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This mad diet wheel
On the carnivore (Paleo Ketogenic Diet) I was advised to eat the meat, offal and eggs (400g of beef liver per week) which after 14 months made me very unwell; surely because of an overload of vitamin A.
To detox from high vitamin A, I moved into the Karen Hurd’s diet followed by Grant’s diet (meat, beans and rice). This diet is high in beans which makes is quite high in oxalates.
Looking at a low oxalate diet by Sally Norton (meat, cheese, eggs and low oxalates vegetables) I see that it is pretty high in vitamin A.
Can you see the problem?
Yes! It’s a minefield working out what to do. I think different diets work for different people. If you process vA very well in the liver/bile and have good gut bacteria then I’m sure you can eat quite a lot of vA without problem. If you have a rich microbiome with plenty of bacteria that break down oxalates then you can probably eat plenty of oxalates without problem. Once it goes wrong people tend to get stuck in negative vicious cycles (this is how I see it) which unless identified are difficult to get out of.
Probably the sickest should stick to beef+starch and later expand, once the health is at least partly recovered(could take many months .. even years).
Also starch seems to be the best carb source by itself:
https://academic.oup.com/ajcn/article-abstract/26/11/1180/4732762
And the worst could be fructose...
https://file.scirp.org/pdf/OJI20110200003_20641104.pdf
[Fructose and Sucrose Inhibit Biologic Functions of MBL]
Mannose-binding lectin (MBL), a mammalian lectin, is a pattern recognition molecule of the innate immune system and recognizes carbohydrates that are exposed on pathogens.
The importance of dietary sugar interaction with MBL is underscored by our studies on two common pathogens. Using both viral and bacterial pathogen binding to MBL, we demonstrate that dietary sugars, specifically fructose has a dramatic negative consequence. Mannan, fructose and sucrose had similar low level, inhibition of MBL binding to immobilized pathogens. However, the biologic pathways, activation of the lectin complement pathway and coagulation, downstream of MBL are significantly down regulated, particularly in presence of sucrose and fructose. Using an established bacterial and viral phagocytosis assay we show that fructose neutralizes pathogen entry into phagocytes, such as macrophages and neutrophils, the primary cell defense in innate immunity..
Our results also suggest that dietary sugars, in particular fructose has negative effect on innate immunity in a dose dependent manner. Therefore, it is conceivable that dietary sugars at low concentrations may not have any pathological consequence. It has been observed that in fructose fed rat, fructose concentration in the hepatic portal vein reaches to 0.4 mg/ml, which significantly inhibited MBL-mediated biologic functions in our study [55]. Consumption of these dietary sugars, more so for fructose, has skyrocketed in recent years and has been linked to a recent increase in metabolic disease, including diabetes and obesity [5-7]. It is also know that diabetic patients have increased susceptibility to infection [6], which has been attributed to a poor circulation in these patients. Our findings would suggest that those dietary sugars might also be responsible by directly reducing innate immune functions as blood fructose levels reportedly increase after fructose consumption in diabetes [56]. Therefore, one can speculate that intake of high levels of dietary sugar may induce a similar situation to MBL deficiency, which has been associated with infection susceptibility [25].
...
We propose that dietary sugars, in particular high dose of fructose weakens the innate immune protection, which is initiated by pattern recognition molecules, including MBL (Figure 5(b)). It is also conceivable that pattern recognition molecules may play roles in maintaining healthy commensal microbiota by fending off pathogenic bacteria [58,59]. In turn, the healthy microbiota would stimulate and strengthen the innate immune defense mechanisms. Diet can also affect defense mechanisms. Diet can also affect microbiota composition in mice underscoring the tight link between diet and metabolism of intestinal bacteria [60]. Thus, elucidating the relationships between diet, microbiota and innate immune system will be central to our understanding of human health...
The first, holistic immunological model of COVID-19: Implications for prevention, diagnosis, and public health measures:
https://onlinelibrary.wiley.com/doi/10.1111/pai.13271
...
MANNOSE-BINDING LECTIN
Mannose-binding lectin plays a pivotal role in innate immunity, interacting with surface sugars of a wide series of microorganisms as a pattern-recognition receptor.92 Thus, MBL (i) activates the lectin complement pathway; (ii) promotes opsonophagocytosis93; and (iii) modulates inflammation.
...
7.1 Evidence suggesting that MBL may protect in the early stages of SARS-CoV-2 infection
...
These results suggested that MBL may contribute to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for the acquisition of SARS
...
An smart old guy in my life convinced me that starch is much different than sugar and not to lump them together. (like low carb people do) I think he was right. A meal of rice isn't going to mess you up like a meal of dessert will.
I was thinking about Beata's topic here and musing that eventually we will be detoxing on pure white table sugar, LOL. I always thought it was interesting that Matt Stone would talk about his use of candy in his latter days on the interwebs. But now rockarolla has pointed out that fructose is bad. (table sugar is made up of glucose and fructose). LOL and sigh.
Eh, in large amounts sugar gives me a stomach ache.
I used to make a nice gluten-free potato starch/corn starch/rice flour blend (hopefully I'm remembering that right) ... It was pretty useful for getting calories and not horrible to bake with, easy to find the ingredients too. Probably low VA.
