haidut

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I am posting this study just as an example of how important the role of endotoxin is in insulin resistance and diabetes. Similarly to the human study with aspirin, sterilizing the gut with antibiotics did not reduce the weight in the obese subjects (in this case mice). So, obesity may be a less important factor in diabetes than leaky gut and compromised liver function as a result of endotoxin overload.
In confirmation of Peat's views, the improvement of insulin sensitivity was associated with decrease in fatty acid metabolism and increase in glucose metabolism, as a result of antibiotic treatment. So, once again, burning fat may make you lean but will probably make you insulin resistant and as soon as you stop the fasting, exercising or low carb diet, the weight will massively pile on. Thus, lean often does not mean healthy, especially if the leanness is maintained with exercise, fasting, or carb restriction.

@Travis

https://www.nature.com/articles/s41467-018-05336-9
"...Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions. However, unlike germ-free mice, the effects of AIMD on host metabolism remain incompletely understood. Here we show the effects of AIMD to elucidate its effects on gut homeostasis, luminal signaling, and metabolism. We demonstrate that AIMD, which decreases luminal Firmicutes and Bacteroidetes species, decreases baseline serum glucose levels, reduces glucose surge in a tolerance test, and improves insulin sensitivity without altering adiposity. These changes occur in the setting of decreased luminal short-chain fatty acids (SCFAs), especially butyrate, and the secondary bile acid pool, which affects whole-body bile acid metabolism. In mice, AIMD alters cecal gene expression and gut glucagon-like peptide 1 signaling. Extensive tissue remodeling and decreased availability of SCFAs shift colonocyte metabolism toward glucose utilization. We suggest that AIMD alters glucose homeostasis by potentially shifting colonocyte energy utilization from SCFAs to glucose."

"...We then assessed the effects of AIMD on glucose homeostasis. AIMD induced a lower fasting blood glucose level compared to vehicle-treated mice (Fig. 2a) after a 4-h fast or a 16-h fast. Glucose clearance was much faster in AIMD mice, with glucose levels lower in the AIMD group compared to the vehicle-treated controls (Fig. 2b). The area under the curve (AUC) above baseline for AIMD mice was less than half of that of vehicle-treated mice (Fig. 2c). An insulin tolerance test (ITT) showed that AIMD mice had increased sensitivity to insulin compared to vehicle-treated controls (Fig. 2d). However, fasting insulin levels was not significantly different between AIMD-treated and vehicle-treated mice (Fig. 2e)."

"...To better understand the altered glucose homeostasis associated with AIMD, we investigated the expression of genes involved in metabolic pathways. Most strikingly, AIMD leads to extensive reconfiguration of the cecal enterocytes’ metabolism. The decrease in luminal SCFAs, particularly of butyric acid (Fig. 3a) and BAs (Fig. 3b, c), suggests difficulty in the absorption of fatty acids, the primary source of nutrients for enterocytes. Accordingly, compared to vehicle-treated mice, AIMD mice down-regulate genes involved in fatty acid metabolism (Fig. 6a). A schematic of transcriptional changes in the cecum is illustrated in Fig. 6b. There is a downregulation of fatty acid receptors and transporters such as free fatty acid receptor 2 (Ffar2/Gpr41) and fatty acid-binding proteins (e.g., Fabp2). SCFAs are imported into the mitochondria by carnitine palmitoyltransferases (Cpt1a, Cpt2) and processed by acyl-CoA synthetases (Acss1), both of which are downregulated in AIMD mice. Similarly, all the enzymes of fatty acid β-oxidation are downregulated in AIMD mice, including acyl-CoA dehydrogenases (Acadl, Acad8, Acad12), enoyl CoA hydratases (Echdc2), 2,4-dienoyl CoA reductase (Decr1, Decr2), hydroxyacyl-coenzyme A dehydrogenase (Hadh, Hadhb), and acetyl CoA acyltransferase (Acaa1a, Acaa1b). A parsimonious explanation of the consistent downregulation of β-oxidation genes is that the enterocytes are not using SCFAs for cellular metabolism."

