Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[Spondive]

This is from Wikispooks.. the CIA misdirection arm itself, but the devil always mixes lies with the truth

TreatmentEdit

• Stopping high Vitamin A intake is the standard treatment. Most people fully recover.[1]
• Phosphatidylcholine (in the form of PPC or DLPC), the substrate for Lecithin retinol acyltransferase, which converts retinol into Retinyl esters (the storage forms of vitamin A).
• Vitamin E may alleviate hypervitaminosis A.[32]
• Liver transplantation may be a valid option if no improvement occurs.[33]

If liver damage has progressed into fibrosis, synthesizing capacity is compromised and supplementation can replenish PC. However, recovery is dependent on removing the causative agent: halting high Vitamin A intake.[34][35][36][37]


HistoryEdit
Vitamin A toxicity is known to be an ancient phenomenon; fossilized skeletal remains of early humans suggest bone abnormalities may have been caused by hypervitaminosis A.[20]

Vitamin A toxicity has long been known to the Inuit and has been known by Europeans since at least 1597 when Gerrit de Veer wrote in his diary that, while taking refuge in the winter in Nova Zemlya, he and his men became severely ill after eating polar bear liver.[38]

In 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned (and Mertz died) from eating the livers of their sled dogs during the Far Eastern Party.[39] Another study suggests, however, that exhaustion and diet change are more likely to have caused the tragedy.[40]


Other animalsEdit
Some Arctic animals demonstrate no signs of hypervitaminosis A despite having 10–20 times the level of vitamin A in their livers as other Arctic animals. These animals are top predators and include the polar bear, Arctic fox, bearded seal, and glaucous gull. This ability to efficiently store higher amounts of vitamin A may have contributed to their survival in the extreme environment of the Arctic.[41]

TreatmentEdit
These treatments have been used to help treat or manage toxicity in animals. Although not considered part of standard treatment, they might be of some benefit to humans.

• Vitamin E appears to be an effective treatment in rabbits,[42] prevents side effects in chicks[43]
• Taurine significantly reduces toxic effects in rats.[44] Retinoids can be conjugated by taurine and other substances. Significant amounts of retinotaurine are excreted in the bile,[45] and this retinol conjugate is thought to be an excretory form, as it has little biological activity.[46]
• Cholestin – significantly reduces toxic effects in rats.[47]
• Vitamin K prevents hypoprothrombinemia in rats and can sometimes control the increase in plasma/cell ratios of vitamin A.[48]

 

[Lynne]

What symptoms do you get from tryptophan?

Yeah @Cirion , I'd also be interested to know. Is it serotonin syndrome kinda symptoms? Are you sensitive to tyramine and Mao inhibiting foods too? I seem to be.

 

[Amazoniac]

- Carotenoids - Volume 5: Nutrition and Health (978-3-7643-7500-3)

"A question that frequently arises is whether any effect attributed to a carotenoid is in fact due to a metabolite/breakdown product rather than to the intact carotenoid itself[.] For any carotenoid, there are many products, as complex mixtures. Any one, or combination, could have some biological activity. The roles of vitamin A and retinoic acid are well known but evidence is accumulating to suggest that other non-retinoid breakdown products may be biologically active. Some possibilities that have been suggested are:

1. β-Carotene cleavage products of different chain length or cleavage products of other carotenoids, bearing structural features (end group or chain) in common with retinoids, could act as retinoid agonists or antagonists.
2. Many carotenoid oxidation products have reactive α,β-unsaturated aldehyde structures. By binding to side-chain amino groups or, for dialdehydes, cross-linking, these could modify properties and activity of enzymes or other proteins.
3. The biological activity of many compounds is based on size, shape and position of functional groups. Although otherwise structurally unrelated, a carotenoid breakdown product could have the right topography to mimic some other molecule, e.g. vitamin D, hormones, and act as an agonist or antagonist."