There is a “rice porridge” served to the ill and convalescent people in China called congee. It is made with rice boiled for several hours till almost smooth. Often the chicken stock or bone broth is used in place of water.
Makes sense!
@jaj. I have often thought about the healthiest people on Earth; they eat local, seasonal, not too much and a variety of foods. I tinkered with my food since I was 13 and before that western medicine made sure my microbiome got to be a total mess (lots and lots of antibiotics). Now it seems that when I work on one thing, something else is becoming unbalanced. I despair. 🙈
@rockarolla, I lost a few friends as I refuse to eat their lovingly prepared desserts. I found that white organic Thai Jasmine rice agrees with me nicely. I ofter take breaks from it but it looks like there is nothing to worry about. Thanks for the interesting links.
@lil-chick. I had a similar thought today. Eating seems to be hazardous to my health. Anyone knows anything about how to do the sun gazing and quit eating all together?? (Gasp) Why such a basic function became so difficult?
There is the famous Kempner rice diet, which also involved some whipping for noncompliance and one patient ending up a sex slave to Kempner. The rice diet seemed to be effective for its purpose. Garrett Smith has mentioned that rice has arsenic, which might be bad for someone who has issues with detoxification.
@Retinoicon
Yes, rice absorbs arsenic but half the globe eats rice 3 times per day with good results.
I choose organic Thai Jasmin rice as it has the least amount of arsenic, hoping to avoid any arsenic issues.
Your comment is yet another prove that eating is hazardous to health!
I read years ago that a certain amount of arsenic is needed by the heart, makes it run "smoother" or more strong and reliable. So maybe the small amount of arsenic in rice is a health benefit. Also it is common to wash rice in Asia; if the arsenic is coming from atmosphere pollution, the washing should deal with that.
yeah, arsenic is not that bad esp. in small quantities, i've already posted it somewhere
also, maybe it's the meat(balanced in proteins and fats) that should be the main staple and rice' role is to serve as a decoration/ketosis prevention(as an alternative to proteins overdosing), then very little amount is required like 60..100 grams/day, depending on lifestyle
It was believed that with prolonged consumption of small doses of arsenic, the body develops immunity. This fact has been established for both humans and animals. There are cases when habitual arsenic consumers immediately took doses several times higher than the lethal dose and remained healthy. Experiments on animals have shown the originality of this habit. It turned out that an animal, accustomed to arsenic when consumed, quickly dies if a significantly lower dose is injected into the blood or under the skin. However, this "addiction" is very limited, in relation to the so-called. "Acute toxicity", and does not protect against neoplasms. However, the effect of microdoses of arsenic-containing drugs as an anticancer agent is currently being investigated.
Both organic and inorganic arsenic compounds are toxic to living organisms in high concentrations. Nevertheless, in small doses, some arsenic compounds promote metabolism, strengthen bones, have a positive effect on hematopoietic function and the immune system , and increase the absorption of nitrogen and phosphorus from food. With plants, the most noticeable effect of arsenic is to slow down metabolism, which lowers yields, but arsenic also stimulates nitrogen fixation . [12] [13]
It was noted that for a growing organism in humans and animals, micro doses of arsenic contribute to the growth of bones in length and thickness, and in some cases, bone growth under the influence of micro doses of arsenic was noted during the period of the end of growth [14] .
Some authors consider arsenic as a vital microelement and class it among ultramicroelements - trace elements necessary in especially low concentrations (like selenium , vanadium , chromium and nickel ). The required daily dose for humans is 10-15 mcg. [12]
Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity
https://pubmed.ncbi.nlm.nih.gov/29225114/
Traditionally, the leading hypothesis regarding the development of obesity involves caloric imbalance, whereby the amount of calories consumed exceeds the amount of calories burned which causes obesity. Another hypothesis for why we get fat has surfaced in the last decade which is the idea that the overconsumption of added sugars and refined carbohydrates induce insulin resistance and high insulin levels causing obesity. While insulin is a fat-storing hormone, this hypothesis does not explain visceral adiposity, or why certain people are found to have fat stored in and around their organs. We propose a new mechanism for body fattening, particular visceral adiposity. This hypothesis involves the overconsumption of fructose, which leads to inflammation in all cells that metabolize it rapidly. When fructose is metabolized in subcutaneous adipocytes, the subsequent inflammation leads to an increase in intracellular cortisol in order to help squelch the inflammation. Unfortunately, the increase in intracellular cortisol leads to an increased flux of fatty acids out of the subcutaneous adipocytes allowing more substrate for fat storage into visceral fat tissue. Moreover fructose-induced inflammation in the liver also leads to increased intracellular cortisol via an upregulation of 11-B hydroxysteroid dehydrogenase type 1 causing increased fat storage in the liver (i.e., fatty liver). In essence, the fructose-induced inflammatory cortisol response causes "thin on the outside, fat on the inside" (TOFI). Furthermore, fructose in the brain, either from fructose uptake via the blood brain barrier or endogenous formation from glucose via the polyol pathway stimulates an increased release of cortisol causing hepatic gluconeogenesis leading to overall insulin resistance and further body fattening. This review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity.