PUFAs Better Than Saturated Fats?

[RWilly]

@RWilly
I know your not saying those things. What I'm asking is why eat nuts in the first place? We know that PUFA isn't good and they are a significant source of PUFA. They also have minimal nutrient supply considering all of the digestive inhibitors which includes the phytic acid. Thus, the only thing that is left is perhaps the fiber and the polyphenols, in which case why not just eat fruit/ juice/ tubers/ veg?

Also, Vit e does not fully protect against the effects of PUFA in the body. Also, any Vit E in the nuts is most likely mitigated by the PUFA present concurrently.

I'm not saying that the vitamin E in nuts is protecting us from body stores of PUFA ... but I'm saying that vitamin E in the nut is protecting the amount of PUFA that is in that nut. I believe the E will continue that in vivo for that amount of PUFA.

A nut is more than PUFA though. Even in an apple, there are thousands of compounds that we don't even know about yet.

Phytochemical composition of nuts. - PubMed - NCBI
"Observational studies suggest nut consumption is inversely associated with the incidence of cardiovascular disease and cancer."

Many of those "anti-nutrients" still have benefits in certain doses. Phytic acid for instance, chelates iron and zinc, making copper more available, which is really important when dealing with infection.

 

[raypeatclips]

Hopefully you read my article, as that really explains it all, and I list a ton of studies there too. But I'll add more research here that I didn't use in the article.

Also, keep in mind that it is going to depend on what kind of microbes the person has.

Low-Carb and Ketogenic Diets in Type 1 and Type 2 Diabetes
"Reducing CHO [carb] intake with an LCD [low carb diet] is effective in reducing body weight and, in patients with type 2 diabetes, improving glycemic control, with a stronger effect with a very low carb diet (KD). However, LCD [low carb diet] and KD [ketogenic diet] may not be appropriate for all individuals. Especially in patients with type 2 diabetes, it is necessary to balance the potential increase in cardiovascular risk because of the unfavorable lipid profile observed with KD with the benefits deriving from weight loss and improvement of glycemic control. Moreover, long-term compliance with low-CHO diets is still an issue."

https://www.hindawi.com/journals/jdr/2015/206959/
"The present study uncovered a significant relationship between dairy consumption and reduced insulin sensitivity in middle-aged, nondiabetic women, suggesting that higher intakes of dairy products may be associated with greater insulin resistance."

Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia
"In recent years accumulating research has investigated the link between dietary fat and endogenous endotoxin in relation to metabolic inflammation [12,13]. Current evidence suggests that dietary fat augments circulating endotoxin concentrations and the resultant postprandial endotoxemia leads to low-grade systemic inflammation which has been implicated in the development of several metabolic diseases [1,3,14]. Intestinal derived endotoxin and the subsequent acute endotoxemia are considered major predisposing factors for inflammation associated diseases such as atherosclerosis, sepsis, obesity, type 2 diabetes and Alzheimer's [15-17]. However, the ability of different types of oil and fatty acids to facilitate uptake of intestinal endotoxin has been poorly characterized. Interestingly, saturated and n-3 polyunsaturated fatty acids (PUFA) have been shown to reciprocally modulate the LPS receptor, TLR4, and cell membrane lipid rafts [18]. This is postulated to be due to saturated fatty acids (SFA) such as lauric and myristic acid being part of the fatty acyl side chain composition of Lipid-A component of endotoxin and the ability of n-3 PUFA to reduce the potency of endotoxin when substituted in place of saturated fatty acids in lipid-A [19,20]. Thus, there is clear linkage between fatty acids (saturated, n-3 polyunsaturated, monounsaturated etc. …) and endotoxin signaling.


Dietary Fat and Risk for Type 2 Diabetes: a Review of Recent Research
https://www.sciencedirect.com/science/article/abs/pii/S0026049598900804
High-Fat Diet Is Associated with Obesity-Mediated Insulin Resistance and β-Cell Dysfunction in Mexican Americans
https://physiology.org/doi/abs/10.1152/ajpendo.1986.251.5.E576
High Fat Diet Produces Brain Insulin Resistance, Synaptodendritic Abnormalities and Altered Behavior in Mice
A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain
Short-term feeding of a ketogenic diet induces more severe hepatic insulin resistance than an obesogenic high-fat diet. - PubMed - NCBI
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Are We Going Nuts on Coconut Oil? - PubMed - NCBI


I should also mention, that 'dairy fat' is a little too inclusive for all types of dairy. Cream for instance, has a high endotoxin response. I however think that the bacterial action done to make butter (thus butyrate), along with vitamin A to help deal with pathogenic bacteria, is different. Thus, reasons for mixed results. (And I'm still on the fence about butter by the way.)

The cream endotoxin study has been debunked so many times, the cream has carageenan in it. Unless there is a new study done on it, but everyone I've seen talk about this just quotes the same stupid study.

 

[RWilly]

Very true, environment also matters. I am not looking forward to winter as such. Just have to take extra care to keep home warm, and bundle up excessively if necessary whenever going outside. Last winter I was the "weird guy" who would wear a ski mask frequently to work on cold days. It kept my face warm, so I didn't care how I looked. I also like to double, triple, quadruple, quintuple up on layers to really stay warm on the torso in particular. I think most people under-dress for the cold. I feel like you should dress warmly enough to stay reasonably comfortable for upwards of an hour (or more) of being outside. Most people only dress warm enough to survive the 5 minute walk in the parking lots.

I have low waking basal temps, which can be down to 95.7 ... yet, I'm always hot. I can usually get my temps up to about 97.3 during the day. I've had a few days at 98. I'm at high altitude though.

 

[RWilly]

Perhaps this is the mechanism that gives Omega 3 some of its anti-inflammatory properties:

Understanding intestinal lipopolysaccharide permeability and associated inflammation

"Dietary long chain n-3 PUFA such as eicosapentaenoic acid (EPA) and docoasahexaenoic acid (DHA) have been shown to antagonize LPS signaling."