"Although it is clear that carotenoids can serve as antioxidants in vitro, there is no unequivocal evidence for their functioning in this way in vivo. Indeed, carotenoid concentrations are low compared to those of recognized antioxidants such as vitamins C and E, so activity as a general antioxidant seems unlikely, but some specialized action in a particular sub-cellular environment such as a membrane, or in particular tissues, cannot be ruled out. All aspects must be considered. It is suggested, for example, that protection of LDL by lycopene as an antioxidant may be a factor in reducing risk of CHD. If this is looked at carefully, calculations show that, on average, there is only about one carotenoid molecule per four LDL particles. This does not seem compatible with a major antioxidant rôle."​

- Vitamin A signaling and homeostasis in obesity, diabetes, and metabolic disorders (it's almost a book authored by just one guy)

"Until recently, it had been thought that most or all of retinoic acid actions in the body could be explained by its actions in the nucleus (Chambon, 1996; Gudas, 2011; Al Tanoury et al., 2013). However, recent work has suggested a role for retinoic acid outside of the nucleus, where retinoic acid acts in a non-genomic manner (Al Tanoury et al., 2013; Rochette-Egly, 2015; Park et al., 2018). These non-genomic actions are proposed to involve a number of different processes including ones involving RARs located outside of the nucleus and cellular retinoic acid-binding protein, type 1 (CRABP1). The non-genomic actions of retinoic acid are considered in greater detail in reviews by Rochette-Egly and colleagues (Al Tanoury et al., 2013; Rochette- Egly, 2015)."

"Since the discovery and first description of RBP4 in the late 1960s, the sole function of RBP4 in the body had been thought to be the mobilization of retinol from vitamin A stores and deliver it to target tissues requiring vitamin A actions (Kanai et al., 1968; Soprano & Blaner, 1994). However, Kahn and colleagues reported studies that allowed them to suggest that RBP4 synthesized in adipose tissue acts as a signal that lessens insulin responsiveness in the body (Yang et al., 2005; Graham et al., 2006)."

"It is important to note that HSCs, which play the central role in the storage of vitamin A in the body, are also a central cell type involved in the development of hepatic disease (Tsuchida & Friedman, 2017). Hepatic injury activates HSCs resulting in the acquisition of a proliferative myofibroblast-like phenotype. HSC activation is accompanied by a complete loss of the vitamin A-containing HSC lipid droplets and greatly increased HSC production of extracellular matrix. Thus, HSCs not only store the majority of vitamin A that is present in the body but they also are centrally involved in the development of hepatic fibrosis, cirrhosis and hepatocellular carcinoma."

"Although the hepatocyte is the cellular site where most postprandial vitamin A is cleared from the circulation (Cooper, 1992; Abumrad & Davidson, 2012), during chylomicron remodeling in the circulation, some chylomicron retinyl ester is hydrolyzed by LpL. This results in the product retinol being taken up by extrahepatic tissues where LpL is expressed, especially adipose tissue (Blaner et al., 1994; van Bennekum et al., 1999). This LpL-dependent process confers to adipose tissue, a key organ contributing to metabolic disease development, a role in vitamin A storage and metabolism."

"Adipose tissue accumulates both retinol and retinyl esters (Tsutsumi et al., 1992)."

"As discussed earlier in the text, vitamin A is required for mediating many physiologically important processes in the body, involving multiple genes and signal transduction pathways. Moreover, some of the processes for metabolism and storage of vitamin A overlap with lipid-related parameters (related to cholesterol and triglyceride metabolism) that when dysregulated contribute to disease progression. Consequently, it is not too surprising that the literature has implicated vitamin A and/or vitamin A-related parameters (vitamin A-binding proteins and enzymes involved in vitamin A metabolism) to have a role, or actually multiple different roles, in metabolic disease development. However, at present, there is little consensus in this literature regarding how vitamin A causes or prevents metabolic disease development. In fact, much of this literature is controversial and/or contradictory."

"The literature is convincing that impairments in vitamin A signaling and metabolism can contribute to nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH), as well as later stage liver disease (fibrosis, cirrhosis, and hepatocellular carcinoma (HCC)). But the underlying mechanisms responsible for this remain to be completely established."

"Since both hepatocytes and HSCs play key roles in hepatic vitamin A metabolism and storage, it should be noted that the early stages of liver disease usually involve insults to hepatocytes (Tsuchida & Friedman, 2017). This is true for both NASH and viral infection. Mediators released by injured hepatocytes promote HSC activation facilitating later stage hepatic disease."

