Ray Peat Interview - June 1st, 2019 With Jodelle - Cortisol, Low Testosterone, Dangers Of A No Sugar

yerrag

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As to heart rate going up after meals, I also wonder about that. Is it because the blood sugar is higher after meals that heart rate is up? Or is it because digestion is an energy-intensive process that it demands more energy, and so metabolism and heart rate naturally has to increase?

@CLASH I think the heart rate after meals shouldn't be relied upon as an indication of our metabolic rate. It goes up because there's a deluge of glucose going into the blood, and the body is absorbing it at a high rate, which it can. I tested my blood sugar right after a meal, and my blood sugar was at 140. I was initially shocked at seeing that huge a number, but then realized it must be normal given how fast rice is digested and assimilated into blood. With that much sugar being metabolized, it's likely metabolism would increase, and we would see that in increased heart rates.

On the other hand, I am curious to find out if people with poor tissue sugar absorption - the insulin resistant people - would experience an increase in heart rate. Maybe they would, but the increase in heart rate may be smaller. And it would be interesting to see the effect on heart rate compared between taking sucrose and taking glucose for insulin-resistant people. I would expect increase in heart rate to be more pronounced when they take sucrose.
 

Inaut

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@encerent i think her perspective has changed relatively recently as I also noticed some of her older posts aren’t Peaty in the slightest. I remember her saying that some of the things she advised her clients about in the past is no longer valid and that she has changed her views about a lot of things.... I give her credit though for acknowledging mistakes and being open to new ideas...Sad thing is many people pay for “coaching” from anybody with any internet presence...Not pointing my finger at Jodelle specifically here but that most people don’t have the time nor the energy to do their own research on health. It’s easier to be spoon fed bull****. More ramblings...
 

CLASH

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Good evening everyone,
I havent been posting as much because I’ve been trying to learn wordpress so I can make a blog. After the past few days I’ve been able to create something thats somewhat presentable and I posted 2 short and sweet articles. Hope you guys enjoy. Maybe I should create a forum thread to see what topics you want discussed and what articles you want me to go over in blog posts, also what you guys think about the blog posts themselves (so i dont entirely derail this thread)?
 
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I think a high carb, medium protein, lowish fat diet seems best for me.

The past week I’ve kept a food diary and calculated calories and calcium.

I’ve also felt really crappy which I don’t think is because of my diet (which hasn’t really changed). I think I have had a flu passing over me. But I’ve taken 40g of vitamin C a day, and antibiotics (less than would be prescribed, more than normal) and it is passing me by. Every day I feel better than the day before.

I was going to point out a few things though.

As people age, their metabolism slows down. A lot. Dr. Peat thinks this is due to PUFA accumulation. He recommends lowish fat primarily because all fat contains some PUFA and the PUFA accumulates, depressing metabolism.

I was also going to point out that ground beef is high in endotoxins. I grind my own in the food processor and then I cook it. At the end of the day, endotoxins are probably the OTHER reason we decline so much as we get older.

The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4 | British Journal of Nutrition | Cambridge Core
The ingestion of fatty meals is associated with a transient, low-grade systemic inflammatory response in human subjects, involving the activation of circulating monocytes and the secretion of pro-inflammatory cytokines. However, it is not yet clear how different foodstuffs may promote inflammatory signalling. In a screen of forty filter-sterilised soluble extracts from common foodstuffs, seven were found to induce the secretion of TNF-α and IL-6 from human monocytes in vitro. To investigate what may differentiate inflammatory from non-inflammatory food extracts, stimulants of Toll-like receptor (TLR) 2 and TLR4 were quantified using human embryonic kidney-293 cells transfected with each TLR, and calibrated with defined bacterial lipopeptide (BLP) and lipopolysaccharide (LPS) standards. These assays revealed that while most foods contained undetectable levels of TLR2 or TLR4 stimulants, all TNF-α-inducing foods contained stimulants of either TLR2 (up to 1100 ng BLP-equivalent/g) or TLR4 (up to 2700 ng LPS-equivalent/g) in both the soluble and insoluble fractions. TLR stimulants were present mainly in meat products and processed foods, but were minimal or undetectable in fresh fruit and vegetables. The capacity of food extracts to induce TNF-α secretion in monocytes correlated with the content of both TLR2 (r 0·837) and TLR4 stimulants (r 0·748), and was completely abolished by specific inhibition of TLR2 and TLR4. LPS and BLP were found to be highly resistant to typical cooking times and temperatures, low pH and protease treatment. In conclusion, apparently unspoiled foodstuffs can contain large quantities of stimulants of TLR2 and TLR4, both of which may regulate their capacity to stimulate inflammatory signalling.