 

[CLASH]

These are the studies linked in your article that address saturated fat specifically.

Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study. - PubMed - NCBI

"RESULTS: Participant serum endotoxin concentration was increased during the postprandial period after the consumption of the saturated fat meal but decreased after the n-3 meal (p < 0.05). The n-6 meal did not effect a different outcome in participant postprandial serum endotoxin concentration from that of the control meal (p > 0.05). There was no treatment meal effect on participant postprandial serum biomarkers of inflammation."

I already went over why this ia the case at length above. This study doesnt validate your point. It actually affirms my point with the bolded section.


JBC : Journal of Biological Chemistry

"Saturated fatty acids (SFAs) acylated in lipid A moiety of LPS are essential for biological activities of LPS. Thus, we determined whether these fatty acids modulate LPS-induced signaling pathways and COX-2 expression in monocyte/macrophage cells (RAW 264.7). Results show that SFAs, but not unsaturated fatty acids (UFAs), induce nuclear factor κB activation and expression of COX-2 and other inflammatory markers. This induction is inhibited by a dominant-negative Tlr4. UFAs inhibit COX-2 expression induced by SFAs, constitutively active Tlr4, or LPS. However, UFAs fail to inhibit COX-2 expression induced by activation of signaling components downstream of Tlr4."

All this study shows is that LPS bound to saturated fats activates TLR4 and COX enzymes while unsaturated fats dont, in cultured macrophages. However as I showed you above, the fat based system including chylomicrons, lipoproteins etc. bind the LPS and shuttle it to the liver before the macrophages can get it and induce an inflammatory response. Furthermore, the inflammatory response that the macrophages induce, activates the livers production of more fat based componenets like lipoproteins to further bind the LPS and transport it to the liver for detox. This article doesnt prove anything, especially when I provided the context for what actually occurs with LPS bound to saturated fats in the human body, not a cultured dish with specific cell lines of macrophages.


Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice

"The high-fat diet contained 72% fat (corn oil and lard), 28% protein, and <1% carbohydrate, as energy content (5)."

Besides the fact that the high fat diet used in this study is 72% fat, consisting of corn oil and lard this study is in mice, which I already discussed above. Did you read the studies before you posted them?


Are We Going Nuts on Coconut Oil? - PubMed - NCBI

"Several studies consistently showed consumption of coconut oil increases low-density lipoprotein cholesterol (LDL-C) and thereby could increase adverse cardiovascular health."

This one is a joke right? I posted numerous articles above with quotes showing no relationship with LDL-C as a cause of heart disease, in fact its protective. I also provided the mechanism. Also studies you posted below run contrary to this pretty directly.


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This one is a review in a rat model that the researchers created for type 2 diabetes. It would be a waste of time to go through and refute a specific rat model they developed lol.


Short-term feeding of a ketogenic diet induces more severe hepatic insulin resistance than an obesogenic high-fat diet. - PubMed - NCBI

"We show that, even though KD fed animals appear to be healthy in the fasted state, they exhibit decreased glucose tolerance to a greater extent than HFD fed animals. Furthermore, we show that this effect originates from blunted suppression of hepatic glucose production by insulin, rather than impaired glucose clearance and tissue glucose uptake. These data suggest that the early effects of HFD consumption on EGP may be part of a normal physiological response to increased lipid intake and oxidation, and that systemic insulin resistance results from the addition of dietary glucose to EGP-derived glucose."

This is exactly what I said above and doesnt show anything about endotoxin. All it shows is that when eating mostly fat with little glucose a PHYSIOLOGIC state of supposed "insuline resistance" occurs. This articles shows that the liver responds less to insulin on this diet, while the bodies glucose uptake is not impaired. The only impairment shown is that when insulin is present the liver doest shut down its glucose production as much in this state. This would make sense, if little sugar is available in the diet, and a constant supply of sugar is needed then the liver has to upregulate gluconeogenesis to meet the demand, which is what you see here. I dont know why you posted this study to he honest.



A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain

"Despite being 15% lighter (P< 0.001) than RC-fed mice because of a 17% increase in energy expenditure (P < 0.001), KD-fed mice manifested severe hepatic insulin resistance, as reflected by decreased suppression (0% vs. 100% in RC-fed mice, P < 0.01) of endogenous glucose production during the clamp"

This shows the same thing i described above. With less glucose coming in the liver produces more glucose and is less responsive to insulin, i.e. it doesnt stop producing glucose even when insulin is present.


High Fat Diet Produces Brain Insulin Resistance, Synaptodendritic Abnormalities and Altered Behavior in Mice

Another study showing physiologic insulin resistance under low carbohydrate feeding. I dont know why you posted these studies, they are somewhat irrelevant to my question and points.

https://physiology.org/doi/abs/10.1152/ajpendo.1986.251.5.E576

More of the same, all in rats, as i touched on above. Furthermore, alot of these diets are 60% fat and greater of mostly non-saturated fat sources.


https://academic.oup.com/jn/article/143/4/479/4571560

In the pictures attached for this one you'll see the fat contents of the different diets in question. The low fat diet ate 63g, the medium 75g, and the high 76g. Saturated fat content went 20g, 25g, 26g respectively. I fail to see what this study shows on the points i presented. The fat contents of the diet are marginal, especially if we look at saturated fat, unless you want to make the case that an extra 6g of saturated fat per day increase your risk of diabetes....
Furthermore the fat percentages differences where about 1-2% from the highest to lowest intakes and the BMI's only changed by 2 points from what I can see.


https://www.sciencedirect.com/science/article/abs/pii/S0026049598900804

Yes, on a 50% fat diet insulin sensitivity will decrease, however is this pathologic and from endotoxin? Also, I cant see the diet to see what fats where fed, doubt it was saturated. The change in insulin sensitivity was 6% in comparison to a 20% fat diet. More studies that affirm what I discussed with little relevance to my question.