"Human observational studies exploring relationships between serum/plasma RBP4 and NAFLD occurrence are largely in agreement with the conclusion that serum/plasma RBP4 levels are elevated in patients with NAFLD. A representative sample of, but not all correlative studies, include ones involving patients with type II diabetes (Wu et al., 2008), obese children (Romanowska et al., 2011), healthy 6- to 12-year-old children (Huang & Yang, 2013), subjects diagnosed with NAFLD but not type II diabetes (Yan et al., 2013), obese and lean patients diagnosed with NAFLD (Zwolak et al., 2016), postmenopausal women diagnosed with NALFD (Cai et al., 2018) and a community-based cross-sectional study involving 2938 participants 40-70-year-olds (Chen et al., 2017). Each of these studies reported significantly elevated serum/plasma RBP4 concentrations for patients with NAFLD but provided little insight into possible cause/effect relationships."

"The older literature reports that some proteins can become post-translationally modified through the covalent addition of a retinoic acid molecule to the protein, see [(Brun et al., 2013)] for review. This process is referred to as protein retinoylation."

"A recent publication from Yang et (2018) reports very rigorous investigations that led these authors to conclude that ALDH1A1 functions within adipose tissue to modulate adipogenesis and adipocyte differentiation through mechanisms that are independent of both retinaldehyde and retinoic acid."

"Retinol saturase (RetSat), which catalyzes the conversion of all-trans-retinol to all-trans-13,14-dihydroretinol, saturating the 13-14 double bond of all-trans-retinol, has also been implicated as having a role in adipogenesis (Moise et al., 2004). RetSat is expressed in many tissues and all-trans-13,14-dihydroretinol is found in these tissue (Moise et al., 2004). Interestingly, Rühl et al. (2015) have suggested that RetSat may have a role in generating 13,14- dihydroretinols that are precursors needed for 9-cis-13,14-dihydroretinoic acid synthesis." "A number of published studies establish a role for RetSat in promoting adipogenesis (Schupp et al., 2009; Moise et al., 2010; Pang et al., 2017)."

"Some APL [Acute Promyelocyric Leukaemia] patients receiving [an] effective therapeutic dose develop a potentially fatal syndrome referred to as “Retinoic Acid Syndrome” or more recently as “Differentiation Syndrome” (Montesinos & Sanz, 2011). Amongst the many adverse symptoms associated with this dose of all-trans-retinoic acid are elevated blood cholesterol and/or triglyceride levels (up to 60% of patients) and weight gain (23% of patients) ((Agadir & Chomienne, 1999; Fenaux et al., 1999). Moreover, excessive weight gain is considered to be one of the symptoms that might be indicative of onset of Differentiation Syndrome (Fenaux et al., 1999; Montesinos & Sanz, 2011). Similarly, the usage of 13-cis-retinoic acid (a naturally occurring form of vitamin A (Kane et al., 2008b)) in clinical dermatology has established that administration of large doses of this naturally occurring retinoic acid form can result in a high risk of hyperlipidemia and other components of the metabolic syndrome in treated patients, including increased fat accumulation in adipose tissue (Rodondi et al., 2002)."

"Until 2005, the sole known function for RBP4 was to mobilize retinol from tissue stores and deliver it to vitamin A-responsive cells where it can be converted to retinoic acid for use in regulating vitamin Adependent transcription and functions. In 2005, Kahn and colleagues reported that circulating RBP4 levels affect glucose clearance, with high RBP4 levels inducing insulin resistance (Yang et al., 2005; Graham et al., 2006). Specifically, Kahn and colleagues proposed that adipocyte-derived RBP4 is a signal that contributes to the pathogenesis of type 2 diabetes, linking obesity with type 2 diabetes, as well as other obesity-related metabolic diseases."

"Working with mice that fail to express the glucose transporter GLUT4 in adipose tissue, Kahn and colleagues showed that that RbP4 expression was elevated in adipocyte-specific male Glut4-null mice (Yang et al., 2005). These investigators showed further that serum RBP4 levels were elevated in the insulin-resistant mice but this could be normalized upon treatment with rosiglitazone, an insulin-sensitizing drug. Both male transgenic mice overexpressing RBP4 and injection of RBP4 into the circulations of normal mice were found to be associated with insulin resistance. Moreover, increased serum RBP4 levels were found to induce hepatic expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase and to impair insulin signaling in muscle. Male Rbp4-null mice showed better responsiveness to challenges with either glucose or insulin. Based on these data, Kahn and colleagues proposed that RBP4 is an adipocyte-derived signal that may contribute to impaired glucose and insulin responsiveness and the pathogenesis of type 2 diabetes (Yang et al., 2005)."

