The Travis Corner

[Terma]

I must say that my memory and mental clarity is better now that I've stopped drinking milk.

Mine as well (no such improvement from cutting out wheat), and taking folinic acid. Good posts btw (Travis's extremely informative as well, but no surprise there).

 

[allblues]

@Travis To what extent do you avoid plastics, especially in the way of food packaging etc, if at all? Would you eat a goat cheese contained in a soft plastic packet, for instance? (This is a decision I am currently pondering)

 

[Travis]

Is there any way someone can negate the antigen formation for those that still want to drink milk? And not just bypassing it with high doses of (6S)-5-methyltetrahydrofolate or (6S)-folinic acid. Would that be possible?

Yes, you'd have to completely break down the proteins in the milk by thoroughly digesting it.

Raising antibodies in response to ingested food antigens is in no way certain. Immune cells require that an amino acid be a minimum of ~10 amino acids in length before it will form a corresponding antibody. Should an ingested protein be hydrolyzed completely in the stomach into free amino acids, antibody formation is impossible—even di- and tripeptides are too short & nonspecific to be antigenic. Wheat forms the most antibodies out of any common food because it has gliadins that are characterized by an unusually-high density of proline, the only amino acid forming a unique peptide bond. The sp² hybridization of the connecting nitrogen has a geometry not conducive to efficient proteolysis, perhaps not matching catalytic sites of sp³-specific digestive enzymes. The prolyl peptide bond is also uniquely capable of cis-trans isomerization—perhaps also conferring enzymatic resistance, somehow... Regardless of how exactly proline peptide bonds resist digestion, it has been experimentally-confirmed that they do.

Stomach pH, salt concentration, intestinal permeability, pepsin activity, gastric bacteria, and food matrix effects are just a few things either preventing or facilitating food-antibody formation. The prevention of wheat-antibody production can be accomplished though sourdough fermentation, a process using certain strains of Lactobacilli which have protease activity against proline peptide bonds. The ability of either Lactobacillus sanfranciscensis or prolyl-endoprotease capsules to make wheat gliadins non-immunogenic has been experimentally-verified. Since the immunogenicity of the most difficult-to-digest and most antigenic food protein can be reliably circumvented, a person could rightly assume that bovine folate receptor-α could be similarly neutralized.

But then again: the half-life decay rate for antibodies in on the order of months, so you'd have to be especially diligent:

 

[Travis]

Edit: Also, what would you consider a high dose of (6S)-5-methyltetrahydrofolate and (6S)-folinic acid to be?

I think a few milligrams per day would be beneficial, but there seems to be no practical limit to how much you can take. Children have been given milligrams per day, per kilogram, so I don't think safety is much of a consideration. But since (6S)-5-methyltetrahydrofolate is stereochemically-pure, I think a person could get by using less than the larger doses of racemic folates reported in the published clinical case reports.

 

[Hans]

Since the immunogenicity of the most difficult-to-digest and most antigenic food protein can be reliably circumvented, a person could rightly assume that bovine folate receptor-α could be similarly neutralized

"Relatively new data on actual concentrations in different dairy products show folate-binding proteins (FBP) to occur in unprocessed milk, but also in pasteurised milk, spray-dried skim milk powder and whey. In contrast, UHT milk, fermented milk and most cheeses only contain low levels or trace amounts."
Folates and dairy products: a critical update. - PubMed - NCBI

 

[Travis]

@Travis To what extent do you avoid plastics, especially in the way of food packaging etc, if at all? Would you eat a goat cheese contained in a soft plastic packet, for instance? (This is a decision I am currently pondering)

I used to eat just that: raw goat cheddar wrapped in polyethylene.

Of the class of plasticizers bisphenol A has gotten the most publicity, yet since this is exclusive to polycarbonates it can be ignored. Of concern in the case of cheese are phthalates, perhaps being leeched from the polyvinylchloride or polythylene packaging. On warm days, goat cheese will 'sweat' or exude a liquid oil and it' seem reasonable to suppose that this—caproic acid fatty acid trigylcerides—would make a suitable phthalate solvent. ['Phthalate' is actually my favorite nine-letter word having four consecutive consonants!]

​

Phthalates are benzenedicarboxylic acids. The butyl and ethylhexyl esters of ortho-pthalic acid are the most commonly used PVC plasticizers. Toxicological interest in ortho-pthalic acid esters had begun in 1970 with the finding of diethylhexyl phthalate in the organs of patients previously intubated with PVC tubing.

​

Pthalic acid esters appear to have a low acute toxicity and little carcinogenic potential. Dibutyl phthalate appears to be more toxic that diethylhexyl phthalate, yet is still a relatively safe molecule.

'These plasticizers give the polymer the desired flexibility and softness and may account for up to 40% of the final weight of the material. They are not chemically bound to the polymer, but dispersed in the matrix of the polymer chains...' ―Autian

'Diethylhexyl phthalate (DEHP) has an extremely low order of acute toxicity. The LD₅₀ values in several species of animals indicate that extremely large doses. Fourteen to greater than 50 g/kg of the compound are necessary to produce lethal effects. In fact, this agent would be classified as "practically nontoxic" by the toxicity rating system of Gleason et al.' ―Autian

'Rats fed diets containing 0.01, 0.05, and 0.25% dibutyl phthalate showed no toxic reactions after 1 yr. Of those fed 1.25%, half died during the first week of the experiment, but those which survived grew normally,' ―Autian​

Diethylhexyl phthalate is readily absorbed. Most of the diethylhexyl phthalates that enter the body are transformed into their corresponding monoethylhexyl esters by uncharacterized enzymes distributed ubiquitously (i.e. ghost enzymes). Cleavage of both alkyl esters rarely occurs, yielding phthalate, although this does occur in the liver with phthalates having shorter alkyl substituents (i.e. dimethylphthalate). Elimination is quick, and the monoethylhexyl form appears in the urine either conjugated with glucose or unchanged. This efficient detoxification process is not complete, however, and some diethylhexyl phthalate does remain in adipose tissue with a half-life on the order of months.