Dietary Fat and Risk for Type 2 Diabetes: a Review of Recent Research

"According to findings from five meta-analyses, whereas fish and marine n-3 fatty acid consumption among Asian populations was associated with a decreased risk for type 2 diabetes, fish and marine n-3 fatty acid consumption among western Europeans and Americans was associated with increased incidence of the disease [7–9, 10•, 11]."

"Zhou et al. [11] reported that consuming fish about four times per month and consuming about 0.1 g of marine n-3 fatty acids per day increased the risk for type 2 diabetes. These results were based on 13 prospective cohort studies conducted in Western populations. Zheng et al. [10•], however, showed that in pooled analyses from 24 prospective cohorts, that whereas studies conducted in Western populations observed positive associations between fish and marine n-3 fatty acid consumption and type 2 diabetes, those studies conducted in Asian populations observed an inverse association."

"No clinical trials have shown that fish consumption or marine n-3 fatty acids contribute to diabetes risk [5]. Further, biomarker data from prospective cohorts that aimed to assess the fatty acids present in human plasma and serum and risk for type 2 diabetes indicate no increased risk associated with marine n-3 fatty acids and type 2 diabetes among two Finnish cohorts and one American cohort (Table (Table2)2) [28, 29, 33]. Data from Finnish men enrolled in the Metabolic Syndrome in Men Study indicated that total n-3 polyunsaturated fatty acids elucidated from erythrocyte membranes were not associated with worsening hyperglycemia or type 2 diabetes [28]. Data from another cohort of Finnish men, from the Kuopio Ischaemic Heart Disease Risk Factor Study, indicated that the highest versus the lowest quartile of eicosapentaenoic acid (EPA) + docosapentaenoic acid (DPA) + docosahexaenoic acid (DHA) from serum was associated with 33% lower risk for type 2 diabetes [29]. Similarly, in a US cohort of men and women from the multi-Ethnic Study of Atherosclerosis (MESA), higher diabetes incidence was observed for individuals with serum total n-3 fatty acid levels below the 75th percentile [33]. No associations with diabetes were observed for those with serum total n-3 fatty acids above the 75% percentile [33]. Whereas these data indicate no detrimental association between serum and plasma n-3 fatty acids and type 2 diabetes in Western cohorts, it is still difficult to draw any definitive conclusions based on them."

So we have evidence against fish oil, evidence neutral and evidence for, with conclusions of "we don't know"; this is only for insulin sensitivty. In the contrary we know is oxidizes easily and damages the liver and vasculature, while depleting antioxidants. Also, this has little to do with my questions or arguments, but even on this, there isnt support for your point.

"In a prospective study of Australian men and women, whereas total dairy consumption was not associated with type 2 diabetes or metabolic syndrome, a leading risk factor for the development of type 2 diabetes, the highest versus the lowest quartile of regular-fat dairy consumption was inversely associated with metabolic syndrome [18]. Further, in a cohort of Swedish men and women, the highest versus the lowest quintile of regular-fat dairy consumption was associated with 23% less incidence of type 2 diabetes [19]."

"Several of the fatty acids derived from milk have been neutrally or inversely associated with type 2 diabetes in prospective analyses. A meta-analysis designed to investigate the associations between saturated and trans-fat consumption and risk for chronic diseases indicated that saturated fat consumption was not associated with type 2 diabetes and ruminant derived trans-palmitoleic acid (trans-16:1, n-7) was associated with 42% lower risk for type 2 diabetes [39]. Four large cohorts, the Cardiovascular Health Study, the Multi-Ethnic Study of Atherosclerosis, the Nurses’ Health Study, and the Health Professionals Follow-Up Study cohorts, were included in the meta-analysis. Prospective biomarker data from these cohorts indicated inverse associations between circulating trans-palmitoleic acid (trans-16:1, n-7) and insulin resistance [25, 40] and incident type 2 diabetes [25, 35, 40]. Data from a smaller cohort from the USA, however, indicated that serum trans-palmitoleic acid (trans-16:1, n-7) had no association with risk for type 2 diabetes [27]."

"Prospective studies have also indicated an inverse association between saturated fats derived from dairy foods and type 2 diabetes. In Swedish men and women from the Malmö Diet and Cancer Cohort, the highest versus the lowest quintiles of saturated fatty acids with four to ten carbons, lauric acid (12:0), and myristic acid (14:0) were associated with decreased risk for type 2 diabetes [19]. The dietary assessment was an interview-based diet history method that combined a diet-recall and food-frequency questionnaire with the interview [19]. Biomarker data from plasma fatty acids has also indicated inverse associations between milk fat consumption and reduced risk for type 2 diabetes. Prospective data from 659 multi-ethnic men and women from the Insulin Resistance Atherosclerosis Study and 3333 men and women from the Nurses’ Health Study and the Health Professionals Follow-Up Study indicated that serum pentadecanoic acid (15:0), a short-term marker of milk fat consumption, was associated with 27% and 44% lower incidence of type 2 diabetes, respectively [27, 35]. Heptadecanoic acid (17:0), another short-term marker of milk fat consumption, was also inversely associated with type 2 diabetes in the Nurses’ Health Study and Health Professionals Follow-Up Study cohorts [35]."

The statements above speak for themselves. So, the only evidence in contrary to my point in the entire article was this below:


"the highest versus the lowest quartile of saturated and animal fat consumption was associated with the incidence of type 2 diabetes [21]. These findings were in agreement with those from the Malmö Diet and Cancer Cohort in which the highest versus the lowest quintile of meat consumption was associated with increased risk for type 2 diabetes [19]. Whereas these data indicate an association between meat consumption and risk for type 2 diabetes, more research is necessary to test these observations."

