@Elephanto
Have you looked for foods with opiates aside from dairy?
Have you looked for foods with opiates aside from dairy?
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@Elephanto
Have you looked for foods with opiates aside from dairy?
Fructose is found in fruit, does not generate an insulin response, and is very sweet.
intermediary metabolites from fructose metabolism overwhelm hepatic mitochondrial capacity, which promotes de novo lipogenesis and leads to hepatic insulin resistance, which drives chronic metabolic disease.
Some of the fatty acyl-CoA products from DNL escape packaging into VLDL for export and instead accumulate as lipid droplets in the hepatocyte (48), driving hepatic steatosis, similar to ethanol. In doing so, the enzyme JNK-1 (49) is activated, which induces serine phosphorylation of IRS-1 in the liver (50), thereby preventing normal insulin-mediated tyrosine phosphorylation of IRS-1 and promoting hepatic insulin resistance. This drives hyperinsulinemia
Eventually, in response to the hepatic insulin resistance, gluconeogenesis, and the phenomena of glucotoxicity, lipotoxicity, endoplasmic reticulum stress (53–56), and the unfolded protein response (57) at the β-cell, this leads to inadequate insulin secretion in relation to the degree of peripheral insulin resistance and type 2 diabetes (58).
Not all of these studies found consistent effects for all parameters, however. In the study by Lê et al. (6), where 1.5 g fructose/kg body weight were consumed during a 4-week period, fasting lipids and glucose were affected, but insulin resistance, as determined by a euglycemic-hyperinsulinemic clamp, did not change. However, their study only tested fructose, without comparison with other sugars. Furthermore, relatively high amounts of fructose were consumed in most of these studies, reaching up to 25% of total energy intake. In a recent intervention study in healthy Swiss men, we found adverse effects of low to moderate amounts of fructose—but also glucose and sucrose—on fasting glucose and inflammatory markers, whereas only beverages containing fructose seemed to negatively affect LDL particle size. Even though fasting glucose was altered, none of the interventions showed any effect on glucose tolerance or on indices of insulin sensitivity calculated during an oral glucose tolerance test
During each intervention, subjects were supplied with SSB containing different sugars in different concentrations: medium fructose (MF), 40 g/day; high fructose (HF), 80 g/day; high glucose (HG), 80 g/day; and high sucrose (HS), 80 g/day. The drinks were provided in containers of 200 mL each, with blinded content, and the subjects had to consume three drinks (total, 600 mL) daily. The sugar concentrations of the drinks were 66.5 g/L for the medium concentrations and 133.5 g/L for the high concentrations. Subjects were advised to consume the drinks together with the three main meals.
The observations that knockdown of TLR-4 and MyD88 can alter hepatic lipid content by reducing food intake underline the critically important fact that genetic manipulations in immune pathways in rodents can often lead to subtle alterations in appetite, activity, energy expenditure or other parameters that affect development of ectopic lipid deposition and insulin resistance, ultimately leading to flawed interpretations of experimental data if not taken properly into account. We further found that mice deficient of the TLR-4 receptor were not protected from saturated fat-induced hepatic steatosis, hepatic DAG accumulation, PKCε activation or insulin resistance as assessed by hyperinsulinemic-euglycemic clamp studies, when the decreased caloric intake was compensated for. In contrast to the proposed mechanism where activation of TLR-4 leads to activation of hepatic ceramide synthesis [3], TLR-4 deficient mice had increased hepatic ceramide content when fed the saturated fat diet.
In conclusion we found that: 1) both saturated- and unsaturated fat-feeding results in hepatic DAG accumulation, activation of PKCε and hepatic insulin resistance through impairment of insulin signaling at the level of IRS-2, 2) both saturated and unsaturated fat feeding induced hepatic insulin resistance independent of changes in hepatic ceramide content in normal rodents, and 3) TLR-4 receptor signaling is not required for saturated fat-induced accumulation of ceramides, triglycerides, DAGs or impairment of hepatic insulin signaling and lipid-induced hepatic insulin resistance.