'MEHP in blood, ostensibly a product of DEHP hydrolysis by blood esterases, equilibrates between free and albumin-bound forms.' ―Kluwe

'Whether administered by oral or parenteral routes, DEHP and di-n-butyl phthalate (DBP), the two compounds studied most extensively, are rapidly cleared from the body. The bulk of the chemicals is cleared within 24 hr and nearly none is left 3-5 days after exposure; there is little or no evidence of tissue accumulation or prolonged tissue retention.' ―Kluwe

'Phthalate esters with longer chain lengths, however, such as DEHP, must undergo further modification after hydrolysis to the monoester to achieve sufficient polarity for renal excretion.' ―Kluwe

'The ferret, African Green monkey and man form glucuronide conjugates of MEHP, as well, but rats appear to be unable to do so. Recent evidence indicates that hamsters, guinea pigs and mice also excrete glucuronide conjugates of MEHP.' ―Kluwe

'The primate/rat difference in ability to form glucuronide conjugates of MEHP is suggestive of a major species difference in chemical metabolism. Whether or not such a difference renders the rat an unsuitable model of human response to DEHP exposure awaits elucidation of the mechanisms of DEHP toxicity in rats.' ―Kluwe

'The generally rapid clearance and low potential for tissue accumulation of the dialkyl phthalate esters, however, is at least consistent with, if not the cause of, their low toxic potencies in both acute and chronic studies.' ―Kluwe​

Some could actually be burned for energy. The attached lipid chains can become sequentially oxidized eventually forming acetyl groups:

'Following initial oxidation of the terminal (ω) or adjacent (ω − 1) carbon atom in the side chain to an alcohol, aldehydes, ketones and carboxylic acids are formed via successive oxidations. Compounds with long (six or more linear carbons) alkyl chains may undergo β-oxidation and the loss of two-carbon fragments.' ―Kluwe​

This class of plasticizers appears to be relatively safe by comparison to bisphenol A, pesticides, and most other environmental toxins—those that work specifically on cellular targets. Phthalate esters exhibit a nonspecific colligative toxicity at only at very high doses, and the main concern appears to be the amount stored in adipose tissue.

Phthalate esters appear to be an unavoidable consequence of eating cheese. Even in cheese shops that cut sections off of wheels, wrap them in wax paper, and then place them in a paper bag: the 70 pound wheels still often come wrapped in PVC—or polyethylene.

[1] Cocchieri, Renata. "A Research Note Occurrence of Phthalate Esters in Italian Packaged Foods." Journal of Food Protection (1986)
[2] Autian, John. "Toxicity and health threats of phthalate esters: review of the literature." Environmental health perspectives (1973)
[3] Kluwe, William. "Overview of phthalate ester pharmacokinetics in mammalian species." Environmental health perspectives (1982)​

 

[allblues]

Superb, thanks @Travis!

 

[Mito]

I think a few milligrams per day would be beneficial, but there seems to be no practical limit to how much you can take. Children have been given milligrams per day, per kilogram, so I don't think safety is much of a consideration. But since (6S)-5-methyltetrahydrofolate is stereochemically-pure, I think a person could get by using less than the larger doses of racemic folates reported in the published clinical case reports.

Some studies suggest a link between folic acid supplements and prostate cancer. Maybe due the type of folic acid (i.e. not (6S)-5-methyltetrahydrofolate)?

Cancer risk with folic acid supplements: a systematic review and meta-analysis. - PubMed - NCBI

“"........Prostate cancer was the only cancer type found to be increased after folic acid supplementation (meta-analyses of six RCTs).......”

 

[Amazoniac]

The Travis Corner

I was thinking just as a one‐time experiment. I would like to match each neurotransmitter to the thought processes, feelings, and idiosyncracies which characterize them; dopamine, histamine, and serotonin are neurotransmitters that I'd like to get a feel for.

Yesterday, I think the serotonin from the massive amounts of chicken eggs had become melatonin—basicially methylated and acetylated serotonin—despite having been in a well‐lit environment. [Now, I do know exactly what melatonin feels like since I have it in the cabinet, and had taken it twice.] It's rather clownish; I had found myself watching music videos on YouTube from the '80s, but actually enjoying them! [⁉]

I usually hate '80s music, but for some reason David Bowie's Let's Dance, Queen's Under Pressure, and even the Talking Heads' Burning Down the House seemed like good things to watch. But thankfully, I'm feeling much better now.

[And also thankful that it wasn't bad enough to watch this.]

The Fly II (0:52 )
You'll thank me on your next experiment.

 

[TreasureVibe]

Hey @Travis, I would be interested in hearing your views on the following topic and the works of Dr. Pantellini! The full texts of the quotes can be found in the topic and on the Pantellini Foundation website.

Potassium Ascorbate With Ribose For Cancer (With Cell Level Explanation Inside) Possible Treatment

Home - Fondazione Valsè Pantellini

Based on the studies of Dr. Pantellini, we are convinced that oxidative stress damages cell membrane structures, in particular the sodium-potassium ATPase (also known as the Na/K pump). This causes (an initially mild) depolarization and an increasingly greater alteration of the active transport mechanism of these two electrolytes, that have very different but fundamental functions in the cellular organization; potassium is the main regulator of intracellular metabolic processes through reversible salification of amino groups and imino of enzymes and proteins in a slightly acid environment; the other, sodium, is the main regulator of the alkaline reserve of the organism at extracellular level, with reversible salification of carboxylic groups of enzymes and proteins in a more or less basic environment.

In this way we obtain an increasingly bigger modification of the acid-based environment and redox-reactions between cytoplasmic molecules.

We are convinced that this fact constitutes the activating mechanism (trigger) for mutation into a cancerogene cell. In fact, research relating to the sarcoma (malignant tumor) of Rous that was already published in the 30′s (Moraveck and Kishi) proved that the neoplastic cell is lacking potassium and rich of sodium, with an increasingly greater imbalance along with the development of cell degeneration.

This seems to be the common denominator in all neoplastic diseases and is also verifiable through a careful evaluation of the four hematic electrolytes (sodium, calcium, potassium, magnesium) in the blood.

The described mechanism turns out to be very dangerous for the cell when:

• it activates a rapid transfer of calcium from intracellular deposits (mitochondria), that could be responsible for mitogenic activation (i.e. cell duplication);

• it allows a considerable transport of glucose into the cytoplasm (together with sodium, SGLUT symport) with a speed that increases along with the increasingly greater alteration of the sodium/potassium pump (which is the only active control element of the two electrolytes).

These processes lead to a modification in cell respiration, with a decrease of oxidative phosphorylation and a substantial increase of glycolysis. The production of lactic acids, formed by pyruvate reduction, is also increased. Moreover, this pyruvate reduction prevents the start of the S-phase of the mitosis and its steady decrease in the cytoplasm (for the conversion into lactic acid) takes this block on mitosis away, pushing the cell towards uncontrolled proliferation.

So we have a modification of the intracellular pH that tends to become lightly alkaline, and a modification of the cellular respiration with a significant alteration of the Krebs cycle.

These facts together tend to result in an alteration in form and action of proteins and cytoplasmic enzymes, leading to a polymerization of RNA and a transfer of incorrect information between the ‘periphery’ and the ‘operative center’ (DNA). This leads to the mutation of the nuclear DNA and carcinogenesis.

In conclusion, the following hypothesis on which we are working now is that degeneration does not arise from a direct damage in the nuclear DNA, but from a problem in the cytoplasm, which means the damage occurs at the peripherical level (cell membrane). This would actually mean that operation of DNA can be strongly influenced by various components of the same cellular environment as well as by cell-to-cell signals.

From experience and data of Dr. Pantellini first and those of the Foundation now it seems that potassium ascorbate, also and especially in its newest formula with ribose, interferes with this process in a major way; it protects the cell against oxidative stress and inhibits the uncontrolled proliferation mechanism.

Source: Potassium Ascorbate || Information - Fondazione Valsè Pantellini

GIANFRANCESCO VALSÈ PANTELLINI


This is a story about a discovery that occurred by chance, as often happens in physics and science. Science is not only about the great events. It is about being able to be wondered by the small things, that makes a person great.


Dr. Gianfrancesco Valsè Pantellini was born on April 2, 1917 in Ruffina, a small village in Tuscany, where he lived together with his father Italo and his mother Margherita until 1929. Paternal influence (his father was a doctor) and the boy’s curiosity led him on the path of scientific research and he began to devote himself to electrochemical studies together with the pharmacist of the village.
He continues his studies in Florence, first at the La Querce College and later at the private high school Liceo Michelangelo where he obtained his diploma studying 3 years in just 1 academic year. He enrolled at the University of Florence, Faculty of Chemistry in 1936 and took the specialization Bio-organic Chemistry.
Although the war interrupted his studies, he remained active in this field serving as Chemical Official (officer in chemical engineering) at the Genio Guastatori, a department of the Italian army, and worked at various locations such as Udine (north of Italy), Russia and France. In 1943, he meets the famous mathematician Luigi Fantappiè in Rome.


After the war, he resumes his studies in Florence where he graduated in Bio-organic Chemistry in 1947. He then attends the Institute of Theoretical Physics in Naples for a year. During a stay in Paris, he meets physician Louis Kervran and deepens his research on cold fusion in the human body.
After coming back to Florence again, he decides to go to the Autonomous Tumor Center in Ancona (Centro Autonomo Tumori) where he collaborated for more than a year with professors Protti, Gusso and Neubauer. He had his first experiences here following enzymatic research of yeast and their pyroertic action towards the neoplastic cell.


He returned to Florence in 1949 and while he worked for several small pharmaceutical companies, in private he was dedicated to researching tumors. He personally participated in different congresses on Cancerology including those in Florence, Cremona, Baden Baden and New York. Being part of an international research group on cancer that used non-conventional research methods, he was nominated Member of the prestigious New York Academy of Sciences (NYAS) and the International Society for Cryosurgery.


After the disastrous accident at the Chernobyl nuclear power plant in 1986, he offered his help to the people of the ex-Soviet Union that were directly affected by nuclear radiation, creating appropriate outlines (schemes) based on Potassium ascorbate intake. In honor of these efforts, he was awarded a Red Star Medal by the Russian Academy of Sciences in Moscow. The award certificate of honors mentions ‘outstanding achievements in science aimed at the population of de Soviet Union’ (this was in fact in 1987-1988, the period in which Gorbachev was the President of the USSR).


The discovery really happened by accident in 1947. A Florentine goldsmith named Giovanni that Valsè Pantellini was well acquainted with fell ill with stomach cancer. Prof. Valdoni diagnosed him inoperable, indicating he would just have a few months left to live. Suffering from severe stomach pain, Valsè Pantellini advised the goldsmith to take lemon juice with bicarbonate.
Deeply concerned about the health condition of Giovanni, Pantellini goes to visit the man after one year and finds him completely recovered, fit as a fiddle even. Somewhat surprised he asked him what kind of cure he had been taking. Giovanni answered that he simply continued taking lemon juice with bicarbonate as suggested by Pantellini. He then took a closer look at the jar from which Giovanni had been adding with a teaspoon a small amount of bicarbonate into the lemon juice and saw that the jar had an unusual appearance. He turned it around to read the label and noticed that instead of sodium bicarbonate, he had been taking potassium bicarbonate!


The man lived another twenty years and then died because of a heart attack.
‘It was mind-blowing to see this unexpected miracle, which was actually the result of a misunderstanding’, describes Pantellini one day. ‘I made the radiologists double-check because I thought they made a mistake with the X-rays, but no, the results were real. This fact made me think a lot and I began to wonder what had happened’.


He then retrieved the results of an old research done by Moraweck and Kishi in 1932, in which they emphasized a high percentage of potassium inside healthy cells, and a low percentage of potassium in neoplastic tissue and non-neoplastic tissue that carried a malignant tumor. At that moment, Pantellini’s potassium ascorbate ‘adventure’ started.


We have to underline that the first scientific work of Dr. Pantellini was presented and published in the Journal of Medical Pathology not earlier than 1970, more than 22 years after this important encounter. Dr. Pantellini was part of an (unfortunately increasingly rare) array of people that feels the necessity to verify, experiment, prove again and analyze something in depth before talking about it in public. Only when he was reasonably sure of the credibility and reproducibility of his data, he decided to officially present the fruits of his labor.


This work was followed by another study published 4 years later (1974) in the same Journal and then, apart from Andromeda’s ‘last’ publication ‘The co-factor K+, 50 years of research and therapy against tumors’, further publications ceased. To requests for new publications Pantellini’s answer was always the same: ‘I said what I had to say. Now it is up to others to verify it. I cannot lose time writing, I have to work!’, meaning that he would continuously have to answer people addressing him while he just wanted to continue his research and study in order to discover new pathways and insights on the matter.
This is when he came to the intuitive idea of introducing ribose into the compound.


With this website, we would like to honor the moral and professional stature of this extraordinary man and his great contribution to humanity. He was humble and dignified, always respectful towards people and patients in particular.
In order that Pantellini’s work and insights become more and more noted, the Pantellini Foundation will unworthily and undeservingly continue his work, so that more and more people can experiment and verify that what we present is not just nonsense or worse, speculation, but instead represents an important resource for all of us.