"...Cecal enterocytes could be using SCFAs for energy storage through lipogenesis. However, cecal gene expression profiling again shows that this is not the case (Fig. 6a, b). AIMD mice have a downregulation of fatty acid synthase (Fasn) compared to vehicle-treated mice. There is also a downregulation of the stearoyl-CoA desaturase (Scd1) which elongates palmitate, the end product of fatty acid synthase complex, into oleate. Furthermore, the upregulation of 3-oxoacid CoA transferase (Oxct1) accompanied by a complementary downregulation in the genes involved in ketogenesis, including acyl-CoA thioesterase (Acot7) and HMG-CoA synthase (Hmgcs2), suggested increased utilization of ketone bodies as an energy source."
 
Last edited:

Regina

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I am posting this study just as an example of how important the role of endotoxin is in insulin resistance and diabetes. Similarly to the human study with aspirin, sterilizing the gut with antibiotics did not reduce the weight in the obese subjects (in this case mice). So, obesity may be a less important factor in diabetes than leaky gut and compromised liver function as a result of endotoxin overload.
In confirmation of Peat's views, the improvement of insulin sensitivity was associated with decrease in fatty acid metabolism and increase in glucose metabolism, as a result of antibiotic treatment. So, once again, burning fat may make you lean but will probably make you insulin resistant and as soon as you stop the fasting, exercising or low carb diet, the weight will massively pile on. Thus, lean often does not mean healthy, especially if the leanness is maintained with exercise, fasting, or carb restriction.

@Travis

https://www.nature.com/articles/s41467-018-05336-9
"...Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions. However, unlike germ-free mice, the effects of AIMD on host metabolism remain incompletely understood. Here we show the effects of AIMD to elucidate its effects on gut homeostasis, luminal signaling, and metabolism. We demonstrate that AIMD, which decreases luminal Firmicutes and Bacteroidetes species, decreases baseline serum glucose levels, reduces glucose surge in a tolerance test, and improves insulin sensitivity without altering adiposity. These changes occur in the setting of decreased luminal short-chain fatty acids (SCFAs), especially butyrate, and the secondary bile acid pool, which affects whole-body bile acid metabolism. In mice, AIMD alters cecal gene expression and gut glucagon-like peptide 1 signaling. Extensive tissue remodeling and decreased availability of SCFAs shift colonocyte metabolism toward glucose utilization. We suggest that AIMD alters glucose homeostasis by potentially shifting colonocyte energy utilization from SCFAs to glucose."

"...We then assessed the effects of AIMD on glucose homeostasis. AIMD induced a lower fasting blood glucose level compared to vehicle-treated mice (Fig. 2a) after a 4-h fast or a 16-h fast. Glucose clearance was much faster in AIMD mice, with glucose levels lower in the AIMD group compared to the vehicle-treated controls (Fig. 2b). The area under the curve (AUC) above baseline for AIMD mice was less than half of that of vehicle-treated mice (Fig. 2c). An insulin tolerance test (ITT) showed that AIMD mice had increased sensitivity to insulin compared to vehicle-treated controls (Fig. 2d). However, fasting insulin levels was not significantly different between AIMD-treated and vehicle-treated mice (Fig. 2e)."

"...To better understand the altered glucose homeostasis associated with AIMD, we investigated the expression of genes involved in metabolic pathways. Most strikingly, AIMD leads to extensive reconfiguration of the cecal enterocytes’ metabolism. The decrease in luminal SCFAs, particularly of butyric acid (Fig. 3a) and BAs (Fig. 3b, c), suggests difficulty in the absorption of fatty acids, the primary source of nutrients for enterocytes. Accordingly, compared to vehicle-treated mice, AIMD mice down-regulate genes involved in fatty acid metabolism (Fig. 6a). A schematic of transcriptional changes in the cecum is illustrated in Fig. 6b. There is a downregulation of fatty acid receptors and transporters such as free fatty acid receptor 2 (Ffar2/Gpr41) and fatty acid-binding proteins (e.g., Fabp2). SCFAs are imported into the mitochondria by carnitine palmitoyltransferases (Cpt1a, Cpt2) and processed by acyl-CoA synthetases (Acss1), both of which are downregulated in AIMD mice. Similarly, all the enzymes of fatty acid β-oxidation are downregulated in AIMD mice, including acyl-CoA dehydrogenases (Acadl, Acad8, Acad12), enoyl CoA hydratases (Echdc2), 2,4-dienoyl CoA reductase (Decr1, Decr2), hydroxyacyl-coenzyme A dehydrogenase (Hadh, Hadhb), and acetyl CoA acyltransferase (Acaa1a, Acaa1b). A parsimonious explanation of the consistent downregulation of β-oxidation genes is that the enterocytes are not using SCFAs for cellular metabolism."

"...Cecal enterocytes could be using SCFAs for energy storage through lipogenesis. However, cecal gene expression profiling again shows that this is not the case (Fig. 6a, b). AIMD mice have a downregulation of fatty acid synthase (Fasn) compared to vehicle-treated mice. There is also a downregulation of the stearoyl-CoA desaturase (Scd1) which elongates palmitate, the end product of fatty acid synthase complex, into oleate. Furthermore, the upregulation of 3-oxoacid CoA transferase (Oxct1) accompanied by a complementary downregulation in the genes involved in ketogenesis, including acyl-CoA thioesterase (Acot7) and HMG-CoA synthase (Hmgcs2), suggested increased utilization of ketone bodies as an energy source."
Now you tell me. (Just kiddink).
I'm happy to be facing the truth. Very grateful.
 

MrSmart

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It's amazing the amount of diseases antibiotics can target, the pathological gut flora balance in our digestive tracts today is worse than a sterile gut, which in turn would have been considered ill before the 20th century. That tells you how deteriorated health has become.
 

SOMO

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So, obesity may be a less important factor in diabetes than leaky gut and compromised liver function as a result of endotoxin overload.
In confirmation of Peat's views, the improvement of insulin sensitivity was associated with decrease in fatty acid metabolism and increase in glucose metabolism, as a result of antibiotic treatment. So, once again, burning fat may make you lean but will probably make you insulin resistant and as soon as you stop the fasting, exercising or low carb diet, the weight will massively pile on. Thus, lean often does not mean healthy, especially if the leanness is maintained with exercise, fasting, or carb restriction.

Accordingly, compared to vehicle-treated mice, AIMD mice down-regulate genes involved in fatty acid metabolism (Fig. 6a). A schematic of transcriptional changes in the cecum is illustrated in Fig. 6b. There is a downregulation of fatty acid receptors and transporters such as free fatty acid receptor 2 (Ffar2/Gpr41) and fatty acid-binding proteins (e.g., Fabp2). Similarly, all the enzymes of fatty acid β-oxidation are downregulated in AIMD mice...
...accompanied by a complementary downregulation in the genes involved in ketogenesis, including acyl-CoA thioesterase (Acot7) and HMG-CoA synthase (Hmgcs2), suggested increased utilization of ketone bodies as an energy source
."

I think even non-diabetics can achieve a level of blood ketones that becomes metabolically disruptive, but LC definitely causes insulin resistance.
14 Years on a Low-Carb/Ketogenic Diet:
HVW2Nnr.png
Xoilnwh.png


(Being in a state of Ketosis and supposed Fatty Acid Oxidation obviously does not result in all of the fat on your body supposedly being burned off via FAO or lipolysis.)

I absolutely despise when people body-shame others, especially the obese who are often struggling greatly to sort out their health problems, but this guy makes a living peddling this low-carb bull**** even though it's clearly not working for him. I've read research on this board that indicates an increase in carbohydrate consumption also causes increase in Glucose Oxidation, but there is no parallel mechanism when it comes to fat intake - that is, FAO is not increased just because you consume more fat, even in a Low-Insulin state. I think an organization called NuSI also ran a study that showed a small increase in FAO during low-carb diets, but it was not enough to offset the increase in fat intake and/or calories.

@haidut Do you think disproportionate central abdominal obesity could be evidence that LPS/endotoxin damage can be limited solely to the gut? Do you think it is possible that LPS can stay quarantined within the intestinal tract (without systemic absorption) and cause abdominal obesity? By extension, can LPS that is absorbed systemically travel to another part of the body and cause visible fat gain there?
I ask because it seems like this guy has true abdominal fat which is disproportionate to the rest of his body. His abdominal area is in the morbidly obese range, but his arms and legs aren't nearly as big proportionately. It's possible antibiotics may help this guy, but someone with his diet and size taking antibiotics - I believe the "die-off" of bacteria killed by the antibiotic could be re-absorbed and cause more issues, if someone's gut barrier has already been damaged by LPS (which I believe he has.) And combination with charcoal would decrease effectiveness of the antibiotic itself, yes?




It's very interesting that different people deposit fat in different parts of their body, and some deposit it pretty equally all throughout. I know LPS that enters the bloodstream can cause cardiac destruction, but assuming it is neutralized by the immune system before it gets too far from the intestinal tract, is it possible local adiposopathy would develop, but other areas of the body would be unaffected? I've also seen women with disproportionately large buttocks, generally African or Hispanic, so would sterilizing the gut cause "spot reduction" of gluteal fat? Mainstream says you can't reduce fat in one spot (spot reduction), but this has not been my experience, and it seems the opposite is true - that you can gain fat in one area but not in others (within some threshold.)

Image-240.png

NSFW historical photos
C8LXQ_7UIAAKe3g.jpg
 
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haidut

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14 Years on a Low-Carb/Ketogenic Diet:
HVW2Nnr.png
Xoilnwh.png


(Being in a state of Ketosis and supposed Fatty Acid Oxidation obviously does not result in all of the fat on your body supposedly being burned off via FAO or lipolysis.)

I absolutely despise when people body-shame others, especially the obese who are often struggling greatly to sort out their health problems, but this guy makes a living peddling this low-carb bull**** even though it's clearly not working for him. I've read research on this board that indicates an increase in carbohydrate consumption also causes increase in Glucose Oxidation, but there is no parallel mechanism when it comes to fat intake - that is, FAO is not increased just because you consume more fat, even in a Low-Insulin state. I think an organization called NuSI also ran a study that showed a small increase in FAO during low-carb diets, but it was not enough to offset the increase in fat intake and/or calories.

@haidut Do you think disproportionate central abdominal obesity could be evidence that LPS/endotoxin damage can be limited solely to the gut? Do you think it is possible that LPS can stay quarantined within the intestinal tract (without systemic absorption) and cause abdominal obesity? By extension, can LPS that is absorbed systemically travel to another part of the body and cause visible fat gain there?
I ask because it seems like this guy has true abdominal fat which is disproportionate to the rest of his body. His abdominal area is in the morbidly obese range, but his arms and legs aren't nearly as big proportionately. It's possible antibiotics may help this guy, but someone with his diet and size taking antibiotics - I believe the "die-off" of bacteria killed by the antibiotic could be re-absorbed and cause more issues, if someone's gut barrier has already been damaged by LPS (which I believe he has.) And combination with charcoal would decrease effectiveness of the antibiotic itself, yes?




It's very interesting that different people deposit fat in different parts of their body, and some deposit it pretty equally all throughout. I know LPS that enters the bloodstream can cause cardiac destruction, but assuming it is neutralized by the immune system before it gets too far from the intestinal tract, is it possible local adiposopathy would develop, but other areas of the body would be unaffected? I've also seen women with disproportionately large buttocks, generally African or Hispanic, so would sterilizing the gut cause "spot reduction" of gluteal fat? Mainstream says you can't reduce fat in one spot (spot reduction), but this has not been my experience, and it seems the opposite is true - that you can gain fat in one area but not in others (within some threshold.)

Image-240.png

NSFW historical photos
C8LXQ_7UIAAKe3g.jpg

Yes, endotoxin can and IS usully localized mostly to the gut. Its absorption into the bloodstream is due to several factors such as eating foods that promote the gut leakiness due to various gum additives or PUFA content, excessive alcohol intake which does the same, and above all chronic stress. Peat wrote a few times that even several minutes of notable stress causes measurable increase in endotoxin levels in the blood. With age, the combination of these factors over the years results in chronically compromised gut barrier and thus chronic low-grade endotoxemia. Taking low dose antibiotics as Peat does 2-3 times weekly is probably warranted for most people over 40 who carry extra weight in the abdominal area.
 

bzmazu

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" Taking low dose antibiotics as Peat does 2-3 times weekly is probably warranted for most people over 40 who carry extra weight in the abdominal area." Didn't know this...could you elaborate?....
 

haidut

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" Taking low dose antibiotics as Peat does 2-3 times weekly is probably warranted for most people over 40 who carry extra weight in the abdominal area." Didn't know this...could you elaborate?....

It is scattered around the forum, but when asked about keeping gut clean aside from carrot salad and charcoal, he said taking lower dose penicillin or tetracycline (~50mg) a few times weekly keeps the bacteria from overgrowing. It does not sterilize the gut though, for that much higher doses and longer treatment is needed. But the lower dose antibiotics keep the bacteria from overpopulating.
 

lvysaur

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but other areas of the body would be unaffected? I've also seen women with disproportionately large buttocks, generally African or Hispanic, so would sterilizing the gut cause "spot reduction" of gluteal fat?

African people have higher estrogen than whites, who in turn have higher estrogen than Asians. This pretty much corresponds perfectly to butt size, with black > white > Asian.

The Hispanic connection is overrated, and whatever trend exists does so solely because of the presence of African ancestry mixed into many Hispanic people. Actual American Natives, both north and south, have very flat butts.

Additionally, the women you posted are not typical Africans, but instead San people, who have even larger butts. I'm not aware of their estrogen levels.

Regarding spot reduction, I remember seeing things about beta adrenaline and gluteal fat burning. Lower body fat stores are more polyunsaturated than upper body ones, so I've always thought of them as an adaptation to starvation--for example Asians have the flattest butts, but are also the skinniest in general. Lactase persistence is probably also a starvation adaptation, and Anglos definitely have more weight problems than Slavs--and of course Asians are the only race without any widespread lactase persist.
 
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dbh25

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So, once again, burning fat may make you lean but will probably make you insulin resistant and as soon as you stop the fasting, exercising or low carb diet, the weight will massively pile on.
I'd try the fasting or exercising, and wouldn't stop the regimen if it worked, instead of being overweight and pretending it is healthy.
 

haidut

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I'd try the fasting or exercising, and wouldn't stop the regimen if it worked

The point is that it does not work, and by work I mean keep you healthy. By exercising, you are forcefully burning calories through stress (cortisol/adrenaline) and that has been shown to be highly detrimental. The only exercise that is beneficial is glycogen-bound - e.g. weight lifting done in a way that builds muscle and keeps lactate at bay, walking at a pace that allows you to hold a conversation without breathing through your mouth, maybe even running (subject to the same restrictions). Exercise may work when you are in your 20s and can produce enough DHEA to counter the cortisol/adrenaline from the exertion. Once your gonadal steroids and pregnenolone/DHEA start to decline (30+ yo) then exercise (at least the officially recommended forms of it) becomes nothing but serious stress that is entirely detrimental and it pushes you further into the hole of insulin resistance and obesity. It fits perfectly into the narrative "life is a struggle" and that gets applied into every aspect of your life - your health, your work, your personal relationships, even your pastime activities. Who do you think benefits from that narrative?
Countless human experiments showed that only higher average/sustained RMR is associated with better health. In other words, higher metabolic rate (MR) that is NOT due to exertion. Elevated MR due to exertion, or lowered MR due to fasting are not healthy and invariably lead to serious issues down the road. Nobody is saying obese people are healthy. But, on average, they are probably far less unhealthy than the lean ghosts running around to exhaustion. If somebody is lean without working themselves to death, then yes, that is good sign. But if somebody is lean only because they keep driving themselves into the wall...well, I think it is quite obvious how healthy that is.
We must have discussed this at least 100 times on the forum. Namely, weight gain and obesity are endocrine problems, driven by low thyroid, cortisol, adrenaline, estrogen, and PUFA. Gorging yourself in SFA may also make you fat but it is much harder to accomplish simply because eating a diet containing mostly SFA is not nearly as easy to accomplish as loading up on PUFA from virtually anything commercial we buy. Piling stress on top of that is the last thing anybody needs.
https://raypeatforum.com/community/...-requires-cortisol-blockade-to-reverse.20121/