So 2 studies are quoted here:

1)https://www.ncbi.nlm.nih.gov/m/pubmed/25832335/
" RESULTS: Total intake of high-fat dairy products (regular-fat alternatives) was inversely associated with incident T2D (HR for highest compared with lowest quintiles: 0.77; 95% CI: 0.68, 0.87; P-trend < 0.001). Most robust inverse associations were seen for intakes of cream and high-fat fermented milk (P-trend < 0.01) and for cheese in women (P-trend = 0.02). High intake of low-fat dairy products was associated with increased risk, but this association disappeared when low- and high-fat dairy were mutually adjusted (P-trend = 0.18). Intakes of both high-fat meat (P-trend = 0.04) and low-fat meat (P-trend < 0.001) were associated with increased risk. Finally, we did not observe significant association between total dietary fat content and T2D (P-trend = 0.24), but intakes of saturated fatty acids with 4-10 carbons, lauric acid (12:0), and myristic acid (14:0) were associated with decreased risk (P-trend < 0.01)."

So meat was associated with diabetes but not total fat and saturated fat was associated with decreased risk... High fat dairy had the lowest risk, especially for some of the individual fatty acids found surprisingly in coconut oil myristic and lauric acid.

2) https://academic.oup.com/ajcn/article/105/3/723/4569701

In this study the highest intake of fat was associated with more diabetes, the thing is the highest intake of fat had 30% of calories from vegetable fats while the lowest intake had 17%. So doubling your vegetable based fat intake increases your risk of diabetes, how interesting. The difference in saturated fat intake in the lowest was 7.8% calories in lowest and 11.5% in highest. Meanwhile the change in PUFA percentage was 4.8 in the lowest and 7.2 in the highest. Linoleic acid change was 3.9% calories in the lowest and 6.1% in the highest. Furthermore if you look at the P-values the relationships are only significant for the vegetable fat, PUFA, and total fat categories, not the animal fat or saturated fat categories lol. This article, atleast if I am reading it correctly supports my point of view. See attached photos (thanks for the article btw, I think I'll use it in the book).

 

[CLASH]

@raypeatclips

I posted a cream study showing increased endotoxin with serum levels seeen as high as a gram negative infection, however the participants had no inflammatory mediators present with the high serum lps. Its a few posts back. If people actually read what I posted, it would destroy the saturated fat/ endotoxin argument totally.

 

[CLASH]

@RWilly
I posted a study showing that the vit E isn't entirely sufficient to protect against PUFA.

I'm not sure chelating zinc is a good idea in an infection. Also, does phytic acid actually chelate iron out of the bodies stores? If it doesnt, how helpful is it in an infection? Also, why not just use coffee, aspirin, pomegranate, cranberry, blood donation? I dont see the point in the nuts. There are better foods that dont have its negative effects.

 

[RWilly]

However as I showed you above, the fat based system including chylomicrons, lipoproteins etc. bind the LPS and shuttle it to the liver before the macrophages can get it and induce an inflammatory response. Furthermore, the inflammatory response that the macrophages induce, activates the livers production of more fat based componenets like lipoproteins to further bind the LPS and transport it to the liver for detox. This article doesnt prove anything, especially when I provided the context for what actually occurs with LPS bound to saturated fats in the human body, not a cultured dish with specific cell lines of macrophages.

Yes... and this is one of the methods of becoming insulin resistant if the LPS level is more than what the liver can handle, especially if choline is low ... and this is a precursor to fatty liver and diabetes.

Besides the fact that the high fat diet used in this study is 72% fat, consisting of corn oil and lard this study is in mice, which I already discussed above. Did you even read the studies before you posted them?

You were asking about a high fat diet in general. I stuck some SFA and PUFA studies in there (as this is also a PUFA thread), because I don't think a high fat diet is beneficial when dealing with gram negative bacteria, whether it is SFA, MUFA or PUFA.

Another study showing physiologic insulin resistance under low carbohydrate feeding. I dont know why you posted these studies, they are somewhat irrelevant to my question and points.

I'm not sure how these studies are irrelevant. You've been asking about fats and diabetes. Diabetes starts with insulin resistance.

Usually if a diet is high fat, it tends to be low carb. Just as a high carb diet often tends to be low fat.

But, there are studies too on over-feeding, with both high carb and high fat that cause insulin resistance.

But then again ... we also need to consider protective nutrients in combined meals, because I do think that it is possible to have both, such as having OJ after a McDonald's meal.

And lastly, here's a good read on low fat diets if you haven't read it yet by Denise Minger

In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)

I also just want to say again, that I think what Peat teaches us, is how a healthy body without the influence of microbes should function. We are however more microbe than human. And these microbes change much of our physiology. This is where we get metabolic syndrome.

 

[RWilly]

@RWilly
I posted a study showing that the vit E isn't entirely sufficient to protect against PUFA.

I'm not sure chelating zinc is a good idea in an infection. Also, does phytic acid actually chelate iron out of the bodies stores? If it doesnt, how helpful is it in an infection? Also, why not just use coffee, aspirin, pomegranate, cranberry, blood donation? I dont see the point in the nuts. There are better foods that dont have its negative effects.

Zinc is important. Heck... zinc moves copper to deal with infection. However, the body also needs to absorb copper. Iron and zinc are absorbed first, unless there is calcium. With lots of zinc and iron in a meal, we may not absorb the copper that we need. This to me is where phytic acid comes in handy. There are health benefits to phytic acid. (Again... it's the dose that matters.)

We have beneficial bacteria that can break down phytic acid and use its nutrients.

And, I agree the coffee, aspirin, pomegranate, cranberry and blood donation are all good things. But sometimes even those things are not enough.

 

[CLASH]

"Yes... and this is one of the methods of becoming insulin resistant if the LPS level is more than what the liver can handle, especially if choline is low ... and this is a precursor to fatty liver and diabetes."

Ok even so, but does this occur from eating saturated fat? I havent see a single piece of evidence that says yes. In fact I have presented a picture, and used the studies you posted to show otherwise.



"You were asking about a high fat diet in general. I stuck some PUFA studies in there too (as this is also a PUFA thread), because I don't think a high fat diet is beneficial when dealing with gram negative bacteria, whether it is SFA, MUFA or PUFA."

This is what I was asking. Its about saturated fat specifically.