Source: Gianfrancesco Valsè Pantellini || Informazioni - Fondazione Valsè Pantellini

Subject to the same condition of the previous experiments I started a new experiment by administering Potassium ascorbate to various cancer patients: each patient was given a dose of 0.90 gr. in two 0.45 gr. dose twice a day, 45 minutes before the main meals. In about 20 days a more or less marked improvement was reported for the first time in almost each pateint. The improvement was characterized by: recovery of strenght and appetite, reduction of pains, increased body weight, normalization of the blood formula. Some patients improved to the point of resuming their normal activities. This improvement lasted a few years for some patients, for others just a few months, then the disease resumed its evolution till the end. This is concisely what was observed both by myself and the doctors assisting me in the course of the experiments. I haven’t prepared any statistic. I can only say that one thing has been definitely ascertained,, i.e. the administration of potassium ascorbate does improve the general condition of a cancer patient.


POTASSIUM ASCORBATE; SUPPOSED TRIGGERING PROCESS

According to a huge bibliography on the matter, K+ Cation is always located inside the cell wall of tissuses and erythrocytes in the form of Potassium protein and hemoglobin. On the contrary NA+ Cation is prevailing in the pericellular fluid and in the serum. Said Cations are physically and chemically similar as they belong to the same group of alkalines, and they appear to be in a mutual equilibruim inside our body thanks to the buffer process. It still remains unknown why K+ Cation is contained inside cell walls (separation interface) and NA+ Cation is outside the walls, while HCO3 3 Ll-,PO - ecc. Run freely both ways without any difficulty. This process is governed by catalysis activity of Carboanydrase. To explain the physical and chemical condition of said cations it would not be sufficient to appeal to the phenomena of osmotic pressure, or of PH, or H pressure (rH), or electrostatic equilibrium, or cell wall potentials. I do believe this phenomenon may be rightly defined only from a chemical point of view, that is to say that thanks to its chemical affinity Potassium does salify hydrogen atoms present in the amino acid groups inside the cells and the erythrocytes; the same cannot be said of Sodium as it has less chemical affinity for said hydrogenated groups, therefore it is shut out. It is thus established that, due to chemical affinity, Sodium truly regulates, both in serum and in pericellular fluids, the alkali reserve whereas Potassium, due to its affinity with the hydrogen groups of amino acids present inside the cell walls, does regulate actively the phenomena of oxide-reducing interchanges of the same, maintaining at a constant level the proteic level needed for an orderly structuring of the complex cell framework. Furthemore, it is actively involved in the oxidation phenomena of the same. The following schematic diagram allows a clear exact look of the this phenomenon.


THE PYRROLIC RING AND ITS IMPORTANCE IN THE LIVING MATTER STRUCTURE: ANALOGIES WITH FURANOSIC AND THIOPHENIC RINGS

The importance of the Pyrrolic ring and its relationship with many fundamental products of the animal and vegetable life is unquestionable. Both the blood hemoglobin and the plant chlorofyll contain pyrrolic rings in their molecule; furthermore many fundamental amino acids are to be considered pyrrole derivatives. It is to be noted that the black pigaments of animals, i.e. skin, hair, moles or bith-marks, ect are in close relationship with pyrrole black spots, which allows the assumption that said pigaments are oxidized compounds and polycondensed compounds having a pyrrolic structure.

A similiar reaction occurs inside the cell during the cellular self-analysis. In lieu of DK hemoglobinate the formation of K proteinate takes place. Pyrrole, thiophene and furan are similar and isologous among themselves and therefore in the formation of their compounds they follow the rule of analogies (Angeli). It is therefore reasonable to assume that during the biological process of protein derivatives from such compounds there may occur chemical and a physiological relationship and that under some particular condition a pyrrolic group may be replaced by a similar thiophenic or furanoid group.

Both potassium hemoglobinate and potassium proteinate, contain structures which can be salified with KNCO3. Now it happens that potassium ascorbate contains in its molecule a furanosic group which by analogy may replace one of the pyrrolic groups of potassium proteinate and hemoglobinate. These groups appear to have been definitely inactivated at the beginning of cancer growth. It is very likely that the starting point of a neoplasia is the peptide molecule containing pyrrolic groups at the RNA level. My assumption is that the opening of the pyrrolic molecule (Ciamician effect) may- in particular physiologic condition - give rise to a triggering of RNA polymerization, this being the beginning of the phase of a neoplasia.

In the tissuses will then appear polymerized monomers which physical tension forces are established (Van der Waals forces). These forces are quite different from the common electrostatic forces. Hence it is of no use to interefere with the growth of neoplasia through chemical substances or drugs capable of generating forces of electrochemical nature, as they will never be able to counter efficaciously the physical forces established among the various polymers of the neoplasia.

CONCLUSION

In view of the above it is my opinion that:
1.-The specific action of potassium ascorbate is due to said cation salified at the ascorbic acid furanosic ring. This group may well be replaced by a analogy of the pyrrolic group believed to be inactivated restoring the structuring phenomena of cellular auto-synthesis to the required physiological normality.
2.-The invariable polymerization energy which is present in the neoplastic phase is interrupted by introducing into the cell the a group formed by potassium ascorbate, thus reestablishing the equilibrium amongst the intermolecular forces of the peptide groups which are present inside the cell membrane.

https://www.curezone.org/upload/PDF/studies_ascorbate.pdf

Hindawi Oxidative Medicine and Cellular Longevity Volume 2017, Article ID 4256519, 12 pages https://doi.org/10.1155/2017/4256519 2017

Concerning ascorbic acid (AA), since the ‘70s, there has been a controversy on its use against cancer. Cameron and Pauling showed that high doses of intravenously injected vitamin C increased 20-fold the average time of survival in advanced cancer patients [28, 29], but this study was denied by other researchers who obtained negative results [30, 31]. This dispute has lasted until recently, when Pauling’s hypothesis was confirmed by a study published in 2015 by Yun et al., who demonstrated that vitamin C (sodium ascorbate) selectively kills KRAS and BRAF mutant colorectal cancer cells [32]. The hypothesized mechanism of action is based on the fact that AA, at concentrations higher than 1 mM, can cause a build-up of hydrogen peroxide (H2O2), which is preferentially toxic toward tumor cells [33]. However, PAR might have more potent and different effects than those elicited by AA, due to the presence of two other components, potassium and ribose, the synergic action of which allows the correction of the hypokalemic condition found in cancer cells [20]. Consistently with the synergic action of individual components, our results revealed that PAR started to be cytotoxic even at the dose of 100 μM in melanoma cells and the cytotoxic response was dose-dependent (100 μM–2 mM). Cell proliferation is not the only altered aspect in cancer. The gap junction proteins, connexins, are important regulators of intercellular communication and cell growth, and mutations or loss of function of gap junctions have been found in a few diseases, including cancer.