According to your own citation, consumption of carbohydrates in general is no good. Not particularly credible for your argument.
Here's the full study. Check the methods. Diabetes Care
They had individual drink 200mL of glucose, sucrose, fructose in addition to their meal for every meal. Do you think their diets might have been just a tad bit hypercaloric? Seems like these researchers have a bit of an agenda to design such a silly study.
So why do I mention hypercaloric diets? Eating too much of anything will induce insulin resistance. Just pick an energy substrate, head on over to pubmed, and you can scare yourself away from eating anything.
Effects of a hypercaloric diet on β-cell responsivity in lean healthy men. - PubMed - NCBI
Lipid-induced hepatic insulin resistance
Context is everything. Eat sufficient calories. Eat varied nutrient-dense foods. Leverage fruits as a means to replenish hepatic glycogen, especially if you're trying to recover it after years of habits detrimental to it, but probably don't chug pure fructose on top of a full meal every meal. That's it. Context.
In closing, I'd also like to mention that you didn't address the fact that starchy foods have a higher glycemic index than even pure table sugar. What are your thoughts there? How does that fit into your perspective?
FWIW, hairloss, or lack thereof, is %100 about a clean and healthy gut, in my experience.
@Elephanto I really enjoy beverages, but wondering which are acceptable to drink? With the peat diet, I have been enjoying coke and OJ. Coke has actually become my favourite so would love to keep it in the diet if I could.
It's a big part but not 100%. Try to find pictures of people with Cushing's Syndrome (extremely high cortisol), most are bald. People who do coke and crack. Stress and adrenaline are another reason. Try to find people in hemochromatosis meeting (very high iron), most are bald. People who stress and hyperventilate in general have bad hairline, hyperventilation is another reason. Estrogen is a major one, endotoxin is one of the main reasons to have high estrogen but not the only one. Eating estrogenic foods, drinking a lot of alcohol and smoking weed, using certain herbs, stressing in general and fapping too much would be other reasons to have high estrogen. If you look at the recent study I posted in the Scientific Studies section, IGF-1 : IGFBP3 is the main predictor of balding, so ingesting things that literally contain IGF-1 like milk in large enough quantity would be another reason. Check out the Masai tribe, all their males are bald.
That said, that's why I put coconut oil and bicarbonate sodium in the drastic tier of my recommendations, on its own killing endotoxin will do most of the job. Regrowth is another story, decalcification must be done.
Well coke is done with corn starch syrup, and corn is pretty estrogenic because of the pesticides they use on corn crops ("turn the frogs gay"), I read that even mexican coke doesn't use pure sugar anymore. If you can find some indie carbonated drinks that have pure sugar or cane sugar, it would already be better. Or you could just get some carbonated source water and add some simple syrup (water + table sugar boiled). Anyway, don't worry too much. I was drinking coke during the time I was regrowing. If you want to be optimal, I'd say to have some white rice with your meals and treat sugar of any kinds as a dessert. Boiled apples seem to be one of the safest fruits right now, taste like apple pie. Avoid the OJ and citruses though, you probably already have high histamine from what you said earlier.
Stress constricts the intestines and colon. So chronic stress likely consitpates and creates build up in the intestine. I have seen plenty of very high stress people with full heads of hair, but they are usually the type that doesn't eat much. I've seen heavy coke users that have full heads of hair, same with crack heads.
Even the Masai women have very high hair lines, so I think there is something else going on there. None of them
Have vertex balding either.
I think there many things than can cause issues with digestion, but I do believe digestion is the primary issue in hairloss.
I've seen people that have grown hair back from fasting, which is completely contrary to the stress causes hairloss theory.
Of course I don't know. This is all theory. But I have a hunch it's almost always related to the condition of the gut.
