High PUFA Diet Effectively The Same As Diabetes, Aging And Cancer

haidut

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This must be one of the most comprehensive and convincing studies I have come across in the last year. Both a human and a rodent study combined into one. Pretty telling as to whether you want to eat high PUFA or glucose. The patients were on a high-fat diet (35% of calories) and the fat was at least 80% PUFA. Keep in mind that this actually is NOT a high fat diet, and is close to what most people eat on a daily basis. High fat diet is clinically defined as 45% of calories or more.
Such a good study on so many levels. I suggest it strongly to everyone who has the time to read it!

Several key points:

1. The high fat (PUFA) diet induced the same negative effects on oxidative phosphorylation as established diabetes.

2. Fasting has the same effect on oxidative metabolism as a high fat (PUFA) diet and induced a diabetes-like state.

3. Free fatty acids are NOT elevated by high fat (PUFA) diet but fat influx into the muscle IS elevated and that is what drives the process of insulin resistance.

4. Free fatty acids directly inhibit insulin signaling. So, burning fat is not desirable even if it is saturated fat.

5. High fat (PUFA) diet induced strong inhibition of cytochrome C oxidase (-27%) and PGC1a/b by about 40%.

6. In Peatarian terms - high fat (PUFA) diet creates the same field as fasting, aging, diabetes, and cancer - i.e. inhibition of the ability to oxidize glucose.

http://www.ncbi.nlm.nih.gov/pubmed/15983191

"...In conclusion, HFDs in both insulin-sensitive humans and mice were associated with reduction in the expression of genes involved in oxidative capacity (e.g., genes of the electron transport chain), nuclear genes encoding mitochondrial proteins (e.g., mitochondrial carrier proteins), and those involved in mitochondrial biogenesis (e.g., PGC1α and PGC1β). These studies support the novel hypothesis that HFDs or high-fat flux explain the reduction in OXPHOS genes seen in aging, the prediabetic state, and in overt diabetes."

"...Numerous studies have implicated reduced mitochondrial biogenesis and OXPHOS in the pathogenesis of insulin resistance and type 2 diabetes (31). Our studies suggest that dietary fat is an important factor in the observed reduction in OXPHOS genes in insulin-resistant states. Microarray analysis and real-time quantitative RT-PCR results revealed a downregulation of OXPHOS genes in young men consuming a HFD, as well as transcription factors and cofactors. Additionally, we have shown that the reductions in genes involved in OXPHOS and mitochondrial biogenesis were recapitulated in an animal model of dietary-induced obesity and insulin resistance (32) and were of a much greater magnitude in mice compared with man."

"...The 3-day isoenergetic HFD significantly changed the expression of 297 genes (P < 0.01; Supplemental Table 2). By the HFD, 163 genes were upregulated, and 135 were downregulated. Six were known to be involved in OXPHOS by visual inspection or through gene ontogeny analysis (P < 0.001; Table 3). All of the OXPHOS genes were downregulated. Four genes are components of complex I, and one is a component of complex II. The remaining regulated gene is involved in mitochondrial solute transport."

"...We sought to confirm expression of these six OXPHOS genes by real-time quantitative RT-PCR. All six microarray “hits” displayed the same downward trend with quantitative RT-PCR, and three genes were “confirmed” (Fig. 1A): NDUFB5 (3.19 ± 0.26 to 2.12 ± 0.20 AU [arbitrary units], P < 0.01), SDHB (0.26 ± 0.02 to 0.19 ± 0.02 AU, P < 0.05), NDUFS1 (0.28 ± 0.03 to 0.21 ± 0.02 AU, P = 0.05), SLC25A12 (0.29 ± 0.04 to 0.19 ± 0.02 AU, P = 0.0838), NDUFB3 (0.39 ± 0.05 to 0.26 ± 0.034 AU, P = 0.1355), and NDUFV1 (0.36 ± 0.05 to 0.30 ± 0.04 AU, P = 0.3191). The magnitudes of these changes (∼20–30%) are strikingly similar to the decreases demonstrated by microarray analysis of reduced skeletal muscle OXPHOS gene expression found by Patti et al. (4) and Mootha et al. (3) in diabetic subjects."

