body of information suggests that ODC plays an important role in both normal cellular proliferation, and the growth and development of tumors polyamines.' ―Ahmad​

 

[Wagner83]

Fasting used to be researched; there are a few older studies circa 1910. There are a few newer studies, but it's always been a fringe topic like 'ultra‐weak fluorescence.' But it's clear that fasting will change the mRNA produced, both by sensing—or not sensing—tryptophan . . . and a few other signalling amino acids such as leucine can be sensed by the body (through mTOR). There is enough science behind fasting to feel comfortable and confident in doing so, and it's main opponents appear to be the food industry and that residual primitive folklore in our psyche passed on throughout the generations (think about that stereotypical, slightly overweight aunt who always tries to feed you cookies.)

What about the higher cortisol, increased fat-oxidation of fasting and the gh promoting effects of intermittent fasting? How to know if the overall effects are positive?

 

[raypeatclips]

It could be better than eating seeds, which are also high in zinc. But with shellfish, you have peculiar toxins which need to be considered; some religions avoid these entirely. I think we need to search for the best zinc food, because when I do the cronometer I get over 100% on essentially everything besides zinc and selenium. But after reading about selenomethionine and selenocysteine, I'm starting to wonder how selenium in foods is measured. Perhaps it is underestimated in plants due to them measuring only the free, inorganic form?

But I remember seeing some seeds high in zinc, yet these are too high in linoleic acid for rational consumption. I bet there's some seafood out there which has zinc yet doesn't have anything shellfish toxins.. .

Thanks for the reply. Maybe simply a bit of beef would be best for trying to get zinc, instead of overthinking it trying to eat seafood etc, I've never particularly enjoyed seafood anyway.

 

[Hans]

This means during an intermittent fast, cellular lipids will be β-oxidized for fuel. This would mean a relatively rapid depletion of prostaglandin potential.

Does this mean during intermittent fasting or ketogenic dieting, prostaglandin synthesis is reduced? Or could you explain about the depletion of the prostaglandin potential.

 

[Obi-wan]

I have prostate cancer. Fasting started the wasting process for me. Rather do just low PUFA

 

[haidut]

Sounds like Estrogen and Prostaglandin E2 have things in common

Yep, they promote each other's synthesis. Prostaglandins increase aromatase activity (hence why aspirin is can lower estrogen) and estrogen promoted the synthesis of prostaglandins from arachidonic acid. Estrogen also promotes leukotriene synthesis from arachidonic acid. So, estrogen activates both COX and LOX which are responsible for 80%+ of the inflammatory cascade.