@RWilly
Keto diets induce a state of adapted insulin resistance, however it is reversible, and I don't think it is due to endotoxin. With this in mind, I am not a fan of keto diets, I was merely making a point.

Can you please post studies showing that a high saturated fat diet induces diabetes specifically because of endotoxin?

I don't think this is true at all and I have posted quite a bit of evidence directly to the contrary, with plausible mechanisms explained. Also, I think to be realistic we have to clairfy what a high saturated fat diet is? I highly doubt a diet based on fruit, juice, meat, specific seafood, possibly dairy, possibly tubers and saturated fat sources like butter, coconut oil, cocoa butter, beef tallow is going to induce diabetes. I would say even 30-40% of calories from mostly saturated fat sources would pose no real issue, especially not diabetes, heart disease or even obesity.

"Usually if a diet is high fat, it tends to be low carb. Just as a high carb diet often tends to be low fat."

I think researchers define high fat as anything greater than 30% energy. This can also have a high amount of carbs.



"I'm not sure how these studies are irrelevant. You've been asking about fats and diabetes. Diabetes starts with insulin resistance."

Theres a difference between diabetes and a diabetic like state. Diabetes is from an infection, a diabetic state, which is reversible can be induced by high fat feeding. You havent shown any evidence that this high fat state causes diabetes from endotoxin, merely that eating less glucose makes the liver still produce glucose even tho insulin is present, which makes sense considering the context.



"But, there are studies too on over-feeding, with both high carb and high fat that cause insulin resistance."

Yes.



"But then again ... we also need to consider protective nutrients in combined meals, because I do think that it is possible to have both, such as having OJ after a McDonald's meal."

Yes fruit/ Juice and saturated fats are both very protective against endotoxin.



"And lastly, here's a good read on low fat diets if you haven't read it yet by Denise Minger"

In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)

Yes, I've read it, thank you.



"I also just want to say again, that I think what Peat teaches us, is how a healthy body without the influence of microbes should function. We are however more microbe than human. And these microbes change much of our physiology. This is where we get metabolic syndrome."

I agree, microbes, PUFA, iron, other heavy metals, radiation, starvation, stress, etc. are all strongly implicated in disease. Saturated fat is not, in fact it helps to protect against the microbes.

 

[RWilly]

I agree, microbes, PUFA, iron, other heavy metals, radiation, starvation, stress, etc. are all strongly implicated in disease. Saturated fat is not, in fact it helps to protect against the microbe

I guess I'm still not seeing where saturated fat is protective against microbes. I want to, but I'm still not seeing proof.

Here's additional studies:
https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=3795&context=etd;Understanding

"Furthermore, oils rich in saturated fatty acids, such as coconut oil, augmented LPS permeability and postprandial endotoxemia"

"Saturated fatty acids stimulate the TLR4 to localize into rafts and start the inflammatory signaling cascade whereas n-3 PUFA’s prevent the stimulation and localization into lipid raft (Wong et al., 2009)"

"High saturated fats have been shown to up- regulate mir-143, which plays a major role in the pathophysiology of obesity (Takanabe et al., 2008)."

Postprandial Endotoxemia Linked With Chylomicrons and Lipopolysaccharides Handling in Obese Versus Lean Men: A Lipid Dose-Effect Trial. - PubMed - NCBI

"Postprandial endotoxemia is modulated by ingested fat amount in obese men. LPS handling in plasma through chylomicrons and LBP seems critical in driving the acute inflammatory response. The pathophysiological importance of repeated postprandial endotoxemia excursions and their contribution to a vicious cycle of LBP-driven low-grade inflammation deserve further investigation in the nutritional management of cardio-metabolic risk prevention."

(Saturated fat forms chylomicrons)

Science of Fatty Acids and Inflammation

"Researchers have known for decades that gut microbes could be a source of systemic bacterial infection leading to sepsis and organ failure under a variety of medical circumstances (21). Yet, it was only recently that researchers reported that dietary fat could promote endotoxin absorption. Cani et al. (22) reported that feeding mice a diet very high in fat (i.e., 72% of total energy) over 4 wk significantly elevated circulating endotoxin concentrations compared with mice fed a low-fat control diet. The data suggest that high-fat feeding results in a chronic elevation in circulating endotoxin throughout the day and night. The authors reported that the high-fat diet altered the distribution and numbers of some of the microbial populations found in the gut. Interestingly, the authors went on to demonstrate that high-fat feeding affected a number of metabolic processes associated with metabolic syndrome (e.g., hepatic TG accumulation, elevated fasting insulin, visceral adipose tissue accumulation) in a manner similar to infusion of LPS. Elevated expression of a number of inflammation biomarkers, such as TNF-α, IL-1, and IL-6, was observed in the liver, adipose, and muscle. These responses were surprisingly similar in mice infused with LPS compared with those fed the high-fat diet."

"Recently, Mani et al. (27) demonstrated that fat source affected postprandial endotoxin absorption and transport in the sera of domestic pigs. After overnight feed deprivation, pigs were fed a meal containing 12.5% by weight (∼25% of total energy) added fat or saline (control). The meal was consumed within 10 min, then blood samples were taken hourly for 5 h. Pigs fed coconut oil, rich in SFAs, had the highest circulating concentrations of endotoxin followed by those that were fed vegetable oil and then those fed fish oil."

Diet and Diabetes: Why Saturated Fats Are the Real Enemy - UC Davis Integrative Medicine
(This is a good article on meat consumption, which is high in SFA, and the risk of type 2 diabetes.)


Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars
"Macronutrient composition of excess energy influences pathways of IHTG [intrahepatic triglyceride]: CARB increases DNL, while SAT increases and UNSAT decreases lipolysis. SAT induced the greatest increase in IHTG, insulin resistance, and harmful ceramides. Decreased intakes of SAT could be beneficial in reducing IHTG and the associated risk of diabetes."