-

Dr. Peat has said dairy is best because the animal filters out a lot of the toxins that are in its environment. I think this includes and maybe especially pertains to endotoxins in our food. Endotoxins are low/non existent in most vegetable products, but today there are many toxins in food especially in the fat of industrial meat animals.
 

yerrag

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was also going to point out that ground beef is high in endotoxins. I grind my own in the food processor and then I cook it.
Why would you say they're high in endotoxins but not mentioning bacteria as well? Is this because bacteria is killed while cooking while the toxins remain? Considering that ground beef has been the subject of recalls in the past due to e. coli outbreaks from unsanitary sourcing and processing techniques.
 
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Why would you say they're high in endotoxins but not mentioning bacteria as well? Is this because bacteria is killed while cooking while the toxins remain? Considering that ground beef has been the subject of recalls in the past due to e. coli outbreaks from unsanitary sourcing and processing techniques.

the endotoxins are not destroyed with cooking. There are bacteria of course.

The food industry applies chemicals to disinfect meat parts and uses this to produce ground meat. The endotoxins are not destroyed but are concentrated. There is no testing for it, only bacterial counts are tested for.
 

CLASH

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@ecstatichamster
Theres endotoxin on everything, especially if the meat or veg has been chopped up increasing surface area. I’m not so sure its such a big deal. The study you posted is in vitro. I think it may be different in the GI tract or everyone buying bagged salad and eating burgers, sausage, etc. Would be keeling over with inflammation:


Identification of Sources of Endotoxin Exposure as Input for Effective Exposure Control Strategies
“A large variation in the endotoxin levels was found on samples of potatoes, onions, and seeds (overall geometric standard deviation 17), in the range between 0.7 EU g−1 to 16400000 EU g−1. The highest geometric mean endotoxin levels were found in plant material (319600 EU g−1), followed by soil material (49100 EU g−1) and the outer side of products (9300 EU g−1), indicating that removal of plant and soil material early in the process would be an effective exposure control strategy.“


Stimulants of Toll-like receptor (TLR)-2 and TLR-4 are abundant in certain minimally-processed vegetables. - PubMed - NCBI
“Of 5 classes of MPV and 3 classes of related vegetable products considered to be likely to contain a high microbial load, diced onion and bean sprouts contained the highest levels of stimulants of TLR2 (up to 18.5 μg Pam(3)CSK(4)-equivalents per g) and TLR4 (up to 11.4 μg LPS-equivalents per g). By contrast, the majority of fresh whole vegetables examined reproducibly contained minimal or undetectable levels of TLR2- or TLR4-stimulants”


Accumulation of stimulants of Toll-like receptor (TLR)-2 and TLR4 in meat products stored at 5 °C. - PubMed - NCBI
“TLR-stimulants reached the highest levels (approximately 80 μg lipopeptide-equivalents per gramme and approximately 7 μg lipopolysaccharide-equivalents per gram) in meat that was minced rather than intact, and when stored in air rather than under a modified atmosphere.”

*also I think the dairy is low in endotoxin, not because the cow is filtering it out but because the milk is antibacterial at first and there isnt much bacteria in it to start due to compounds in the milk limiting growth. Then the milk is pasteurized and vaccum sealed so there really isnt a chance for hacteria to populate it. Fermented dairy has endotoxin from what I understand.