"...As a subsequent step in elucidating effects of the diet intervention on expression of genes involved in mitochondrial function, we examined mRNA for genes in complexes III and IV using quantitative RT-PCR (Fig. 1A). Cytochrome C (complex III) and Surfeit one (complex IV) expression levels were reduced (1.13 ± 0.07 to 0.85 ± 0.05 AU, P < 0.01, and 1.10 ± 0.05 to 0.90 ± 0.05 AU, P < 0.01)."

"...Because expression levels of genes involved in the function of mitochondria decreased, we examined expression of genes known to be involved in mitochondrial biogenesis. We observed a 20% and a 25% reduction in mRNA levels in PGC1α and PGC1β, respectively (Fig. 2A); PGC1α (1.44 ± 0.08 to 1.13 ± 0.06 AU, P < 0.01) and PGC1β (2.12 ± 0.16 to 1.59 ± 0.18 AU, P < 0.05). Mitochondrial transcription factor A, TFAM, a key activator of mitochondrial transcription and its genome replication, was not significantly changed (2.00 ± 0.19 to 1.79 ± 0.19 AU, P = 0.3784), nor was nuclear respiratory factor 1, NRF1 (1.89 ± 0.13 to 1.56 ± 0.16 AU, P = 0.1398) (Fig. 2A)."

"...We next tested whether the changes in gene expression we found in the clinic were present in a murine model of HFD-induced obesity. We fed C57Bl/6J mice either a 10 or 45% fat diet for 3 weeks. We chose two murine genes from complex I; one gene each from complexes II, III, and IV; and one mitochondrial carrier protein from the human experiments. Decline in gene expression was of a greater magnitude than those seen in the human experiments. As measured by real-time quantitative RT-PCR, each gene was downregulated in high-fat–fed mice compared with controls (Fig. 1B): NDUFB5 (24.05 ± 7.89 to 2.10 ± 0.44 AU, P < 0.01), NDUFB3 (19.02 ± 6.25 to 1.82 ± 0.29 AU, P < 0.01), SDHB (10.84 ± 3.58 to 1.05 ± 0.20 AU, P < 0.01) SLC25A12 (6.14 ± 1.99 to 0.45 ± 0.11 AU, P < 0.01), CYC1 (10.41 ± 3.40 to 0.79 ± 0.13 AU, P < 0.01), and SURF1 (175.50 ± 57.35 to 13.81 ± 3.20 AU, P < 0.01)."

"...In parallel to the human experiment, we measured both PGC1α and PGC1β mRNA in these same mice. A 90% reduction in mRNA levels was observed for both PGC1α and PGC1β (Fig. 2B): PGC1α (34.63 ± 12.57 to 2.67 ± 0.31 AU, P < 0.01) and PGC1β (25.75 ± 9.03 to 1.85 ± 0.30 AU, P < 0.01)."

"...PGC1α and cytochrome C protein expression levels were reduced by ∼40% in mice consuming a HFD (Fig. 2B): PGC1α (1.31 ± 0.19 to 0.84 ± 0.07 AU, P < 0.05) and cytochrome C (1.35 ± 0.17 to 0.76 ± 0.09 AU, P < 0.01)."