This Kind of Fat Lowers Your Risk For Diabetes
"In one study, published in the American Journal of Clinical Nutrition, researchers from Harvard University and the Universitat Rovira i Virgili in Spain tracked 3,349 Spanish adults for about 4.5 years. Overall, they found that people who consumed higher amounts of saturated fats and animal fats were twice as likely to develop diabetes than those who consumed a lower amount.

When the researchers broke down the results by specific food type, the consumption of butter (at 12 grams a day) and cheese (at 30 grams a day) were both linked to an increased risk of diabetes. On the other hand, people who ate whole-fat yogurt actually had a lower risk than those who didn’t."

"in the Journal of Clinical Investigation, German scientists asked 14 healthy men to drink either a glass of plain water or a drink made with palm oil that contained as much saturated fat as a cheeseburger and French fries. When the participants drank one of these beverages, they experienced a reduction in insulin sensitivity, an increase in fat deposits in the liver and changes in their metabolism similar to those experienced by people with diabetes."

"For healthy people, the authors say, the occasional fatty meal likely won’t cause any permanent damage. But people who regularly eat foods high in palm oil or other saturated fats may face bigger long-term consequences, like chronic insulin resistance and fatty liver disease. Both are risk factors for diabetes."

Eat more healthy fat to reduce the risk of type 2 diabetes
"Results suggested that consuming foods rich in monounsaturated fat or polyunsaturated fat had a positive effect on blood glucose control, compared with consumption of dietary carbohydrate or saturated fat."

"for each 5 percent of dietary energy that was switched from carbohydrates or saturated fats to mono- or polyunsaturated fats, they found a drop of around 0.1 percent in HbA1c - a blood marker of long-term glucose control.

Previous research has suggested that for each 0.1 percent decrease in HbA1c, the incidence of type 2 diabetes drops by 22 percent and the chance of developing cardiovascular diseases falls by 6.8 percent."

(I believe it's the saturated fat that causes poor carb metabolism.)

https://medicalxpress.com/news/2017-02-consuming-saturated-animal-fats-diabetes.html
'Many cross-sectional or case-control studies have compared dietary fat intake of diabetic patients and healthy subjects. In the multinational, multicentre study of the Mediterranean Group for the Study of Diabetes, dietary surveys were conducted in 6 countries. The results showed that recently-diagnosed diabetics had both higher relative intake of total fat and SFA from animal fat sources compared with healthy controls. Furthermore, subjects with undiagnosed type 2 diabetes had significantly higher intake of saturated fat compared with controls [16]. The latter is relevant because these subjects did not have the chance to change their diet due to diagnosis of type 2 diabetes or dietary treatment [16].

The problem of confounding still remains. Nonetheless, these data are in line with a Dutch study on patients with newly-diagnosed diabetes; subjects who had a higher intake of total fat (40% energy, E), and in particular, saturated fat (15% E) [17]. It should be noted that cross-sectional observational studies investigating links between dietary fat quality and prediabetes/diabetes require cautious interpretation due to several sources of bias, e.g., change of diet due to obesity or prediabetes, or failure to make detailed adjustments for adiposity or physical activity."

"Diabetes incidence was positively associated with the proportions of palmitic (16:0), palmitoleic (16:1n-7), and dihomo-gamma-linolenic (20:3n-6) acids, and inversely associated with the proportion of linoleic acid in cholesterol esters. In phospholipids, there was a positive association between SFA (palmitic and stearic acid) and diabetes risk [25]."

"In this study, a 5% replacement of SFA with MUFA or carbohydrates is associated with respective risk reduction of cardiovascular disease in diabetics of 37% and 22%. Nuts, an important food source of PUFA and MUFA in this population, have been associated with lower risk of diabetes in women even after adjusting for fibre intake and various lifestyle factors"

"In a cross-sectional study of elderly Swedish men, dairy fat intake was inversely associated with several metabolic anomalies, including elevated fasting plasma glucose concentrations [36]. It was also significantly correlated with 15:0 and 17:0 in serum lipids, which can be considered biomarkers of dairy fat intake. In contrast, plasma phospholipid concentrations of 15:0 were inversely related to incidence of type 2 diabetes in a case-cohort study with 4 years of follow-up [26]. Pereira et al. found that among young adults who were overweight at baseline (but not among leaner individuals), dairy consumption was also inversely related to the incidence of metabolic factors associated with insulin resistance"

 

[CLASH]

@RWilly
It's clear to me that you either havent been reading the studies I've posted, or are either unable or unwilling to understand what I have presented to you in terms of medical information.

I'll try one last time:

"Here's additional studies:
https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=3795&context=etd;Understanding

"Furthermore, oils rich in saturated fatty acids, such as coconut oil, augmented LPS permeability and postprandial endotoxemia"

"Saturated fatty acids stimulate the TLR4 to localize into rafts and start the inflammatory signaling cascade whereas n-3 PUFA’s prevent the stimulation and localization into lipid raft (Wong et al., 2009)"

"High saturated fats have been shown to up- regulate mir-143, which plays a major role in the pathophysiology of obesity (Takanabe et al., 2008)."

Postprandial Endotoxemia Linked With Chylomicrons and Lipopolysaccharides Handling in Obese Versus Lean Men: A Lipid Dose-Effect Trial. - PubMed - NCBI

"Postprandial endotoxemia is modulated by ingested fat amount in obese men. LPS handling in plasma through chylomicrons and LBP seems critical in driving the acute inflammatory response. The pathophysiological importance of repeated postprandial endotoxemia excursions and their contribution to a vicious cycle of LBP-driven low-grade inflammation deserve further investigation in the nutritional management of cardio-metabolic risk prevention."