Dysregulation of connexin channels has been described to either enhance or suppress tumorigenesis and metastasis. For example, in melanoma, like in other cancers, gap junctions and connexins, specifically Connexin 43, are upregulated in invasive lesions and in cells that disseminate to the lymph nodes [34]. By contrast, a more recent study showed that the increased expression of Connexin 43 in melanoma suppresses cell proliferation and anchorage-independent growth and also reduces the size of melanoma when grown in an ex vivo system [35]. Therefore, the role of connexins in cancer and cancer cell dissemination is highly controversial and apparently difficult to be reconciled. Nevertheless, the bulk of the literature reports a reduced gap junctional communication in many tumor types, as a result of either downregulated expression of connexins or their inability to form functional junctions. In a recent study, Tittarelli et al. reported that Connexin 43 downregulation induced an increased proliferation in four melanoma cell lines, while its overexpression reduced melanoma cell growth in vivo [36]. According to these results, the increase in Connexin 43 expression that we found after PAR treatment in the 2D model was associated to a significant inhibition of cell proliferation and viability.

Such a growth inhibition by PAR was confirmed in the 3D model, where the twodimensional size and volume of spheroids decreased. In addition, the increase in functional gap junctions by 500 μM PAR, that we observed in the 3D structures by using the florescent dye lucifer yellow, was confirmed by the SEM analysis, showing that cells of treated spheroids appeared to be suffering and with abnormal intercellular contacts. In a clinical perspective, this result suggests that the PARinduced increase in tumor compactness could potentially impair the metastatic potential and facilitate cancer mass removal by surgery. We have shown that 2 mM PAR prevented the assembly of the 3D structures; leading to a significant percentage of dead cells in the 2D model, supporting the efficacy of this drug against melanoma cells. This result is extremely important, considering that normal cells are insensitive to 20 mM ascorbate [26]. Taken together, our results show the efficacy of PAR treatments against melanoma cells, according to data from literature where this adjuvant therapy has shown to exhibit beneficial effects in vivo, on precarcinogenic conditions, and in vitro, on tumor cell types different from melanoma cells. The view that PAR could be used as adjuvant compound (alternative to interferon-α) in melanoma therapy is also supported by the fact that it is a nontoxic compound, is easy to administer, has no short-term side effects, and is not expensive.

https://pdfs.semanticscholar.org/698e/9a49fa79e7b4502e6b65ce10fb66b70d8f25.pdf

Feel free to give your comments on it here or in that topic, I am very curious to hear your opinion! Thank you.

 

[Travis]

Some studies suggest a link between folic acid supplements and prostate cancer. Maybe due the type of folic acid (i.e. not (6S)-5-methyltetrahydrofolate)?

Cancer risk with folic acid supplements: a systematic review and meta-analysis. - PubMed - NCBI

“"........Prostate cancer was the only cancer type found to be increased after folic acid supplementation (meta-analyses of six RCTs).......”

This seems plausible on account if its metabolites.

Folic acid, as such, is enzymatically inactive yet its use is justified by its potential to become a proper folate. Folic acid can become fully-active (6S)-folates needed for one-carbon metabolism and dNA synthesis, yet there is a limit as to how much humans can convert at any given time. Pharmacological studies reveal that anything under ~300·μg is completely reduced to dihydro- and tetrahydro-folates, while anything dose above this value leads to detectable plasma concentrations of 'unmetabolized folic acid.'⁽¹⁾

Yet the presence or absence of 'unmetabolized folic acid' in the plasma says nothing about the stereochemistry of those metabolized, or what I like call 'improperly metabolized folic acid.' Carbon #6 of folic acid's pteridine ring is sp² hybridized and thus has no stereogenic center, and the same can be said about dihydrofolate (the once-reduced metabolite). However: upon reduction to tetrahydrofolate, folic acid's #6 carbon will acquire a stereogenic center: It will become either the (6R)-tetrahydrofolate or (6S)-tetrahydrofolate, the latter being the non-methylated mono-γ-glutamated precursor of all enzymatically-active biofolates. The former species on the other hand, (6R)-tetrahydrofolate, is not only inactive but serves to inhibit brain transport of those that are.⁽²⁾ Due to their structural similarity with (6S)-tetrahydrofolates, enzymes requiring them for activity also have affinity for both folic acid and (6R)-folates—which they serve to inhibit. Seen in this way, 'unmetabolized folic acid' and 'improperly metabolized folic acid' are antifolates.

Dihydrofolate reductase is tautologically responsible for reducing dihydrofolate into tetrahydrofolate. Because studies reveal that this enzyme always produces the (6S)-form,⁽³⁾ it had long been assumed that all ingested folic acid is so converted. However, the only study that had actually bothered to determine the stereochemistry of metabolized folic acid had shown this assumption false:⁽⁴⁾

Disregarding the the poor formatting of this chart—the main headers designating the two enantiomers are confusingly-close to the '5-MTHF' subsidiary category—it is apparent that the ingestion of folic acid produces the (6R)-enantiomer. The two subcategories marked simply as '5-MTHF' depict the stereochemical and pharmacokinetic parameters of subjects given racemic 5-methyltetrahydrofolate so those results are expected, yet folic acid's ability to also lead to (6R)-forms is not. Since dihydrofolate reductase produces solely the (6S)-enantiomer you are forced to conclude that: (1) some other enzyme is responsible for producing the (6R)-folate; (2) folic acid is reduced spontaneously in solution, perhaps by a quinone; or (3) the authors had made a technical error. The only other enzyme shown to reduce folates, dihyrobiopterin reductase, would also be expected to produce exclusively (6S)-folates.*

Folic acid has been consistently associated with cognitive decline, however it is difficult to conclusively incriminate it. This proto-vitamin B₉ is commonly found associated with wheat, to which its added, and thus folic acid is associated with gluten exorphin B5 and aluminum (via baking powder). Both the consumption of folic acid and the serological presence of its unmetabolized form are also associated with education. However, I still personally suspect that folic acid and its dextrorotatory isomer are in fact partially responsible for the correlations attributed to to. Any patho-stereoisomeric folates that enter the brain are inhibitory, veritable antifolate drugs, and my personal experience using a commercial B-vitamin cocktail (the NOW™ brand) lends support to this idea.

The Cahn–Ingold rules give the proper stereoisomer as 'S,' corresponding to the 'L' isomer in this case. You will often find biologically-appropriate folates sold as L-5-methyltetrahydrodrofolate, synonymous with (6S)-5-methyltetrahydrodrofolate and (−)-5-methyltetrahydrodrofolate. Although the attached γ-glutamate also has a stereogenic center, you'd have to use one of folate's alternative names—i.e. (6S)-tetrahydropteroyl-L-γ-glutamic acid—to designate the stereochemistry of that.