"The mouse model studies were followed-up by studies of RBP4 levels in lean, obese and diabetic human subjects (Graham et al., 2006). Studies involving 3 distinct cohorts, ones from San Diego California, Leipzig Germany, and Göteborg Sweden, allowed Kahn and colleagues to reach the identical conclusion from their human studies as they did for the mouse studies. Human RBP4 was found to be an adipocyte-secreted molecule that is elevated in human serum before the development of frank diabetes. The authors proposed that elevated serum RBP4 levels identified insulin resistance and associated cardiovascular risk factors in subjects with varied clinical presentations."

"Nearly all investigators exploring the relationship between circulating RBP4 levels and disease have measured circulating levels of total RBP4 (apo- + holo-RBP4). However, in the circulation both apo- and holo-RBP4 are present, with holo-RBP4 accounting for approximately 85% of the total RBP4 present in the circulations of healthy individuals (the remaining 15% is present as apo-RBP4) (Soprano & Blaner, 1994). Two published reports have provided measures of both apo- and holo-RBP4 levels in patients. One study of normal and obese men and women, reported that total serum RBP4 was strongly associated with both BMI and measures of insulin resistance (Mills et al., 2008). For this study, serum apo-RBP4 levels were approximately two-fold higher in obese patients compared to controls and the retinol:RBP4 ratio, a measure of relative apo- and holo-RBP4 levels, was reported to be significantly lower in obese patients (Mills et al., 2008). Other investigators have reached the same conclusion that excess RBP4 relative to retinol (increased apo-RBP4) is more indicative of type 2 diabetes than total RBP4 levels (Erikstrup et al., 2009). These investigators also reported a positive correlation between adipose tissue RBP4 mRNA levels and plasma tumor necrosis factor-α (TNF-α) levels. This later finding raises a question regarding the possible role of adipose inflammation in RBP4-related disease (Erikstrup et al., 2009). Collectively, these two reports raise a question as to whether both apo- and holo-RBP4 levels should be routinely measured for assessing linkages between circulating RBP4 levels and disease incidence. Importantly, they also raise a caveat for interpreting reports were only total RBP4 was reported."

"Circulating RBP4 levels have also been associated with risk of coronary heart disease (Sun et al., 2013). The authors assessed plasma RBP4 levels for 468 women who developed coronary heart disease and for 472 matched controls in the Nurses’ Health Study cohort during 16 years of follow-up. Higher levels of circulating RBP4 were associated with increased risk of coronary heart disease in a time–dependent manner. In another study, a significant correlation was identified between serum RBP4 levels and various established risk factors for cardiovascular disease in women (Alkharfy et al., 2012). This study which involved 139 male and 145 female patients was unable to establish this relationship in men (Alkharfy et al., 2012). Feng et al. (2015) reported that blood RBP4 levels were positively correlate with carotid atherosclerosis in type 2 diabetes patients for a study involving 1,076 patients."

"The literature concerning the actions of retinoic acid in metabolic disease is strong and points to the conclusion that normal retinoic acid signaling is required for preventing disease. This is especially true for preclinical studies of NAFLD where it is clear from the literature that dysregulation of retinoic acid signaling mediated by RARs contributes to hepatic disease development and progression. The actions of retinoic acid in white adipocyte differentiation are also clearly defined but it remains unclear whether this involves only RAR signaling and/or PPARβ/δ signaling as proposed by some authors. This literature also convincingly suggests a role for retinoic acid in the browning of WAT and in maintaining normal BAT functions. These actions of retinoic acid will undoubtedly receive further research attention in the future.