(Saturated fat forms chylomicrons)

Science of Fatty Acids and Inflammation

"Researchers have known for decades that gut microbes could be a source of systemic bacterial infection leading to sepsis and organ failure under a variety of medical circumstances (21). Yet, it was only recently that researchers reported that dietary fat could promote endotoxin absorption. Cani et al. (22) reported that feeding mice a diet very high in fat (i.e., 72% of total energy) over 4 wk significantly elevated circulating endotoxin concentrations compared with mice fed a low-fat control diet. The data suggest that high-fat feeding results in a chronic elevation in circulating endotoxin throughout the day and night. The authors reported that the high-fat diet altered the distribution and numbers of some of the microbial populations found in the gut. Interestingly, the authors went on to demonstrate that high-fat feeding affected a number of metabolic processes associated with metabolic syndrome (e.g., hepatic TG accumulation, elevated fasting insulin, visceral adipose tissue accumulation) in a manner similar to infusion of LPS. Elevated expression of a number of inflammation biomarkers, such as TNF-α, IL-1, and IL-6, was observed in the liver, adipose, and muscle. These responses were surprisingly similar in mice infused with LPS compared with those fed the high-fat diet."

"Recently, Mani et al. (27) demonstrated that fat source affected postprandial endotoxin absorption and transport in the sera of domestic pigs. After overnight feed deprivation, pigs were fed a meal containing 12.5% by weight (∼25% of total energy) added fat or saline (control). The meal was consumed within 10 min, then blood samples were taken hourly for 5 h. Pigs fed coconut oil, rich in SFAs, had the highest circulating concentrations of endotoxin followed by those that were fed vegetable oil and then those fed fish oil"

I went over this ad nauseum for you. Elevated post prandial LPS doesnt mean anything if it isnt causing inflammation. Saturated fats elevate LPS post prandially, yes we get it. Did you not read what I quoted for you before? Even with the elevated LPS, there isnt a concurrent increase in inflammation with saturated fats. If you saw serum levels of endotoxin that you see with people who just ate a high saturated fat meal in people who havent eaten the meal they would be in, if not on the verge of sepsis/ shock. These post prandial elevations studies mean absolutely nothing, especially in the context of how the entire lipoprotein/ bile/ chylomicron/ alkaline phosphatase system works (Which I showed you with articles I quoted previously).


"Diet and Diabetes: Why Saturated Fats Are the Real Enemy - UC Davis Integrative Medicine
(This is a good article on meat consumption, which is high in SFA, and the risk of type 2 diabetes.)"

This is a garbage article, propaganda for the plant based BS we see in the news. It doesn't show anything tangible, its some random nutritonists ramblings on saturated fat/ meat and diabetes with some observational, correlational studies thrown in, where she didnt even look at the data herself. This is like quoting webMD.


"Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars
"Macronutrient composition of excess energy influences pathways of IHTG [intrahepatic triglyceride]: CARB increases DNL, while SAT increases and UNSAT decreases lipolysis. SAT induced the greatest increase in IHTG, insulin resistance, and harmful ceramides. Decreased intakes of SAT could be beneficial in reducing IHTG and the associated risk of diabetes."

This is an overfeeding study, in the already overweight by an excess of 1000kcal/ day...


"This Kind of Fat Lowers Your Risk For Diabetes
"In one study, published in the American Journal of Clinical Nutrition, researchers from Harvard University and the Universitat Rovira i Virgili in Spain tracked 3,349 Spanish adults for about 4.5 years. Overall, they found that people who consumed higher amounts of saturated fats and animal fats were twice as likely to develop diabetes than those who consumed a lower amount.

When the researchers broke down the results by specific food type, the consumption of butter (at 12 grams a day) and cheese (at 30 grams a day) were both linked to an increased risk of diabetes. On the other hand, people who ate whole-fat yogurt actually had a lower risk than those who didn’t."

I went over this above, the quotes from this study arent supported by the data, which I pulled out for you in pictures. Read what I wrote, your wasting my time and other peoples in this thread. Stop quoting Time magazine, read the studies directly, please.



"Eat more healthy fat to reduce the risk of type 2 diabetes
"Results suggested that consuming foods rich in monounsaturated fat or polyunsaturated fat had a positive effect on blood glucose control, compared with consumption of dietary carbohydrate or saturated fat."

"for each 5 percent of dietary energy that was switched from carbohydrates or saturated fats to mono- or polyunsaturated fats, they found a drop of around 0.1 percent in HbA1c - a blood marker of long-term glucose control.

Previous research has suggested that for each 0.1 percent decrease in HbA1c, the incidence of type 2 diabetes drops by 22 percent and the chance of developing cardiovascular diseases falls by 6.8 percent."

(I believe it's the saturated fat that causes poor carb metabolism.)"

Lol more observational, correlational studies, in which you dont read the study, you quote summaries of the study from a media outlet. I dont know why you are posting a study showing that PUFA and MUFA improve insulin sensitivity, not only over saturated fat, but over carbohydrate. This study is absolute garbage and not supported by many other studies or mechanisms. Please, read what I posted previously if you want to understand fat based physiology. I dumped a ton of information in this thread, not even covering peroxidation or inflammatory mediators, solely focusing on the endotoxin issue.



https://medicalxpress.com/news/2017-02-consuming-saturated-animal-fats-diabetes.html
'Many cross-sectional or case-control studies have compared dietary fat intake of diabetic patients and healthy subjects. In the multinational, multicentre study of the Mediterranean Group for the Study of Diabetes, dietary surveys were conducted in 6 countries. The results showed that recently-diagnosed diabetics had both higher relative intake of total fat and SFA from animal fat sources compared with healthy controls. Furthermore, subjects with undiagnosed type 2 diabetes had significantly higher intake of saturated fat compared with controls [16]. The latter is relevant because these subjects did not have the chance to change their diet due to diagnosis of type 2 diabetes or dietary treatment [16].

The problem of confounding still remains. Nonetheless, these data are in line with a Dutch study on patients with newly-diagnosed diabetes; subjects who had a higher intake of total fat (40% energy, E), and in particular, saturated fat (15% E) [17]. It should be noted that cross-sectional observational studies investigating links between dietary fat quality and prediabetes/diabetes require cautious interpretation due to several sources of bias, e.g., change of diet due to obesity or prediabetes, or failure to make detailed adjustments for adiposity or physical activity."