FYI, many doctors in smaller clinics around the USA are starting to use glucocorticoid antagonists like RU486 for treating diabetes and pre-diabetes. Big Pharma is racing to approve 11b-HSD1 inhibitors (to lower cortisol synthesis) for treating the same conditions. I wonder why...Probably because exercise "works" so well despite 50+ years of public policy in favor of it. But don't worry, the narrative "life is a struggle" will continue as it is integral in keeping everybody blind and docile.
Selective Inhibitors of 11β-Hydroxysteroid Dehydrogenase Type 1 for Patients With Metabolic Syndrome: Is the Target Liver, Fat, or Both?

And finally, this is from Ray's newsletter dated January 2017.
"...The heart is more susceptible to infarction during fasting than after a meal (Liepinsh, et al., 2014). A two day fast causes both diabetics' and normal people's glucose tolerance to deteriorate, and when diabetic men were put on a 75% carbohydrate diet their glucose tolerance was better than on a 44% carbohydrate diet (Anderson, 1977). The high carbohydrate diet improved the men's insulin sensitivity, and fasting, similar to a high fat diet, impairs insulin sensitivity."

So, all other things being equal, biochemically speaking fasting <=> exhaustive exercise. Especially the "endurance" type promoted so much.
 
Last edited:

LeeRoyJenkins

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The point is that it does not work, and by work I mean keep you healthy. By exercising, you are forcefully burning calories through stress (cortisol/adrenaline) and that has been shown to be highly detrimental. The only exercise that is beneficial is glycogen-bound - e.g. weight lifting done in a way that builds muscle and keeps lactate at bay, walking at a pace that allows you to hold a conversation without breathing through your mouth, maybe even running (subject to the same restrictions). Exercise may work when you are in your 20s and can produce enough DHEA to counter the cortisol/adrenaline from the exertion. Once your gonadal steroids and pregnenolone/DHEA start to decline (30+ yo) then exercise (at least the officially recommended forms of it) becomes nothing but serious stress that is entirely detrimental and it pushes you further into the hole of insulin resistance and obesity. It fits perfectly into the narrative "life is a struggle" and that gets applied into every aspect of your life - your health, your work, your personal relationships, even your pastime activities. Who do you think benefits from that narrative?
Countless human experiments showed that only higher average/sustained RMR is associated with better health. In other words, higher metabolic rate (MR) that is NOT due to exertion. Elevated MR due to exertion, or lowered MR due to fasting are not healthy and invariably lead to serious issues down the road. Nobody is saying obese people are healthy. But, on average, they are probably far less unhealthy than the lean ghosts running around to exhaustion. If somebody is lean without working themselves to death, then yes, that is good sign. But if somebody is lean only because they keep driving themselves into the wall...well, I think it is quite obvious how healthy that is.
We must have discussed this at least 100 times on the forum. Namely, weight gain and obesity are endocrine problems, driven by low thyroid, cortisol, adrenaline, estrogen, and PUFA. Gorging yourself in SFA may also make you fat but it is much harder to accomplish simply because eating a diet containing mostly SFA is not nearly as easy to accomplish as loading up on PUFA from virtually anything commercial we buy. Piling stress on top of that is the last thing anybody needs.
https://raypeatforum.com/community/...-requires-cortisol-blockade-to-reverse.20121/

FYI, many doctors in smaller clinics around the USA are starting to use glucocorticoid antagonists like RU486 for treating diabetes and pre-diabetes. Big Pharma is racing to approve 11b-HSD1 inhibitors (to lower cortisol synthesis) for treating the same conditions. I wonder why...Probably because exercise "works" so well despite 50+ years of public policy in favor of it. But don't worry, the narrative "life is a struggle" will continue as it is integral in keeping everybody blind and docile.
Selective Inhibitors of 11β-Hydroxysteroid Dehydrogenase Type 1 for Patients With Metabolic Syndrome: Is the Target Liver, Fat, or Both?