[1] Kelly, Patrick. "Unmetabolized folic acid in serum: acute studies in subjects consuming fortified food and supplements." The American journal of clinical nutrition (1997)
[2] Xin, Wang. "Differential stereospecificities and affinities of folate receptor isoforms for folate compounds and antifolates." Biochemical pharmacology (1992)
[3] Charlton, Peter. "Stereochemistry of reduction of the vitamin folic acid by dihydrofolate reductase." Journal of the Chemical Society (1985)
[4] Willems, Frank. "Pharmacokinetic study on 5‐methyltetrahydrofolate and folic acid in patients with coronary artery disease." British journal of pharmacology (2004)
[*] Although this enzyme produces (6R)-tetrahydrobiopterins, these are stereochemically equivalent to (6S)-folates. This unintuitive result derives from a peculiarity of Cahn–Ingold rules, the assigning of priority based on the atomic mass of substituents. Although both having the same pteridine core, their respective substituents on the #6 carbon have different priorities. The (6S)-folates and (6R)-biopterins both rotate light in the same direction, and hence both receive the 'L'—or the levorotary—attribution. ​

 

[Travis]

Hey @Travis, I would be interested in hearing your views on the following topic and the works of Dr. Pantellini! The full texts of the quotes can be found in the topic and on the Pantellini Foundation website.

Potassium Ascorbate With Ribose For Cancer (With Cell Level Explanation Inside) Possible Treatment

Home - Fondazione Valsè Pantellini

Feel free to give your comments on it here or in that topic, I am very curious to hear your opinion! Thank you.

Assuming most cancer stems from a departure from natural eating habits, potassium ascorbate would appear beneficial. Humans eat less fruit and plants than other primates and their evolutionary ancestors, lowering both potassium and ascorbate intakes. Even when they do eat fruit and plants, analogous reductions are observed: Consequent of being cooked and salted sauerkraut has a lower vitamin C content and higher Na⁺∶K⁺ ratio than the cabbage used to produce it; similar things can be said about many other modified foods. As a powder having just potassium and ascorbate, potassium ascorbate can be seen as a partial antidote to modern eating practices—an orthomolecular supplement that 'kills two birds with one stone' by delivering two dietary factors most deficient in Americans. I think this would helpful for just about anybody, and even when somewhat redundant—i.e. to salt-free raw fooders—it should still be safe.

 

[TreasureVibe]

Assuming most cancer stems from a departure from natural eating habits, potassium ascorbate would appear beneficial. Humans eat less fruit and plants than other primates and their evolutionary ancestors, lowering both potassium and ascorbate intakes. Even when they do eat fruit and plants, analogous reductions are observed: Consequent of being cooked and salted sauerkraut has a lower vitamin C content and higher Na⁺∶K⁺ ratio than the cabbage used to produce it; similar things can be said about many other modified foods. As a powder having just potassium and ascorbate, potassium ascorbate can be seen as a partial antidote to modern eating practices—an orthomolecular supplement that 'kills two birds with one stone' by delivering two dietary factors most deficient in Americans. I think this would helpful for just about anybody, and even when somewhat redundant—i.e. to salt-free raw fooders—it should still be safe.

Much appreciated Travis! Thank you. Any thoughts on the safety of D-Ribose though? I read that it could potentiate cancer, but also bypass the lactic acid blockade in cancer, and that it enhances ATP production, there is kind of conflicting information about it circulating on the internet.

 

[Travis]

Much appreciated Travis! Thank you. Any thoughts on the safety of D-Ribose though? I read that it could potentiate cancer, but also bypass the lactic acid blockade in cancer, and that it enhances ATP production, there is kind of conflicting information about it circulating on the internet.

It seems a dangerous thing to use off-hand because ribose is used to make dNA. The fact that strategies which serve to slow dNA synthesis through reducing polyamine synthesis—i.e. methionine restriction, selenomethionine supplementation, methylglyoxal-bis-guanidine—work so well you'd almost have to assume that inhibiting dNA synthesis would be indicated for cancer. This is not to say the use of chain terminators like 5-fluorouracil should be used, only that the logic behind their development was understandable. Ornithine decarboxylase inhibitors are different because inhibiting polyamines has the effect of merely slowing dNA synthesis of housekeeping genes only, not globally-terminating the polymerization of all nucleic acids.

Perhaps it does work, in some unrelated way...

 

[TreasureVibe]

It seems a dangerous thing to use off-hand because ribose is used to make dNA. The fact that strategies which serve to slow dNA synthesis through reducing polyamine synthesis—i.e. methionine restriction, selenomethionine supplementation, methylglyoxal-bis-guanidine—work so well you'd almost have to assume that inhibiting dNA synthesis would be indicated for cancer. This is not to say the use of chain terminators like 5-fluorouracil should be used, only that the logic behind their development was understandable. Ornithine decarboxylase inhibitors are different because inhibiting polyamines has the effect of merely slowing dNA synthesis of housekeeping genes only, not globally-terminating the polymerization of all nucleic acids.

Perhaps it does work, in some unrelated way...

Hmm very interesting, thank you!

 

[Obi-wan]

I think I will try Potassium Ascorbate by itself for now

 

[Amazoniac]

I used to eat just that: raw goat cheddar wrapped in polyethylene.

Of the class of plasticizers bisphenol A has gotten the most publicity, yet since this is exclusive to polycarbonates it can be ignored. Of concern in the case of cheese are phthalates, perhaps being leeched from the polyvinylchloride or polythylene packaging. On warm days, goat cheese will 'sweat' or exude a liquid oil and it' seem reasonable to suppose that this—caproic acid fatty acid trigylcerides—would make a suitable phthalate solvent. ['Phthalate' is actually my favorite nine-letter word having four consecutive consonants!]

View attachment 9535 ​

Phthalates are benzenedicarboxylic acids. The butyl and ethylhexyl esters of ortho-pthalic acid are the most commonly used PVC plasticizers. Toxicological interest in ortho-pthalic acid esters had begun in 1970 with the finding of diethylhexyl phthalate in the organs of patients previously intubated with PVC tubing.

View attachment 9536​

Pthalic acid esters appear to have a low acute toxicity and little carcinogenic potential. Dibutyl phthalate appears to be more toxic that diethylhexyl phthalate, yet is still a relatively safe molecule.