Well women are not immune to balding, it's just that men already have much higher IGF-1 levels in general. So those women that drink enough igf-1 are promoting it, as well as the fact that african womens have higher igf-1. And the distinction between receiding hairlines and full on vertex balding isn't real, the latter is just the progression, or extreme, of the first.
What you say also is true, it's not a black-or-white thing, some people will keep their hair on crack. Usually some genetically very low estrogenic types. And fasting compensates for the stress by the fact that it dramatically lowers IGF-1 on its own, and is even done for this objective by cancer patients. But there are ways that adrenaline, other than increasing endotoxin, promote calcification and balding. And estrogen is very important, there's a link between bald men and prostate cancer.
@Elephanto
What beverages do you recommend drinking between meals?
The problem with both apples and pineapples, I get an allergic reaction.. scratchy itchy throat, inflamed tongue and a cut up feeling in the mouth. Really don't know what fruit I could eat.. had been eating grapes up until you said they were estrogenic. What other fruit can I try?
That would make sense since the prostate is right next to the colon. Endotoxin will increase estrogen. Endotoxin will increase adrenaline as well. I do believe all the factors you mentioned are variables, but I think a toxic system is at the route of all of it. And for the majority of people, their gut is the root of the toxicity.
Yeah I acknowledged that, endotoxin does increase estrogen and adrenaline but there are other ways that they can be increased. Hemochromatosis is a big proof of that, I had seen pictures of people in related forums and pics of their meetings, iron overload will make almost everyone bald by all the oxidation it's causing and the resultant cortisol havoc; and it being a igfbp3 inhibitor on its own. But also, iron will make a good medium to grow bacterias! Not sure about the link with the proximity of prostate and colon, it's really an estrogen-driven cancer.
Gotcha man. I'm not saying you're right or wrong. We could go back and forth forever on this. My point is that everything we know that appears to relate to baldness, are symptoms of endotoxin overload. However, we know that some of these symptoms, when isolated, do not result in baldness. A person can have high estrogen, or high adrenaline, and not have baldness. So therefore these alone can not be the "cause" of baldness. I believe the cause is poor gut health resulting in endotoxin overload, which also results in many other symptoms.
Why do 5AR-II enzyme deficient pseudohermaphrodites don't experience baldness (even Danny admits this), I am pretty sure they would have constipation or other gut related troubles.Gotcha man. I'm not saying you're right or wrong. We could go back and forth forever on this. My point is that everything we know that appears to relate to baldness, can be symptoms of endotoxin overload. However, we know that some of these symptoms, when isolated, do not result in baldness. A person can have high estrogen, or high adrenaline, and not have baldness. So therefore these alone can not be the "cause" of baldness. I believe the cause is poor gut health resulting in endotoxin overload, which also results in many other symptoms. I believe that's the cause of the male pattern baldness "itch." Bacteria is feeding on endotoxin that being released through the skin.
I thought bacteria created endotoxin, BTW what exactly is "endotoxin" that is being released through the skin here?Bacteria is feeding on endotoxin that being released through the skin.
Yeah but then we'll see some morbidly obese people that have perfect hair, they exist. And yet they absolutely have a lot of endotoxins. So a person can have high endotoxin, and not have baldness. Here's a new way I could put it :
Picture Adrenaline-Endotoxin-Estrogen as the points of a triangle, each point increase the two others. And to the side of each points we could write many factors that influence them. To pinpoint it to one of the triangle's points can be true for certain people, untrue or partly true for others. And then some people have a single of the sub-factors of one of the triangle's point as the root cause (like high iron).
Why do 5AR-II enzyme deficient pseudohermaphrodites don't experience baldness (even Danny admits this), I am pretty sure they would have constipation or other gut related troubles.
I thought bacteria created endotoxin, BTW what exactly is "endotoxin" that is being released through the skin here?
I never knew lettuce had opioid effects. I used to eat a few pounds of salad every day for lunch back in high school, and I would always feel intensely sleepy, and my libido would skyrocket during the next class.Yes, gluten and lettuce have similar effects.