And finally, this is from Ray's newsletter dated January 2017.
"...The heart is more susceptible to infarction during fasting than after a meal (Liepinsh, et al., 2014). A two day fast causes both diabetics' and normal people's glucose tolerance to deteriorate, and when diabetic men were put on a 75% carbohydrate diet their glucose tolerance was better than on a 44% carbohydrate diet (Anderson, 1977). The high carbohydrate diet improved the men's insulin sensitivity, and fasting, similar to a high fat diet, impairs insulin sensitivity."

So, all other things being equal, biochemically speaking fasting <=> exhaustive exercise. Especially the "endurance" type promoted so much.

This is the most epic and beautiful retort and wisdom I've read on this site.
 
D

danishispsychic

Guest
Salt water will sterilize the gut better than antibiotics probs.
 
D

danishispsychic

Guest
I am posting this study just as an example of how important the role of endotoxin is in insulin resistance and diabetes. Similarly to the human study with aspirin, sterilizing the gut with antibiotics did not reduce the weight in the obese subjects (in this case mice). So, obesity may be a less important factor in diabetes than leaky gut and compromised liver function as a result of endotoxin overload.
In confirmation of Peat's views, the improvement of insulin sensitivity was associated with decrease in fatty acid metabolism and increase in glucose metabolism, as a result of antibiotic treatment. So, once again, burning fat may make you lean but will probably make you insulin resistant and as soon as you stop the fasting, exercising or low carb diet, the weight will massively pile on. Thus, lean often does not mean healthy, especially if the leanness is maintained with exercise, fasting, or carb restriction.

@Travis

https://www.nature.com/articles/s41467-018-05336-9
"...Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions. However, unlike germ-free mice, the effects of AIMD on host metabolism remain incompletely understood. Here we show the effects of AIMD to elucidate its effects on gut homeostasis, luminal signaling, and metabolism. We demonstrate that AIMD, which decreases luminal Firmicutes and Bacteroidetes species, decreases baseline serum glucose levels, reduces glucose surge in a tolerance test, and improves insulin sensitivity without altering adiposity. These changes occur in the setting of decreased luminal short-chain fatty acids (SCFAs), especially butyrate, and the secondary bile acid pool, which affects whole-body bile acid metabolism. In mice, AIMD alters cecal gene expression and gut glucagon-like peptide 1 signaling. Extensive tissue remodeling and decreased availability of SCFAs shift colonocyte metabolism toward glucose utilization. We suggest that AIMD alters glucose homeostasis by potentially shifting colonocyte energy utilization from SCFAs to glucose."

"...We then assessed the effects of AIMD on glucose homeostasis. AIMD induced a lower fasting blood glucose level compared to vehicle-treated mice (Fig. 2a) after a 4-h fast or a 16-h fast. Glucose clearance was much faster in AIMD mice, with glucose levels lower in the AIMD group compared to the vehicle-treated controls (Fig. 2b). The area under the curve (AUC) above baseline for AIMD mice was less than half of that of vehicle-treated mice (Fig. 2c). An insulin tolerance test (ITT) showed that AIMD mice had increased sensitivity to insulin compared to vehicle-treated controls (Fig. 2d). However, fasting insulin levels was not significantly different between AIMD-treated and vehicle-treated mice (Fig. 2e)."

"...To better understand the altered glucose homeostasis associated with AIMD, we investigated the expression of genes involved in metabolic pathways. Most strikingly, AIMD leads to extensive reconfiguration of the cecal enterocytes’ metabolism. The decrease in luminal SCFAs, particularly of butyric acid (Fig. 3a) and BAs (Fig. 3b, c), suggests difficulty in the absorption of fatty acids, the primary source of nutrients for enterocytes. Accordingly, compared to vehicle-treated mice, AIMD mice down-regulate genes involved in fatty acid metabolism (Fig. 6a). A schematic of transcriptional changes in the cecum is illustrated in Fig. 6b. There is a downregulation of fatty acid receptors and transporters such as free fatty acid receptor 2 (Ffar2/Gpr41) and fatty acid-binding proteins (e.g., Fabp2). SCFAs are imported into the mitochondria by carnitine palmitoyltransferases (Cpt1a, Cpt2) and processed by acyl-CoA synthetases (Acss1), both of which are downregulated in AIMD mice. Similarly, all the enzymes of fatty acid β-oxidation are downregulated in AIMD mice, including acyl-CoA dehydrogenases (Acadl, Acad8, Acad12), enoyl CoA hydratases (Echdc2), 2,4-dienoyl CoA reductase (Decr1, Decr2), hydroxyacyl-coenzyme A dehydrogenase (Hadh, Hadhb), and acetyl CoA acyltransferase (Acaa1a, Acaa1b). A parsimonious explanation of the consistent downregulation of β-oxidation genes is that the enterocytes are not using SCFAs for cellular metabolism."