'These plasticizers give the polymer the desired flexibility and softness and may account for up to 40% of the final weight of the material. They are not chemically bound to the polymer, but dispersed in the matrix of the polymer chains...' ―Autian

'Diethylhexyl phthalate (DEHP) has an extremely low order of acute toxicity. The LD₅₀ values in several species of animals indicate that extremely large doses. Fourteen to greater than 50 g/kg of the compound are necessary to produce lethal effects. In fact, this agent would be classified as "practically nontoxic" by the toxicity rating system of Gleason et al.' ―Autian

'Rats fed diets containing 0.01, 0.05, and 0.25% dibutyl phthalate showed no toxic reactions after 1 yr. Of those fed 1.25%, half died during the first week of the experiment, but those which survived grew normally,' ―Autian​

Diethylhexyl phthalate is readily absorbed. Most of the diethylhexyl phthalates that enter the body are transformed into their corresponding monoethylhexyl esters by uncharacterized enzymes distributed ubiquitously (i.e. ghost enzymes). Cleavage of both alkyl esters rarely occurs, yielding phthalate, although this does occur in the liver with phthalates having shorter alkyl substituents (i.e. dimethylphthalate). Elimination is quick, and the monoethylhexyl form appears in the urine either conjugated with glucose or unchanged. This efficient detoxification process is not complete, however, and some diethylhexyl phthalate does remain in adipose tissue with a half-life on the order of months.

'MEHP in blood, ostensibly a product of DEHP hydrolysis by blood esterases, equilibrates between free and albumin-bound forms.' ―Kluwe

'Whether administered by oral or parenteral routes, DEHP and di-n-butyl phthalate (DBP), the two compounds studied most extensively, are rapidly cleared from the body. The bulk of the chemicals is cleared within 24 hr and nearly none is left 3-5 days after exposure; there is little or no evidence of tissue accumulation or prolonged tissue retention.' ―Kluwe

'Phthalate esters with longer chain lengths, however, such as DEHP, must undergo further modification after hydrolysis to the monoester to achieve sufficient polarity for renal excretion.' ―Kluwe

'The ferret, African Green monkey and man form glucuronide conjugates of MEHP, as well, but rats appear to be unable to do so. Recent evidence indicates that hamsters, guinea pigs and mice also excrete glucuronide conjugates of MEHP.' ―Kluwe

'The primate/rat difference in ability to form glucuronide conjugates of MEHP is suggestive of a major species difference in chemical metabolism. Whether or not such a difference renders the rat an unsuitable model of human response to DEHP exposure awaits elucidation of the mechanisms of DEHP toxicity in rats.' ―Kluwe

'The generally rapid clearance and low potential for tissue accumulation of the dialkyl phthalate esters, however, is at least consistent with, if not the cause of, their low toxic potencies in both acute and chronic studies.' ―Kluwe​

Some could actually be burned for energy. The attached lipid chains can become sequentially oxidized eventually forming acetyl groups:

'Following initial oxidation of the terminal (ω) or adjacent (ω − 1) carbon atom in the side chain to an alcohol, aldehydes, ketones and carboxylic acids are formed via successive oxidations. Compounds with long (six or more linear carbons) alkyl chains may undergo β-oxidation and the loss of two-carbon fragments.' ―Kluwe​

This class of plasticizers appears to be relatively safe by comparison to bisphenol A, pesticides, and most other environmental toxins—those that work specifically on cellular targets. Phthalate esters exhibit a nonspecific colligative toxicity at only at very high doses, and the main concern appears to be the amount stored in adipose tissue.

Phthalate esters appear to be an unavoidable consequence of eating cheese. Even in cheese shops that cut sections off of wheels, wrap them in wax paper, and then place them in a paper bag: the 70 pound wheels still often come wrapped in PVC—or polyethylene.

[1] Cocchieri, Renata. "A Research Note Occurrence of Phthalate Esters in Italian Packaged Foods." Journal of Food Protection (1986)
[2] Autian, John. "Toxicity and health threats of phthalate esters: review of the literature." Environmental health perspectives (1973)
[3] Kluwe, William. "Overview of phthalate ester pharmacokinetics in mammalian species." Environmental health perspectives (1982)​

Semi-god, it reminded me of these:
Estrogenic chemicals often leach from BPA-free plastic products that are replacements for BPA-containing polycarbonate products (!)
https://ehp.niehs.nih.gov/1003220/

They're actually getting paid to publish that, but if their interest is in prooving that disruptive chemicals do leach, then the consumer can benefit from this.

The ‘safer' plastics designed to replace BPA may be just as bad for you

Companies like Vitamix, Blendtec, Ninja, Oster and many others use Tritan cups for their products.

 

[Travis]

Semi-god, it reminded me of these:
Estrogenic chemicals often leach from BPA-free plastic products that are replacements for BPA-containing polycarbonate products (!)
https://ehp.niehs.nih.gov/1003220/

They're actually getting paid to publish that, but if their interest is in prooving that disruptive chemicals do leach, then the consumer can benefit from this.

The ‘safer' plastics designed to replace BPA may be just as bad for you

Companies like Vitamix, Blendtec, Ninja, Oster and many others use Tritan cups for their products.

Living in a world post-Dow and post-IG Farben, we now all have to pay the piper for living on this planet. While good to buy liquids glass-bottled and to eat whole foods—that are not wrapped in anything besides a halo of glory—some plasti-wrapped products are quite difficult to resist.

Coconuts have a good fatty acid profile and don't need protective packaging, unless . . . DDT will lead to thin-shelled coconuts:

'The insidious aspect of this phenomenon is that large concentrations of chlorinated hydrocarbons do not usually kill the bird outright. Rather, DDT and its relatives alter the bird's calcium metabolism in a way that results in thin eggshells. Instead of eggs, heavily DDT-infested Brown Pelicans and Bald Eagles tend to find omelets in their nests, since the eggshells are unable to support the weight of the incubating bird.

Shell-thinning resulted in the decimation of the Brown Pelican populations in much of North America and the extermination the Peregrine Falcon in the eastern United States and southeastern Canada. Shell-thinning caused lesser declines in populations of Golden and Bald Eagles and White Pelicans, among others. Similar declines took place in the British Isles. Fortunately, the cause of the breeding failures was identified in time, and the use of DDT was banned almost totally in the United States in 1972.' ―DDT and Birds​

I feel that I'm fairly low in plasticizers because I eat essentially all whole foods not wrapped in anything. I make coffee with a steel & glass French press, and I only rarely drink water from a plastic bottle.