"Diabetes incidence was positively associated with the proportions of palmitic (16:0), palmitoleic (16:1n-7), and dihomo-gamma-linolenic (20:3n-6) acids, and inversely associated with the proportion of linoleic acid in cholesterol esters. In phospholipids, there was a positive association between SFA (palmitic and stearic acid) and diabetes risk [25]."

lol so diabetes is associated with saturated, monounsaturated and polyunsaturated fats and inversely associated with linoleic acid...... Did you read the info i presented on oxidized cholesterol and heart disease...

"In this study, a 5% replacement of SFA with MUFA or carbohydrates is associated with respective risk reduction of cardiovascular disease in diabetics of 37% and 22%. Nuts, an important food source of PUFA and MUFA in this population, have been associated with lower risk of diabetes in women even after adjusting for fibre intake and various lifestyle factors"

Another summarized excerpt from a media outlet. Plus this is the same study I already went over not only previously but directly above in this same post of yours. Are you reading what your posting? Are you reading what I am writing? I dont think you are. I will attach the pictures for you again. They show the risk of diabetes broken out by types of fat eaten. Vegetable fat, PUFA and linoleic acid were the only significant trends, animal fat, and saturated fats were not.



""In a cross-sectional study of elderly Swedish men, dairy fat intake was inversely associated with several metabolic anomalies, including elevated fasting plasma glucose concentrations [36]. It was also significantly correlated with 15:0 and 17:0 in serum lipids, which can be considered biomarkers of dairy fat intake. In contrast, plasma phospholipid concentrations of 15:0 were inversely related to incidence of type 2 diabetes in a case-cohort study with 4 years of follow-up [26]. Pereira et al. found that among young adults who were overweight at baseline (but not among leaner individuals), dairy consumption was also inversely related to the incidence of metabolic factors associated with insulin resistance"


Now your just quoting random sh*t. This paragraph is stating the opposite of your point of view on saturated fats. I dont know what your doing here. Your not reading what I wrote to you in detail. Your not reading the studies you post. Your links to the studies are summaries posted on media outlets and your quoting contradictory statements to prove your point and stating things like "I feel". I'm all for a constructive debate, but this is boardering a waste of time.

Edit: fixed some grammar and spelling mistakes

 

[RWilly]

@RWilly
It's clear to me that you either havent read a single study I've posted, or are either unable or or unwilling to understand what I have presented to you in terms of medical information.

I'll try one last time here and then your on your own.

lol- I'm thinking the same thing but the other way around. I guess we will have to agree to disagree.

 

[CLASH]

@RWilly
Works for me.

 

[redsun]

I have low waking basal temps, which can be down to 95.7 ... yet, I'm always hot. I can usually get my temps up to about 97.3 during the day. I've had a few days at 98. I'm at high altitude though.

Dude what are you eating that your waking temps are that low and your temp during the day only reaches 97.3? What is your total protein and carbohydrate intake, and total calories?

 

[RWilly]

Dude what are you eating that your waking temps are that low and your temp during the day only reaches 97.3? What is your total protein and carbohydrate intake, and total calories?

Yeah... I know. I'm still playing with macros and total calories, but it doesn't seem to make a difference.

 

[RWilly]

Just came across another study:

Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity. - PubMed - NCBI

A total of 17 subjects - six people with Type II (non-insulin-dependent) diabetes mellitus, six non-obese and five obese people without diabetes - were randomised to spend two 5-week periods on a diet rich in saturated or in polyunsaturated fatty acids, in a crossover design. At the start of the study and after each dietary period, we assessed abdominal fat distribution using magnetic resonance imaging, insulin sensitivity using hyperinsulinaemic-euglycaemic clamps and fasting lipid parameters.

RESULTS:
Dietary compliance, assessed by weekly 3-day dietary records and measurement of biochemical markers, was good. Energy and fat intake appeared to be reduced on the diet rich in polyunsaturated fatty acids although body weights did not change. Insulin sensitivity and plasma low density lipoprotein cholesterol concentrations improved with the diet rich in polyunsaturated fatty acids compared with the diet rich in saturated fatty acids. There was also a decrease in abdominal subcutaneous fat area.

CONCLUSION/INTERPRETATION:
If this result is confirmed in longer-term studies, this dietary manipulation would be more readily achieved by the general population than the current recommendations and could result in considerable improvement in insulin sensitivity, reducing the risk of developing Type II diabetes.

 

[redsun]

Yeah... I know. I'm still playing with macros and total calories, but it doesn't seem to make a difference.

Ever tried just pounding tasty food down your throat? Serious question. Protein will warm you the most, then carbs. And just calories in general. You just need to eat. I only get temps that low if I were to eat like 50g of protein or less a day for a few days. The low protein in my case is obviously killing the thyroid and destroying the body's ability to keep itself warm.

 

[RWilly]

Ever tried just pounding tasty food down your throat? Serious question. Protein will warm you the most, then carbs. And just calories in general. You just need to eat. I only get temps that low if I were to eat like 50g of protein or less a day for a few days. The low protein in my case is obviously killing the thyroid and destroying the body's ability to keep itself warm.

I used to do a lot of red meat, and found that I'm definitely better off not doing red meat. However, now that I'm not doing red meat, I do find it hard to get the protein in.

Interestingly, I had a Justin's Peanut Butter cup about 30 minutes ago, and I'm thrilled to say I hit the 98 mark just now! Woot!

 

[redsun]

I used to do a lot of red meat, and found that I'm definitely better off not doing red meat. However, now that I'm not doing red meat, I do find it hard to get the protein in.

Interestingly, I had a Justin's Peanut Butter cup about 30 minutes ago, and I'm thrilled to say I hit the 98 mark just now! Woot!

Well if your temp got lower when you stopped red meat, then you are not better off. It doesnt have to be red meat though, I never mentioned that. But it does have to be animal products, which are the most bioavailable proteins. Lean chicken, seafood, eggs, dairy are viable options to increase protein intake.