Although the literature proposes a number of distinct actions for RBP4 in obesity, insulin resistance, type 2 diabetes, NAFLD and other related metabolic diseases, definitive understanding of how RBP4 contributes to these disease states remains elusive. A majority of the human literature finds associations between circulating RBP4 levels or adipose tissue RBP4 expression and metabolic disease. However, a large number of human studies have failed to establish associations between RBP4 levels and disease. It has been suggested that methodological differences in how RBP4 concentrations are measured may account for some of this apparent discrepancy (Graham et al., 2007)."

"The molecular or mechanistic literature regarding RBP4 actions in cells and animal models generally supports the notion that RBP4 has a role in disease causation, although not all published studies support this conclusion. It is the view of this author that RBP4-induced inflammatory responses within adipose tissues are probably responsible for most of these effects, especially RBP4-induced NAFLD and retinal disease. However, the possibility that RBP4 binding to STRA6 may account for some of disease causation cannot be dismissed and this merits further study. A very important question that needs to be addressed is whether circulating RBP4 contributes to disease causation or whether only RBP4 synthesized by adipocytes provokes disease."

"ALDH1A1 (RALDH1) is reported to have a role in a number of key metabolic processes involved in WAT physiology, including the browning of WAT. These actions were originally proposed to involve the actions of retinaldehyde as a transcriptional regulator. Later studies suggested that retinoic acid also contributes to the ALDH1A1-mediated effects in WAT. However, a recently published report proposes that neither retinaldehyde nor retinoic acid is involved in mediating ALDH1A1 actions in WAT, suggesting rather that other ALDH1A1 substrate/product combinations may account for the observed effects of ALDH1A1 in WAT. More research will be required if we are to understand whether ALDH1A1 actions in WAT are related to the role of this enzyme in vitamin A metabolism."

"A number of other proteins involved in vitamin A metabolism and transport, including RetSat, RBP1, RDH1, and CRAPB2, have been proposed to have significant roles in adipose tissue accrual and adipose-related disease. However, the literature regarding the actions of these and other vitamin A-related proteins in metabolic disease is still relatively limited and in its early stages. Clearly more research in this area will be needed if we are truly to understand the actions of these and other vitamin A-related proteins in metabolic disease."​

Haha this exchange was pretty funny.

Psh.

 

[Cirion]

What symptoms do you get from tryptophan?

brain fog, irritability, fatigue, low motivation

 

[tallglass13]

Hopefully somebody can answer this question for me, but if I have access to skim organic raw milk... zero fat nothing added non GMO... would there be any vitamin A??

 

[Dolomite]

The "perfect storm" of Poison/"Vitamin A" problems from dairy products

@tallglass13 , Charlie put this link up on page 193. There has also been a discussion of how milk protein, caisen, is involved.

 

[postman]

brain fog, irritability, fatigue, low motivation

I get that from cooked meat but not with raw meat.

 

[tallglass13]

The "perfect storm" of Poison/"Vitamin A" problems from dairy products

@tallglass13 , Charlie put this link up on page 193. There has also been a discussion of how milk protein, caisen, is involved.

Ok, thanks..just finished reading it.

 

[Pulstar]

I'd tend to agree with what some have said on here about the vitamin D being too low. Whenever I eat liver or take vitamin A for acne it seemed to get worse. Any sort of sunshine even tanning beds always cleared up my face pretty quickly. The two need to be well balanced.

Same here. My skin is actually more or less OK (used accutane many years ago), but whenever I supplement with vitamin A, I'm getting pimples and oily skin, so I don't take it. After reading this thread, Ray's stuff and Grant's book, I'm starting to think that there's something else at play. Possibly my vitamin D is low, I will test it. @Such_Saturation even says that vitamin A is helping his skin.
Anyway, I will try to reduce my vitamin A intake from food and will supplement extra vitamin D and see what happens.

 

[Pulstar]

Folks, can anyone also provide a link where Ray speaks of vitamin A to D ratio or importance of vitamin D in the context of vitamin A. I think I saw something like this, but can't find it.

