Amazoniac
Member
On phytanic acid (again) since it was mentioned recently.
It's a metabolite from the side chain of the chlorophyll molecule.
- Phytanic acid consumption and human health, risks, benefits and future trends: A review
It occurs in large amounts (relative to poisonoids) in some foods such as butter.
- Diet and Refsum's disease. The determination of phytanic acid and phytol in certain foods and the application of this knowledge to the choice of suitable convenience foods for patients with Refsum's disease
You must have noticed on the first images that it's metabolized in a similar way as poisonol, their structure has commonalities as well. This leads us to another publication shared by professor (from prophecy?) Garrett:
- Prevention of Vitamin A Teratogenesis by Phytol or Phytanic Acid Results from Reduced Metabolism of Retinol to the Teratogenic Metabolite, All-trans-retinoic Acid
Note:
"[..]ligand binding to the RXR is not a prerequisite for the formation of RAR-RXR heterodimers[.]"
Why he leaves these details out and continues to neglect RARs?
But in reading the publication, at first the antagonism makes sense, however (as usual) there's no further questioning. The doses of poisonoids used were pharmacological, if the competition was proportional, butter wouldn't be a source of these toxins and have a detectable impact. For some reason this is ignored when claiming that casein has hidden poisonoic acid, why the same protective principle wouldn't apply here since it could contain substantial amounts of these acids?
Those levels were evaluated after dosing, when the body is still metabolizing them, however their behavior after the digestive period passes matters.. and so do the affinities.
- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity
Check out the ranges for each. These numbers are consistent with what the charlatan had posted:
- Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study (subjects tracked for butter and cheese consumption)
He's claiming that it's good because it stems from competition with 9-cis poisonoic acid, which is a metabolite that's not even considered the main ligand candidate anymore. And as they commented above, in extreme levels, issues don't suggest that it's from an interaction with RXR. The guy is spreading confusion on multiple layers.
- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults
It's a metabolite from the side chain of the chlorophyll molecule.
- Phytanic acid consumption and human health, risks, benefits and future trends: A review
It occurs in large amounts (relative to poisonoids) in some foods such as butter.
- Diet and Refsum's disease. The determination of phytanic acid and phytol in certain foods and the application of this knowledge to the choice of suitable convenience foods for patients with Refsum's disease
You must have noticed on the first images that it's metabolized in a similar way as poisonol, their structure has commonalities as well. This leads us to another publication shared by professor (from prophecy?) Garrett:
- Prevention of Vitamin A Teratogenesis by Phytol or Phytanic Acid Results from Reduced Metabolism of Retinol to the Teratogenic Metabolite, All-trans-retinoic Acid
Note:
"[..]ligand binding to the RXR is not a prerequisite for the formation of RAR-RXR heterodimers[.]"
Why he leaves these details out and continues to neglect RARs?
But in reading the publication, at first the antagonism makes sense, however (as usual) there's no further questioning. The doses of poisonoids used were pharmacological, if the competition was proportional, butter wouldn't be a source of these toxins and have a detectable impact. For some reason this is ignored when claiming that casein has hidden poisonoic acid, why the same protective principle wouldn't apply here since it could contain substantial amounts of these acids?
Those levels were evaluated after dosing, when the body is still metabolizing them, however their behavior after the digestive period passes matters.. and so do the affinities.
- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity
"As an important metabolite of chlorophyll, phytanic acid can be produced in ruminating animals by their rumen bacteria. Humans do not efficiently absorb chlorophyll and cannot metabolize it; thus, levels of phytanic acid in the human body are entirely dependent on meat and milk products ingested in the diet. Consequently, phytanic acid cannot be considered as an endogenous ligand in humans, but may potentially act as such in ruminants. Furthermore, its low levels in human questions the physiological relevance of its activities as a nutritional RXR ligand. Thus, in human plasma phytanic acid concentrations ranged around 1.6 μM, which was highly dependent on dietary habits of healthy volunteers, with the highest level (5.8 μM) found in meat eaters and the lowest in vegans (0.9 μM) (Al-Dirbashi et al., 2008; Allen et al., 2008). Phytanic acid levels ranged around 1 μM in mouse plasma, but were approximatively 10-100 times lower in different tissues (Wanders et al., 2011). Such quantities were increased to 10 μM levels under supplementation with high amounts of phytol, a phytanic acid precursor (Wanders et al., 2011). Importantly, disruption of phytanol-CoA hydroxylase, the first enzyme in the α-oxidation in Refsum disease, leads to high accumulations of phytanic acid, which may reach up to 1000 times the level of a healthy person (Verhoeven and Jakobs, 2001), with highest levels found in the liver, heart, adipose and peripheral nervous tissues, and much lower in the brain (Cumings, 1971). Despite the wide range of symptoms, including peripheral neuropathy, retinal degeneration and cerebellar ataxia (see (Verhoeven and Jakobs, 2001) and references therein), no abnormalities relevant to general or even exacerbated RXR signaling were reported like, for instance, decreased thyroid hormone T4 levels, elevated triglyceride levels or reduced food intake. This further questions the relevance of phytanic acid and potential phytanic acid metabolites as RXR ligands."
Check out the ranges for each. These numbers are consistent with what the charlatan had posted:
- Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study (subjects tracked for butter and cheese consumption)
He's claiming that it's good because it stems from competition with 9-cis poisonoic acid, which is a metabolite that's not even considered the main ligand candidate anymore. And as they commented above, in extreme levels, issues don't suggest that it's from an interaction with RXR. The guy is spreading confusion on multiple layers.
- Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults
"Peroxisomes play an important role in the catabolism of hydrogen peroxide, as well as in the shortening of very long fatty acids (which cannot undergo a direct mitochondrial β-oxidation catabolism) and α-oxidation (49). In the latter process, the TPP-dependent enzyme 2-hydroxyacyl-CoA lyase 1 (HACL1) catalyzes the cleavage of 3-methyl-branched and straight chain 2-hydroxy long-chain fatty acids (50). Phytanic acid (a 3-methyl-substituted, 20-carbon branched-chain fatty acid), unlike most fatty acids, is unable to undergo β-oxidation because of an existing methyl group in the 3-position (51). As such, it is broken down by HACL1 by an initial α-oxidation (52, 53). This branched-chain fatty acid is obtained through the diet, specifically from dairy products and red meat. The disruption of phytanic acid catabolism, due to inadequate levels of TPP, leads to triglyceride accumulation, which may cause deleterious effects such as cerebellar ataxia, peripheral polyneuropathy, vision and hearing loss, anosmia, and, in some instances, cardiac dysfunction and epiphyseal dysplasia (54). The symptoms caused by thiamine deficiency are shared by Refsum’s disease, which is caused by pathogenic mutations in HACL1 (55). Some of the symptoms are also observed in the autosomal recessive systemic disorder Zellweger syndrome and other peroxisomal-related diseases including the neonatal adrenoleukodystrophy. Zellweger syndrome is caused by pathogenic mutations in the pexin genes, which encode for proteins essential for the assembly of functional peroxisomes. It is characterized by deficits in the peroxisomal fatty acid oxidation pathway causing severe neurological and liver dysfunction as well as craniofacial abnormalities."
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