*also the fat from the animals doesnt contain endotoxin per say. It just helps to bind it and transport it across the intestinal membrane to the liver. It may induce a small inflammatory response acutely but wether or not this is a bad thing is yet to be proven. From what I understand, in certain experiments of giving people large boluses of fat like cream thier endotoxin levels in the blood went up. However if this was pure endotoxin then the inflammatory response they had gotten should have been massive, however it wasnt. I think the fat is helping to clean out an detoxify endotoxin from the intestine.


Heres a blog post by peter at hyperlipid discussing the cream and endotoxin study:
Hyperlipid: Endotoxin Absorption on a High Fat Diet


Heres the study itself:
High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects


Heres a response by researchers in the form of a letter to the editor discussing the fact that the increased endotoxin in the peoples blood suprisingly didnt induce the massive inflammation it should have:
Comment on: Harte et al. High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects. Diabetes Care 2012;35:375–382


Heres a different study showing that both pure glucose and cream increased endotoxin in general, the difference was cream increased endotoxin in the bloodstream and induced some TLR-4 expression. This was all in mononuclear cells I think, which are white blood cells. If this is the case it seems to me like the cream is detoxifying the endotoxin and stimulating mononuclear cells to possibly help clear out the small intestine. I could be wrong, I have an obvious bias towards higher fat intake based on my experience but its interesting that with increased endotoxin in the blood, there isnt a massive inflammatory response with the fats. Something else is going on. Also interesting is that orange juice didnt stimulate any endotoxin, we’ve seen this before from a study our dear pal haidut posted a while back.
Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3
RESULTS Indexes of inflammation including nuclear factor-κB (NF-κB) binding, and the expression of SOCS3, tumor necrosis factor-α (TNF-α), and interleukin (IL)-1β in MNCs, increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS concentrations increased only after cream intake. The intake of orange juice or water did not induce any change in any of the indexes measured.”


Heres a blog post discussing the use of cholesterol to protect against endotoxin, among other concepts:
Part Five: Cholesterol, Leaky Gut, Endotoxemia and Heart Disease


EDIT: heres an article showing that bile acids breakdown endotoxin and protect rats from endotoxin in the GI tract. Saturated and monounsaturated fats are excellent stimulators of biles acids.
[Bile acids and endotoxins: physico-chemical defense of the body]. - PubMed - NCBI


Heres a study showing alkaline phosphatase is increased by the feeding of fats:
Effect of fat feeding on intestinal alkaline phosphatase activity in tissue and serum. - PubMed - NCBI


Heres a study showing that alkaline phosphatase detoxifies and destroys endotoxin:
Dephosphorylation of endotoxin by alkaline phosphatase in vivo.


*If you put all of this together it seems fats, cholesterol, lipoproteins, alkaline phosphatase and bile acids are all functioning together to detoxify endotoxins and protect against bacteria. In my mind this is especially the case in contexts of studies such as this one:
Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. - PubMed - NCBI
Showing a protection of rats against liver damage by saturated fats despite continued ethanol administration. From what we know on the forum so far, thanks again to studies posted by haidut and thanks to the researchers in this field in general, alcohols main damaging effect is mediated via destruction of the intestinal epithelium allowing endotoxin to leak through. If saturated fats are protecting against this, even in the face of continued alcohol administration it seems that they are serving a protective effect against endotoxin.
 
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thank you @CLASH for the excellent cites. Much appreciated.

I think that Dr. Peat has brought endotoxins to my attention as a source of aging stress, almost as much as PUFA and iron buildup. Endotoxins are a constant stressor and probably produce a lot of the chronic diseases including even Parkinsons.

Hepatic alcohol damage may be ameliorated by sat fat, but that doesn't mean that endotoxins don't take their toll (ha! pun!).