 

[charlie]

Homeopathy shows us a pattern that Poison/"Vitamin A" and nightshades are TOXIC

 

[Amazoniac]

- Vitamins A and E in liver, kidney, and whole blood of East Greenland polar bears sampled 1994–2008: reference values and temporal trends

"Persistent organic pollutant (POP) groups such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), polyaromatic hydrocarbons (PAHs), and pesticides such as dicholorodiphenyltrichloroethane (DDT) and dieldrin have been shown to be related to vitamin A and E metabolism in multiple species (Twaroski et al. 2001; Murvoll et al. 2005; Routti et al. 2005; Novak et al. 2008). As East Greenland polar bears (Ursus maritimus) have been shown to carry some of the highest POP loads of any mammal species (Letcher et al. 2010; McKinney et al. 2011), this population is a relevant one to investigate whether POPs can cause an alteration of the vitamin status in polar bears."

"Gutleb et al. (2010) recently reported an in vitro study showing that the thyroid hormone binding sites on the TTR appeared to be completely saturated by hydroxylated PCB metabolites. In vivo, it has been shown that contaminants explained more than 50% of the TTR-binding activity in 4-month-old polar bear cubs (Simon et al. 2011; Bytingsvik et al. 2013). In addition, many other hydroxylated metabolites of other POPs have been found to disrupt the formation of the RBP–TTR complex (Lans et al. 1993; Meerts et al. 2000; Simon et al. 2013). Also, binding of tetrachlorobiphenyl (TCB) to TTR have been found to reduce serum vitamin A in rats (Brouwer and van den Berg 1986). As the specificity of the binding sites on TTR is not well known, the mechanism may be the same in both cases. The binding of exogenous compounds could also lead to a conformational change in TTR, thus inhibiting the binding of the RBP. In any case, it seems that some exogenous compounds are capable of disrupting the binding of RBP to TTR. This could lead to higher levels of vitamin A in liver over time, or in blood, although the latter is not observed in the present study."

"Cortisol levels have been found to increase significantly over time in polar bear hair (Bechshøft et al. 2012). At the same time, changes in thyroid hormone status in the ani- mals have been found to be correlated with POP loads (Villanger et al. 2011). The fact that vitamin A and vitamin E concentration also appear to be increasing over time makes for a complex interpretation, as all three are bound together in a wide range of hormonal and vitamin cascades."

"Together, these results add to the weight of evidence indicating that some POPs could be disrupting not only polar bear hormone balance but also their vitamin status. While the observed temporal increase in vitamin concentrations is likely related to POPs to some degree, the question remains as to whether this result stems from influence of contaminants only or also changes in prey species and others, or a combination of these factors."​

- Threats to polar bears

- Vitamin A Homeostasis Endangered by Environmental Pollutants
- Grant Genereux's Theory Of Vitamin A Toxicity

Homeopathy shows us a pattern that Poison/"Vitamin A" and nightshades are TOXIC

Hi Karl. This is a hint for how events will unroll: combine the 'protective factors' in foods with eventually starting to acknowledge its therapeutic value as drug and he'll have a creative reasoning to suggest its consumption without having to apologize for the mess.

 

[tankasnowgod]

Iron is given a bad rap because the body has no method of excretion of iron in appreciable quantities and its blamed for many health problems especially in peatland. Its common to suggest avoiding iron especially heme iron and yet if iron was so dangerous why would our bodies hold onto it so desperately?

I think the reason is historical context. Just 150 short years ago, Bloodletting was the go to medical therapy (and was for thousands of years), practically all humans had intestinal parasites (which feed on host blood, lowering iron), and humans were a lot more active, which itself tends to lower iron, through sweat. In this context, there is no need for human bodies to have an iron disposal mechanism, as it was constantly being lost. While a dangerous mineral, it is a necessary one. Without any iron, you are dead.

But times have changed drastically, in addition to those factors, we now have fortification, iron supplements, and more access to iron rich meats. The reason excess iron (key word, excess) gets blamed for so many health problems, is due to the fact that excess iron causes so many health problems. And it's not just Ray Peat that mentions this, You can look up E.D. Weinberg, Dr. Fachinni, Jym Moon, Chris Kresser, and the Zacharsky studies.

On top of all this, over half of the human species does have a mechanism to dispose of excess iron- it's called menstruation. It's only us genetically flawed males that have no easy way to dispose of excess iron.

And the diseases of excess iron tend to strike in old age. If you look at it from an evolutionary perspective, there is no pressure to "select" for an iron lowering mechanism, because the vast majority of people hit with all the excess iron diseases (including cancer, diabetes, and heart disease) are past the age of reproduction. One of the youngest victims of hemochromatosis I've read about was 43, and he was already a father when he was struck down in life.