"...Our results support the hypothesis that HFDs and/or high-fat flux through the mitochondria reduce the expression of nuclear genes encoding mitochondrial proteins and transcription factors involved in mitochondrial biogenesis. Both PGC1α and PGC1β were decreased by ∼20% and accompanied by a 20% reduction in OXPHOS gene expression. Previous studies suggest a link between the downregulation of PGC1 and dysregulation of OXPHOS genes. Our results are consistent with this sequence of events, and three of our OXPHOS genes found by microarray analysis were also present in the analyses of Mootha et al. (3) and Patti et al. (4). Therefore, our findings expand the view beyond the relationship between PGC1 and OXPHOS genes. We move upstream to show that increased fatty acid flux through the mitochondria decreases PGC1 expression and associates with a downregulation of expression of OXPHOS genes. It remains unclear from this experimental data whether it is increased fatty acid mitochondrial oxidation per se or some other pathway triggered by fatty acids that is responsible for the effects on gene expression."

"...Although an increase in free fatty acid concentrations was not seen in this cohort, fatty acid flux through the muscle is by necessity increased in these subjects as demonstrated by a decrease in 24-h respiratory quotient (data not shown) to match fat intake in this experimental paradigm (14). Another explanation for the reduction in the expression of these genes is that HFD decreases insulin-stimulated gene expression. Fatty acids decrease insulin signaling both in vivo and in vitro. Recent microarray studies demonstrate an upregulation of OXPHOS genes after a short-term insulin infusion (36). A reduction in insulin signaling might reduce expression of these same genes. Our studies do not identify the exact mechanism of the reduction in PGC1α, PGC1β, or their downstream targets. Rather, these studies point toward dietary fat, or increased lipolysis, as a potential source of the previously reported reduction in mitochondrial OXPHOS and subsequent mitochondrial dysfunction."

"...Our studies reveal a key question: “why would increased fatty acid flux decrease the expression of genes needed to oxidize these same fatty acids?”. Fasting is another “normal” physiological condition where fatty acid flux through skeletal muscle is increased. Surprisingly, fasting produces changes in gene expression that are strikingly similar to the pattern of fat-induced changes observed in our studies of HFDs. For example, Jagoe et al. (37) found that CASQ2 (calsequestrin 2), NDUFS1, glycogen synthase, and pyruvate dehydrogenase kinase isoenzyme 4, four genes found on our microarray “hit” list (Supplemental Table 2) and confirmed by quantitative RT-PCR (data not shown), were similarly regulated by fasting in rodents. This may explain the paradoxical decrease in systems needed to oxidize fatty acids (nuclear genes encoding mitochondrial proteins, PGC1α) when fat flux is increased during a HFD. In other words, the parallel results between fasting and HFDs suggest that fat flux through the skeletal muscle might be interpreted as a signal of fasting/starvation by the muscle cell itself. Signaling systems normally reserved for responding to energy deprivation (fasting) may be co-opted when dietary fat is increased. This hypothesis is also consistent with observed changes in the transcription of genes involved in nonoxidative metabolism (e.g., glycolysis) found on our microarray “hit” list (Supplemental Table 2)."

One of the substances that can reverse the inhibition of the ability to oxidize glucose is glycine. It successfully reverted aging cells back to their young phenotype. Here is more info:
viewtopic.php?f=75&t=7736
 

milk_lover

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WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.
 

RPDiciple

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If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?
 
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haidut

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milk_lover said:
post 102431 WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.

They said they used standard laboratory diet, which is about 80% omega-6. I sent them an email asking about the exact composition. When they respond I will post their response here.
 
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haidut

haidut

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RPDiciple said:
post 102436 If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?

While you are burning fat you will become temporarily insulin resistant. However, when the excess weight is lost and you start eating properly again there is no evidence that you will not be able to regain your insulin sensitivity. Some people prefer to do it slowly as Ray suggested, but as you can see this study suggests that intramuscular fat is still an issue even if free fatty acid are not elevated. So, losing excess fat weight is paramount for restoring insulin sensitivity. Whether you do it slow or fast would depend on context and other limitations.
 
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hmac

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haidut said:
post 102445
RPDiciple said:
post 102436 If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?