Fresh fruits and vegetables don't have a lot of endotoxins compared to factory-ground meat. The difference is exponential. I think it is a major reason not to eat such beef and to not frequent eat burgers at restaurants.
 

lampofred

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thank you @CLASH
I think that Dr. Peat has brought endotoxins to my attention as a source of aging stress, almost as much as PUFA and iron buildup. Endotoxins are a constant stressor and probably produce a lot of the chronic diseases including even Parkinsons.

Dr. Peat told me constipation is a major cause of Parkinson's. I'm guessing constipation is strongly associated with endotoxin.

According to Wilhelm Reich, armoring is the cause of constipation.
 

CLASH

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CLASH

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@Kartoffel
Omega 3’s seem to lower bile acid content of bile, while omega 6’s seem to increase cholesterol saturation of bile, possibly leading to gallstones. Too low fat in the diet seems to decrease gallbladder emptying and leads to build up of bile in the gallbladder that is stagnant. I think if you couple this with a higher omega 6 diet and subsequent increased cholesterol saturation you’ll find that you may get gallbladder and biliary issues.

http://www.jlr.org/content/34/8/1275.full.pdf

“Hamsters fed the fish oil diet had the total bile salt pool reduced by 48% on average, and the cholic acid pool by 47% as compared with animals fed the safflower oil diet (Fig. 2). Synthesis of cholic acid was higher ( + 5 7 % ;+67%) on the safflower oil diet than on the fish oil or coconut fat diets and was not different between hamsters fed the fish oil or the coconut fat diet (Table 3).”

“Hamsters fed the safflower oil diet showed increased out- put of cholesterol in bile (+95%;P < 0.01) as compared with hamsters on the fish oil diet. O n the coconut fat diet, biliary output of cholesterol was intermediate (Table 4). Cholesterol saturation of bile was increased (P< 0.01) on the safflower oil diet as compared with the fish oil and coconut fat diets.”


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“VLCD (very low calorie diets) have been associated with a gall‐bladder stasis, as a consequence of reduced gall‐bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall‐bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall‐bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. ”



*as a side note here is an interesting article about the role of bile acids as farnesoid x receptor stimulators protecting the distal small intestine from bacterial overgrowth. I know you mentioned at one point the relationship between high fat diets, bile acids and sulphur reducing bacteria such as bilophila wadsworthia.

Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor
 

CLASH

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With all this said, I think the main beneficial effects of the saturated and monounsaturated fats, with avoidance of polyunsaturated fats, as far as digestion goes, takes place in the small intestine. I think the colonic environment is a different story. I think in the colon certain vegatable and fruit fibers may actually be needed and beneficial. I have been increasing my fiber intake from fruits mainly, I already used quite a bit of carrots. I have noticed some benefits in my digestive function so far. I’m going to add in a little starch from some cooked ripe bananas and some boiled purple sweet potato in the next few days and see how it goes. If all goes well, atleast based on my experience, I’d like to be able to say:

1) saturated and monounsaturated fats for the small intestinal health

2) fruit, root, tuber and maybe leafy green fibers for colonic health
 

CLASH

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thank you @CLASH for the excellent cites. Much appreciated.

I think that Dr. Peat has brought endotoxins to my attention as a source of aging stress, almost as much as PUFA and iron buildup. Endotoxins are a constant stressor and probably produce a lot of the chronic diseases including even Parkinsons.

Hepatic alcohol damage may be ameliorated by sat fat, but that doesn't mean that endotoxins don't take their toll (ha! pun!).

Fresh fruits and vegetables don't have a lot of endotoxins compared to factory-ground meat. The difference is exponential. I think it is a major reason not to eat such beef and to not frequent eat burgers at restaurants.

I personally think endotoxin is implicated in almost every common disease at this point, so I would have to agree.

Wether the endotoxin from saturated fat consumption takes its toll overtime is the question. I dont think it does but i’ll have to see ;)

Fair enough. +1 for not eating at restaurants too much in general, atleast in the US.
 
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I watched the Barry Groves video.