Even having said all that, and having been iron loaded previously myself, I still think red meat is excellent, and the heme iron being much less of a concern than it is made out to be.

 

[tankasnowgod]

Folks, can anyone also provide a link where Ray speaks of vitamin A to D ratio or importance of vitamin D in the context of vitamin A. I think I saw something like this, but can't find it.

I've seen lot's of quotes about A, but none in that context. Dan Wich has some excellent Peat related search engines here, this might help you find such a quote easier- PeatSearch: a Ray Peat-specific search engine - Toxinless

 

[Cirion]

It's interesting that, per gram of protein, rice has almost 3 times more tryptophan than beef and almost 5 times more tryptophan than melons.

I don't think this is true... I've been under 1 gram of tryptophan many days now. and was at several grams when my protein intake was high. I'll have a check on chronometer though.

 

[HDD]

Folks, can anyone also provide a link where Ray speaks of vitamin A to D ratio or importance of vitamin D in the context of vitamin A. I think I saw something like this, but can't find it.

@Cheesecake posted this-
I had this response from him when I asked him that question in April last year:
"I don’t think the ratio matters, the need for them can vary in opposite directions, for example, with lots of sunlight there’s no need to supplement D, but the need for A increases. Vitamin E protects against an excess of A."

 

[InChristAlone]

@Cheesecake posted this-
I had this response from him when I asked him that question in April last year:
"I don’t think the ratio matters, the need for them can vary in opposite directions, for example, with lots of sunlight there’s no need to supplement D, but the need for A increases. Vitamin E protects against an excess of A."

There it is. That somehow getting enough of the other fat soluble will protect against toxicity of the other. I have a real life example where that didn't work. My sister who lives in Cali, had severe eczema on her hands, she hates pharmaceuticals yet she has needed to resort to cortisone treatments when it got bad. I told her to try Idealabs vitamin E, she did WITH NO CHANGE. It's possible she wasn't getting enough vitamin D as she works inside, but she is getting higher UV year round than me. She is a healthy person too, doesn't eat junk food.

 

[Rafael Lao Wai]

I don't think this is true... I've been under 1 gram of tryptophan many days now. and was at several grams when my protein intake was high. I'll have a check on chronometer though.

It's true: if you eat 100 grams of protein from beef, you get around 400mg of tryptophan. If you eat 100 grams of protein from white rice, you get around 1200 mg of tryptophan.

Beef, ground, 90% lean meat / 10% fat, raw [hamburger] Nutrition Facts & Calories
Rice, white, long-grain, regular, raw, unenriched Nutrition Facts & Calories

Rice has almost the same amount of tryptophan as chicken breast, given the same amount of protein.

Milk has the highest amount of tryptophan per amount of protein that I have looked into.

 

[Cirion]

Ok, well that's not entirely a fair comparison. No one eats 100 gram of protein from rice lol. I don't notice it because I don't eat 100 gram of protein from rice =P But your comment on milk is probably one of many reasons people don't do well on it. I rarely even eat 100 gram protein total a day anymore. Sometimes half that.

Just like reducing dietary fat automatically brings down pufa, so bringing down dietary protein automatically drops tryptophan.

We must also probably consider density of tryptophan. Even though rice may have more per gram of protein, per gram of RICE has almost none.

 

[Ronald1919]

Homeopathy shows us a pattern that Poison/"Vitamin A" and nightshades are TOXIC

I am not sure what he's trying to say

There it is. That somehow getting enough of the other fat soluble will protect against toxicity of the other. I have a real life example where that didn't work. My sister who lives in Cali, had severe eczema on her hands, she hates pharmaceuticals yet she has needed to resort to cortisone treatments when it got bad. I told her to try Idealabs vitamin E, she did WITH NO CHANGE. It's possible she wasn't getting enough vitamin D as she works inside, but she is getting higher UV year round than me. She is a healthy person too, doesn't eat junk food.

I tanned all summer peak UV. All the while I was consuming liver and eggs to 'balance' things. Guess what? My Seb derm got worse. Ray peat's suggestion are the same as an economist. They sound good on paper but have no application in the real world