"...Cecal enterocytes could be using SCFAs for energy storage through lipogenesis. However, cecal gene expression profiling again shows that this is not the case (Fig. 6a, b). AIMD mice have a downregulation of fatty acid synthase (Fasn) compared to vehicle-treated mice. There is also a downregulation of the stearoyl-CoA desaturase (Scd1) which elongates palmitate, the end product of fatty acid synthase complex, into oleate. Furthermore, the upregulation of 3-oxoacid CoA transferase (Oxct1) accompanied by a complementary downregulation in the genes involved in ketogenesis, including acyl-CoA thioesterase (Acot7) and HMG-CoA synthase (Hmgcs2), suggested increased utilization of ketone bodies as an energy source."
Actually you are not correct about fasting and it " piling on ". Real fasting done correctly actually heals the gut.
 

haidut

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Actually you are not correct about fasting and it " piling on ". Real fasting done correctly actually heals the gut.

It may heal the gut due to lowering endotoxin from undigested food, but chronic fasting (as opposed to intermittent) decreases insulin sensitivity and the net effects is usually a quick "rebound" of weight when the fasting stops. The studies on the Biggest Loser are pretty telling, and some of these people did not do strenuous exercise but only fasted. I am not against fasting, intermittent one can give the gut a break and chance to heal its compromised barrier. But chronic fasting is rarely good simply because it unleashes PUFA from stores and it is hard to imagine any good effects from that.
 
D

danishispsychic

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It may heal the gut due to lowering endotoxin from undigested food, but chronic fasting (as opposed to intermittent) decreases insulin sensitivity and the net effects is usually a quick "rebound" of weight when the fasting stops. The studies on the Biggest Loser are pretty telling, and some of these people did not do strenuous exercise but only fasted. I am not against fasting, intermittent one can give the gut a break and chance to heal its compromised barrier. But chronic fasting is rarely good simply because it unleashes PUFA from stores and it is hard to imagine any good effects from that.
Have you ever tried it? No.
 

haidut

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Have you ever tried it? No.

Oh yes, I tried it for the better part of my 20s and early 30s. The combination of regular fasting, running, and avoiding carbs led me to within an inch of an MS diagnosis and all sorts of other weird neurological symptoms that simultaneously baffled and terrified the 4 different neurologists I saw, and my PCP. Prolactin and cortisol were through the roof, blood glucose was in the 100s despite me being very lean, and I was probably manic from all that cortisol. My former employer loved it. "Look at that guy that can work 24x7 and needs no sleep!", they said. Yet the doctors recommended even more fasting, exercise and avoidance of carbs.
Look, if it works for you then great. I am not here to argue, but I know what does NOT work for me and I found out the hard way.
 
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Dhair

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Oh yes, I tried it for the better part of my 20s and early 30s. The combination of regular fasting, running, and avoiding carbs led me to within an inch of an MS diagnosis and all sorts of other weird neurological symptoms that simultaneously baffled and terrified the 4 different neurologists I saw, and my PCP. Prolactin and cortisol were through the roof, blood glucose was in the 100s despite me being very lean, and I was probably manic from all that cortisol. My former employer loved it. "Look at that guy that can work 24x7 and needs no sleep!", they said. Yet the doctors recommended even more fasting, exercise and avoidance of carbs.
Look, if it works for you then great. I am not here to argue, but I know what does NOT work for me and I found out the hard way.
Haidut, I have always been curious about your neurological symptoms during this period. I think myself and others might be able to relate. Can you please describe them for us?
 
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