While you are burning fat you will become temporarily insulin resistant. However, when the excess weight is lost and you start eating properly again there is no evidence that you will not be able to regain your insulin sensitivity. Some people prefer to do it slowly as Ray suggested, but as you can see this study suggests that intramuscular fat is still an issue even if free fatty acid are not elevated. So, losing excess fat weight is paramount for restoring insulin sensitivity. Whether you do it slow or fast would depend on context and other limitations.
haidut said:
post 102443
milk_lover said:
post 102431 WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.

They said they used standard laboratory diet, which is about 80% omega-6. I sent them an email asking about the exact composition. When they respond I will post their response here.

Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)
 
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Amazoniac

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hmac said:
Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)
Perhaps it's safer in the context of development under concerns of malnourishment. You might find this interesting:
http://edwardjedmonds.com/neonatal-ketosis/
 
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haidut

haidut

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hmac said:
post 102521
haidut said:
post 102445
RPDiciple said:
post 102436 If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?

While you are burning fat you will become temporarily insulin resistant. However, when the excess weight is lost and you start eating properly again there is no evidence that you will not be able to regain your insulin sensitivity. Some people prefer to do it slowly as Ray suggested, but as you can see this study suggests that intramuscular fat is still an issue even if free fatty acid are not elevated. So, losing excess fat weight is paramount for restoring insulin sensitivity. Whether you do it slow or fast would depend on context and other limitations.
haidut said:
post 102443
milk_lover said:
post 102431 WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.

They said they used standard laboratory diet, which is about 80% omega-6. I sent them an email asking about the exact composition. When they respond I will post their response here.

Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)

I think both types of fat cause temporary insulin resistance through the Randle cycle, but the saturated fat does NOT have the negative effects that PUFA has on cytochrome C levels, mitochondrial biogenesis, steroid synthesis enzymes, immune system, etc. In fact, saturated fat is an uncoupler of respiration, so even though it may make you temporarily insulin resistant, it still has beneficial effect on metabolism. But still, even Peat says glucose is a preferable fuel and he tries to limit his fat intake.
I don't know much about the baby metabolism, but according to the study below PUFA is lower during pregnancy and as such in the baby. So, babies have less PUFA to start with and they can probably afford to stay in ketosis without much harm.
http://ajcn.nutrition.org/content/71/5/1262s.full
"...Pregnancy is associated with a decrease in the biochemical PUFA status, and normalization after delivery is slow. This is particularly true for docosahexaenoic acid (DHA) because, on the basis of the current habitual diet, birth spacing appeared to be insufficient for the maternal DHA status to normalize completely. Because of the decrease in PUFA status during pregnancy, the neonatal PUFA status may not be optimal. This view is supported by the lower neonatal PUFA status after multiple than after single births."

So, the above seems to suggest that babies have lower PUFA and especially lower DHA. Quiet contrary to what some "advocates" propose - i.e. babies are high in PUFA/DHA so it must be essential.
 
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hmac

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Amazoniac said:
post 102524
hmac said:
Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)
Perhaps it's safer in the context of development under concerns of malnourishment. You might find this interesting:
http://edwardjedmonds.com/neonatal-ketosis/

That's some interesting reading, thank-you.
 
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hmac

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haidut said:
post 102544
hmac said:
post 102521
haidut said:
post 102445
RPDiciple said:
post 102436 If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?

While you are burning fat you will become temporarily insulin resistant. However, when the excess weight is lost and you start eating properly again there is no evidence that you will not be able to regain your insulin sensitivity. Some people prefer to do it slowly as Ray suggested, but as you can see this study suggests that intramuscular fat is still an issue even if free fatty acid are not elevated. So, losing excess fat weight is paramount for restoring insulin sensitivity. Whether you do it slow or fast would depend on context and other limitations.
haidut said:
post 102443
milk_lover said:
post 102431 WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.

They said they used standard laboratory diet, which is about 80% omega-6. I sent them an email asking about the exact composition. When they respond I will post their response here.

Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)

I think both types of fat cause temporary insulin resistance through the Randle cycle, but the saturated fat does NOT have the negative effects that PUFA has on cytochrome C levels, mitochondrial biogenesis, steroid synthesis enzymes, immune system, etc. In fact, saturated fat is an uncoupler of respiration, so even though it may make you temporarily insulin resistant, it still has beneficial effect on metabolism. But still, even Peat says glucose is a preferable fuel and he tries to limit his fat intake.
I don't know much about the baby metabolism, but according to the study below PUFA is lower during pregnancy and as such in the baby. So, babies have less PUFA to start with and they can probably afford to stay in ketosis without much harm.
http://ajcn.nutrition.org/content/71/5/1262s.full
"...Pregnancy is associated with a decrease in the biochemical PUFA status, and normalization after delivery is slow. This is particularly true for docosahexaenoic acid (DHA) because, on the basis of the current habitual diet, birth spacing appeared to be insufficient for the maternal DHA status to normalize completely. Because of the decrease in PUFA status during pregnancy, the neonatal PUFA status may not be optimal. This view is supported by the lower neonatal PUFA status after multiple than after single births."

So, the above seems to suggest that babies have lower PUFA and especially lower DHA. Quiet contrary to what some "advocates" propose - i.e. babies are high in PUFA/DHA so it must be essential.

Yes, and I remember Peat mentioning that the placenta 'filters out' PUFA during the gestational period so your study would support that claim. As far as I know, one of the main reasons that Glucose is seen as a preferable fuel to SAFA is that it produces more Co2 - interestingly, one of the studies on the page Amazoniac linked to me seemed to suggest that Butyrate was creating more Co2 than glucose. Anyhow, my experiences on low-carb diet were terrible - but I wonder whether it would be different if one had depleted themselves of PUFA before starting.

Do you agree with Peat's assertion that the SFA/PUFA ratio is more important than absolute PUFA intake?
 
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milk_lover

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hmac said:
post 102571 Yes, and I remember Peat mentioning that the placenta 'filters out' PUFA during the gestational period so your study would support that claim. As far as I know, one of the main reasons that Glucose is seen as a preferable fuel to SAFA is that it produces more Co2 - interestingly, one of the studies on the page Amazoniac linked to me seemed to suggest that Butyrate was creating more Co2 than glucose. Anyhow, my experiences on low-carb diet were terrible - but I wonder whether it would be different if one had depleted themselves of PUFA before starting.

Do you agree with Peat's assertion that the SFA/PUFA ratio is more important than absolute PUFA intake?

Can you post the study about Butyrate? This is interesting..
 
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Spondive

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From the stuff Haidut has posted in the past and from my own experience you can get rid of insulin resistance with higher dose niaciamide and thiamine even on a standard diet of 30% fat.. Now I say not to go crazy but incorporating a somewhat Peaty diet.. Also if I was extremely sick such as cancer I would definately do these things and reduce total fat much lower even from more saturated sources to limit pufa
 

Spondive

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I am amazed and I have tried a lot of stuff in my lifetime but I have seen a tremendous effect on my health with adding in higher doses of both niacinamide and thiamine and coffee without being extreme in diet
 

hmac

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milk_lover said:
post 102576
hmac said:
post 102571 Yes, and I remember Peat mentioning that the placenta 'filters out' PUFA during the gestational period so your study would support that claim. As far as I know, one of the main reasons that Glucose is seen as a preferable fuel to SAFA is that it produces more Co2 - interestingly, one of the studies on the page Amazoniac linked to me seemed to suggest that Butyrate was creating more Co2 than glucose. Anyhow, my experiences on low-carb diet were terrible - but I wonder whether it would be different if one had depleted themselves of PUFA before starting.

Do you agree with Peat's assertion that the SFA/PUFA ratio is more important than absolute PUFA intake?

Can you post the study about Butyrate? This is interesting..