 

[Travis]

I just have just received my second bottle of (6S)-5-methyltetrahydrofolate in the mail. These are 1000·μg capsules, an improvement over the now-gone 400·μg dose of last week. After consuming a little cow's cheese a few weeks ago, representing the first time in about 6 months, I am suspecting antifolate antibodies. Autoantibody neogenesis is just like that of any other antibody, and the plasma half life being on the order of months. Below is a graph of antibody titer decay rates raised against the pertussis antigen:

But this is somewhat artificial as aluminum adjuvants adsorb the antigen (or actually encase it, as was done historically through alum precipitation), representing a time-release antigen depot. It is not easy to find such data on antibodies acquired naturally from food, yet below is one on maternally-acquired antimeasles antibodies:

This represents is a more optimistic picture, and could even be more realistic. It is difficult to even get a theoretical answer to food-acquired decay rates because articles on B cell memory draw so heavily upon those assayed post-vaccine, which are designed to prolong antibody formation by associating the antigens with an insoluble compound—usually aluminum phosphate or aluminum oxide hydroxide [sic]. This guarantees that the antigen is not cleared from the body as quickly and would be somewhat akin to a celiac completely ignoring those 'this product had been manufactured in facility manufacturing gluten-based products' warning label and thus eating trace amounts of gluten every day. Low dose antigen can prolong the antibody response, a phenomenon that forms the core principal of immunological adjuvants. This is also used to justify injecting people with aluminum nanoparticles shown to travel to the brain.

 

[squanch]

I used to eat just that: raw goat cheddar wrapped in polyethylene.

Of the class of plasticizers bisphenol A has gotten the most publicity, yet since this is exclusive to polycarbonates it can be ignored. Of concern in the case of cheese are phthalates, perhaps being leeched from the polyvinylchloride or polythylene packaging. On warm days, goat cheese will 'sweat' or exude a liquid oil and it' seem reasonable to suppose that this—caproic acid fatty acid trigylcerides—would make a suitable phthalate solvent. ['Phthalate' is actually my favorite nine-letter word having four consecutive consonants!]

View attachment 9535 ​

Phthalates are benzenedicarboxylic acids. The butyl and ethylhexyl esters of ortho-pthalic acid are the most commonly used PVC plasticizers. Toxicological interest in ortho-pthalic acid esters had begun in 1970 with the finding of diethylhexyl phthalate in the organs of patients previously intubated with PVC tubing.

View attachment 9536​

Pthalic acid esters appear to have a low acute toxicity and little carcinogenic potential. Dibutyl phthalate appears to be more toxic that diethylhexyl phthalate, yet is still a relatively safe molecule.

'These plasticizers give the polymer the desired flexibility and softness and may account for up to 40% of the final weight of the material. They are not chemically bound to the polymer, but dispersed in the matrix of the polymer chains...' ―Autian

'Diethylhexyl phthalate (DEHP) has an extremely low order of acute toxicity. The LD₅₀ values in several species of animals indicate that extremely large doses. Fourteen to greater than 50 g/kg of the compound are necessary to produce lethal effects. In fact, this agent would be classified as "practically nontoxic" by the toxicity rating system of Gleason et al.' ―Autian

'Rats fed diets containing 0.01, 0.05, and 0.25% dibutyl phthalate showed no toxic reactions after 1 yr. Of those fed 1.25%, half died during the first week of the experiment, but those which survived grew normally,' ―Autian​

Diethylhexyl phthalate is readily absorbed. Most of the diethylhexyl phthalates that enter the body are transformed into their corresponding monoethylhexyl esters by uncharacterized enzymes distributed ubiquitously (i.e. ghost enzymes). Cleavage of both alkyl esters rarely occurs, yielding phthalate, although this does occur in the liver with phthalates having shorter alkyl substituents (i.e. dimethylphthalate). Elimination is quick, and the monoethylhexyl form appears in the urine either conjugated with glucose or unchanged. This efficient detoxification process is not complete, however, and some diethylhexyl phthalate does remain in adipose tissue with a half-life on the order of months.

'MEHP in blood, ostensibly a product of DEHP hydrolysis by blood esterases, equilibrates between free and albumin-bound forms.' ―Kluwe

'Whether administered by oral or parenteral routes, DEHP and di-n-butyl phthalate (DBP), the two compounds studied most extensively, are rapidly cleared from the body. The bulk of the chemicals is cleared within 24 hr and nearly none is left 3-5 days after exposure; there is little or no evidence of tissue accumulation or prolonged tissue retention.' ―Kluwe

'Phthalate esters with longer chain lengths, however, such as DEHP, must undergo further modification after hydrolysis to the monoester to achieve sufficient polarity for renal excretion.' ―Kluwe

'The ferret, African Green monkey and man form glucuronide conjugates of MEHP, as well, but rats appear to be unable to do so. Recent evidence indicates that hamsters, guinea pigs and mice also excrete glucuronide conjugates of MEHP.' ―Kluwe

'The primate/rat difference in ability to form glucuronide conjugates of MEHP is suggestive of a major species difference in chemical metabolism. Whether or not such a difference renders the rat an unsuitable model of human response to DEHP exposure awaits elucidation of the mechanisms of DEHP toxicity in rats.' ―Kluwe

'The generally rapid clearance and low potential for tissue accumulation of the dialkyl phthalate esters, however, is at least consistent with, if not the cause of, their low toxic potencies in both acute and chronic studies.' ―Kluwe​

Some could actually be burned for energy. The attached lipid chains can become sequentially oxidized eventually forming acetyl groups:

'Following initial oxidation of the terminal (ω) or adjacent (ω − 1) carbon atom in the side chain to an alcohol, aldehydes, ketones and carboxylic acids are formed via successive oxidations. Compounds with long (six or more linear carbons) alkyl chains may undergo β-oxidation and the loss of two-carbon fragments.' ―Kluwe​

This class of plasticizers appears to be relatively safe by comparison to bisphenol A, pesticides, and most other environmental toxins—those that work specifically on cellular targets. Phthalate esters exhibit a nonspecific colligative toxicity at only at very high doses, and the main concern appears to be the amount stored in adipose tissue.

Phthalate esters appear to be an unavoidable consequence of eating cheese. Even in cheese shops that cut sections off of wheels, wrap them in wax paper, and then place them in a paper bag: the 70 pound wheels still often come wrapped in PVC—or polyethylene.

[1] Cocchieri, Renata. "A Research Note Occurrence of Phthalate Esters in Italian Packaged Foods." Journal of Food Protection (1986)
[2] Autian, John. "Toxicity and health threats of phthalate esters: review of the literature." Environmental health perspectives (1973)
[3] Kluwe, William. "Overview of phthalate ester pharmacokinetics in mammalian species." Environmental health perspectives (1982)​

This wouldn't really be relevant to PE or PP food packaging though, would it?
As far as I know there aren't any plasticizers added to PE or PP because they are already very ductile without it.

What would realistically be the danger of PE or PP? Impurities/residue from the manufacturing process?