He's dead at 77. Ray Peat still lives on and is in his 80s. Barry Groves makes a persuasive case if all his facts do check out, especially with his timeline, especially about brain size of humans getting smaller since humans started to incorporate more carbs into what he eats. Since it is so counter to what Peat says, I have to step back and suspend belief in this. Ray Peat talks about the plentiful availability of sugar being instrumental in the development of brain size.

Groves makes a strong argument about the relative small size of our digestive system being tied to our nature as carnivores, and contrasts it with the large digestive system of herbivores. However, I am not convinced of that arguments as the herbivores' digestive system being large has a lot to do with it being able to digest cellulose. Not all plants are full of cellulose, and our small digestive system can handle the digestion of plants devoid of cellulose. So it makes little sense to argue for humans being carnivores on the basis of the size of his digestive system.

Moreover, being carnivorous makes us deficient in minerals, which are needed to establish a healthy acid-base balance. Eating as a carnivores, we would have an acidic balance and this would place an increasingly taxing burden on our kidneys. Perhaps that's why Groves didn't last as long as Ray Peat, who understands the value of mineral intake as they are alkalizing and would establish a healthier acid-base balance and provide for longevity.

However, I would agree with Barry Groves that meat as well as the accompanying fat that comes with meat is needed to provide nutrition for humans. I would not go low-fat and I would go for saturated fat, which is the fat that comes with eating animal meat (except for the factory farm-raised ones). I value fat as a dense source of energy, as well as for being less useful for bacteria to thrive in our gut.

I have been researching Groves alot lately. Makes very very good points.
The key with a diet like Groves is not to confuse meat and fat. He advocates a high fat diet, not a high protein diet.
We are talking about 60% Fat, 30 Carbs(primarly vegtables+fruit), 20% Protein.

Most people hop on carnivore and go straight into acidosis and tons of ammonia, and the kidneys get destroyed

If you we're to follow such a diet, i would accompany it with plenty of base minerals Pot/Mag/calc from lightly cooked non starch veg and some fruit to save the body the burden of gluconeogensis, also focus on fat, not protein. Like Pork Belly, super fatty steak/gelatin.
 

jet9

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Influence of short-term fasting on the pituitary-testicular axis in normal men. - PubMed - NCBI

“Basal serum T fell from 8.7 +/- 0.7 to 5.7 +/- 0.8 micrograms/l (p less than 0.01), and LH from 6.9 +/- 0.8 to 5.0 +/- 0.7 U/l (p less than 0.01). Serum estradiol (E2) and FSH remained unaffected. T”

“These results imply that: short-term fasting exerts inhibitory influence on Leydig cell function via a mechanism which might involve a reduced hypothalamic and/or pituitary stimulation.”

Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males

“After 8 weeks, the 2 Way ANOVA (Time * Diet interaction) showed a decrease in fat mass in TRF compared to ND (p = 0.0448), while fat-free mass, muscle area of the arm and thigh, and maximal strength were maintained in both groups. Testosterone and insulin-like growth factor 1 decreased significantly in TRF, with no changes in ND (p = 0.0476; p = 0.0397). Adiponectin increased (p = 0.0000) in TRF while total leptin decreased (p = 0.0001), although not when adjusted for fat mass. Triiodothyronine decreased in TRF, but no significant changes were detected in thyroid-stimulating hormone, total cholesterol, high-density lipoprotein, low-density lipoprotein, or triglycerides. Resting energy expenditure was unchanged, but a significant decrease in respiratory ratio was observed in the TRF group.”
@CLASH sorry for bumping old thread, but I have a question:

If sufficient calories are reached during eating window will it prevent lowering testosterone/thyroid?

I mean if from 8am to 1pm I eat 3-3.5k of calories (mostly animal products and fruit) and then fast after am I still damaging my body? Will adding extra meal (say fruit only) at 6pm stop the damage?

I am asking cause I like mental clarity of IF. And I sleep better too. (as long as I have enough calories in morning)
 

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