It is the first study of the post 'neonatal ketosis' on the link Amazoniac posted when quoting me a few posts above this. I can post the study in a separate thread but probably it is slightly tangential to the subject of this one. I am not particularly experienced with interpreting scientific studies so I wouldn't take my word for it!
 
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Binky

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But saturated fat makes so much more ATP, idk if it's the best to go to the extreme low fat, I assume the ability to rest and relax your muscles might depend on ATP? Since rigor mortis is characterized by complete rigidity. obviously nobody in this world has ever gone ridiculously low fat (I mean as a normal diet, not experimental diets) and some like Edward J Edmonds actually believe that saturated fat sources like butter and coconut oil can facilitate EFA deficiencies, albeit in a less aggressive manner than full on low fat.
 

schultz

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Binky said:
But saturated fat makes so much more ATP, idk if it's the best to go to the extreme low fat, I assume the ability to rest and relax your muscles might depend on ATP? Since rigor mortis is characterized by complete rigidity. obviously nobody in this world has ever gone ridiculously low fat (I mean as a normal diet, not experimental diets) and some like Edward J Edmonds actually believe that saturated fat sources like butter and coconut oil can facilitate EFA deficiencies, albeit in a less aggressive manner than full on low fat.

Interesting points you have brought up.

I don't know who Edward J Edmonds is, but he probably has a point about the Sat. Fat and EFA deficiency thing. I guess it depends how you define EFA deficiency? Mead acid ratio? If so, then a zero fat diet is actually inferior to a 20% saturated fat zero PUFA diet. If given equal calories, the latter diet will cause more weight loss and greater EFAD than the zero fat diet.
 

Amazoniac

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schultz said:
post 102678
Binky said:
But saturated fat makes so much more ATP, idk if it's the best to go to the extreme low fat, I assume the ability to rest and relax your muscles might depend on ATP? Since rigor mortis is characterized by complete rigidity. obviously nobody in this world has ever gone ridiculously low fat (I mean as a normal diet, not experimental diets) and some like Edward J Edmonds actually believe that saturated fat sources like butter and coconut oil can facilitate EFA deficiencies, albeit in a less aggressive manner than full on low fat.

Interesting points you have brought up.

I don't know who Edward J Edmonds is, but he probably has a point about the Sat. Fat and EFA deficiency thing. I guess it depends how you define EFA deficiency? Mead acid ratio? If so, then a zero fat diet is actually inferior to a 20% saturated fat zero PUFA diet. If given equal calories, the latter diet will cause more weight loss and greater EFAD than the zero fat diet.

He is (or was) a member of the forum..
 
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schultz

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Amazoniac said:
schultz said:
post 102678
Binky said:
But saturated fat makes so much more ATP, idk if it's the best to go to the extreme low fat, I assume the ability to rest and relax your muscles might depend on ATP? Since rigor mortis is characterized by complete rigidity. obviously nobody in this world has ever gone ridiculously low fat (I mean as a normal diet, not experimental diets) and some like Edward J Edmonds actually believe that saturated fat sources like butter and coconut oil can facilitate EFA deficiencies, albeit in a less aggressive manner than full on low fat.

Interesting points you have brought up.

I don't know who Edward J Edmonds is, but he probably has a point about the Sat. Fat and EFA deficiency thing. I guess it depends how you define EFA deficiency? Mead acid ratio? If so, then a zero fat diet is actually inferior to a 20% saturated fat zero PUFA diet. If given equal calories, the latter diet will cause more weight loss and greater EFAD than the zero fat diet.

He is (or was) a member of the forum..

Ohhhh okay, the forum member with the avatar of a guy holding a coffee mug (presumably himself).
 
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haidut

haidut

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hmac said:
post 102571
haidut said:
post 102544
hmac said:
post 102521
haidut said:
post 102445
RPDiciple said:
post 102436 If one wants to loose fat and eat a no fat/low fat diet but also in a decent calorie deficit this will cause your body to burn alot of bodyfat as fuel. Can you just eliminate this harms with using things like caffeine and aspirin? or do you just have to loose fat very slow to not cause any harm?

While you are burning fat you will become temporarily insulin resistant. However, when the excess weight is lost and you start eating properly again there is no evidence that you will not be able to regain your insulin sensitivity. Some people prefer to do it slowly as Ray suggested, but as you can see this study suggests that intramuscular fat is still an issue even if free fatty acid are not elevated. So, losing excess fat weight is paramount for restoring insulin sensitivity. Whether you do it slow or fast would depend on context and other limitations.
haidut said:
post 102443
milk_lover said:
post 102431 WOW Ray Peat is right again. It's very hard not to be impressed by this genius.. Did the study mention what types of PUFA used? I want to present this study to one of my family members who thinks Omega-6 is bad but Omega-3 is good.

They said they used standard laboratory diet, which is about 80% omega-6. I sent them an email asking about the exact composition. When they respond I will post their response here.

Do you think it's reasonable to assume that if the fat used in the study had the composition of, say, butter (or any mostly saturated fat) that we would have seen the same results?
I wonder whether an influx of saturated fats into the muscle would have still been interpreted as a signal of starvation?
I always have this tedious doubt in the back of my mind regarding fat as an energy substrate (SAFA) that is caused by the equally tedious and over-wrought breast milk argument: If the observations seen in this study are applicable to the burning of all fat, then a breast-fed child would be receiving a metabolically destructive and disease engendering diet... I'm looking for reasons as to why this is a silly argument ;)

I think both types of fat cause temporary insulin resistance through the Randle cycle, but the saturated fat does NOT have the negative effects that PUFA has on cytochrome C levels, mitochondrial biogenesis, steroid synthesis enzymes, immune system, etc. In fact, saturated fat is an uncoupler of respiration, so even though it may make you temporarily insulin resistant, it still has beneficial effect on metabolism. But still, even Peat says glucose is a preferable fuel and he tries to limit his fat intake.
I don't know much about the baby metabolism, but according to the study below PUFA is lower during pregnancy and as such in the baby. So, babies have less PUFA to start with and they can probably afford to stay in ketosis without much harm.
http://ajcn.nutrition.org/content/71/5/1262s.full
"...Pregnancy is associated with a decrease in the biochemical PUFA status, and normalization after delivery is slow. This is particularly true for docosahexaenoic acid (DHA) because, on the basis of the current habitual diet, birth spacing appeared to be insufficient for the maternal DHA status to normalize completely. Because of the decrease in PUFA status during pregnancy, the neonatal PUFA status may not be optimal. This view is supported by the lower neonatal PUFA status after multiple than after single births."

So, the above seems to suggest that babies have lower PUFA and especially lower DHA. Quiet contrary to what some "advocates" propose - i.e. babies are high in PUFA/DHA so it must be essential.

Yes, and I remember Peat mentioning that the placenta 'filters out' PUFA during the gestational period so your study would support that claim. As far as I know, one of the main reasons that Glucose is seen as a preferable fuel to SAFA is that it produces more Co2 - interestingly, one of the studies on the page Amazoniac linked to me seemed to suggest that Butyrate was creating more Co2 than glucose. Anyhow, my experiences on low-carb diet were terrible - but I wonder whether it would be different if one had depleted themselves of PUFA before starting.

Do you agree with Peat's assertion that the SFA/PUFA ratio is more important than absolute PUFA intake?

If Peat is right (and he usually is) that saturated fat can stop the stress response produced by PUFA in its tracks - then yes, the ratio is more important. However, the ingested PUFA will still have to be processed somehow or stored. If it is metabolized it will probably raise inflammation as the study on corn oil I posted shows - i.e. even a low percentage PUFA diet promoted inflammation and liver cancer. If it is stored, then it will have to be detoxified by the liver over time, and that still affects the liver and estrogen levels. Better to not eat it at all.
 
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