Dairy = Essential Or Deadly?

[tankasnowgod]

Last night I had a fair bit of cheese and ice cream. I still will definitely tend to avoid very PUFA rich foods like fatty fish, vegetable oils, nuts, and limit egg intake. I keep going back to a study that was quoted on www.anabolicmen.com which clearly shows that MUFA raises T levels just as much as SFA does (they also found that a high SFA/PUFA ratio is important). I think that's part of the issue. Even when I would go 100-150 gram of fat almost purely from coconut oil, I wouldn't feel right. I now believe that MUFA really are critical for health just like SFA...

Probably one should only restrict PUFA's severely once one only has a few more lbs to lose, and so stores of PUFA are lower. I think @jamies33 said as much also.

Well, if you try and reduce PUFA intake to zero, you are either eating a zero fat diet, or eating only fat from a purely refined source (likely fully hydrogenated). You can run into nutrient deficiencies and other issues with either of these approaches, and it's this very thing that Peat talks about as to why the initial Burr experiments were flawed. In eating normal food, some amount of PUFA and MUFA are unavoidable.

 

[sebastian_r]

What is the mechanism behind which would make that happen?

There are studies showing that Coconut Oil / Lauric acid can block the conversion of DHT by inhibiting 5-ar. There are several post here on the forum about it.

 

[Cirion]

I guess this explains why Peat says the optimal coconut oil intake is very low (maybe 1 or 2 tbsp.)? More may not be better in this case...

@tankasnowgod it seems like only people who are healthy can thrive on a low PUFA diet. RP himself, @Waremu and one or two other people here do well on very low PUFA... but they're already healthy. Probably because someone who is hypo needs more nutrients than someone who is not, and an ultra low pufa diet will be lacking in sufficient nutrients for anyone other than someone healthy who has lower nutritional needs.

 

[Captain_Coconut]

Last night I had a fair bit of cheese and ice cream. I still will definitely tend to avoid very PUFA rich foods like fatty fish, vegetable oils, nuts, and limit egg intake. I keep going back to a study that was quoted on www.anabolicmen.com which clearly shows that MUFA raises T levels just as much as SFA does (they also found that a high SFA/PUFA ratio is important). I think that's part of the issue. Even when I would go 100-150 gram of fat almost purely from coconut oil, I wouldn't feel right. I now believe that MUFA really are critical for health just like SFA...

Probably one should only restrict PUFA's severely once one only has a few more lbs to lose, and so stores of PUFA are lower. I think @jamies33 said as much also.

I had a similar experience when I moved back to olive oil.

 

[Captain_Coconut]

Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids

I find this very interesting:

“Saturated fatty acids represent an essential component of bacterial endotoxins. The lipid A portion of LPS has six saturated fatty acids coupled to this structure through ester or amide bonds. The carbon chain length of these fatty acids in lipid A varies from 12 to 16 carbons. Interestingly, the replacement of these saturated fatty acids by monounsaturated or polyunsaturated fatty acids stops the pro-inflammatory activity of the LPS“

It sounds like the toxic effects of lps depend on its structure of fat saturation, and seemingly sfa is what makes it more toxic. I wonder then if the dietary fats have an influence here as well...

I wish I could find an english translation for this paper:

[The structural diversity of lipid A from gram-negative bacteria]. - PubMed - NCBI

The majority of Gram-negative bacteria are pathogenic to humans and animals. Lipopolysaccharide (LPS) is the most biologically active component of these microorganisms. This compound is also called endotoxin to emphasize its negative impact on a macroorganism. Lipid A, one of the three structural components of the LPS molecule, is responsible for the pathophysiological effects associated with Gram-negative bacteria infections. Although lipid A is considered the conservative component of endotoxin, differences in its structure among species and even strains may occur. These differences concern the type of aminosugars, the degree of substitution of the disaccharide core by fatty acids, phosphate, and/or ethanolamine, and also the type, quantity, and distribution of fatty acids. The lipid A saccharide backbone of the majority of Gram-negative bacteria consists of two glucosamine units in beta (1-->6) glycosidic linkage. Amino groups (at positions 2 and 2') and hydroxy groups (at positions 3 and 3') of glucosamines are commonly substituted by 3-hydroxyfatty acids, most often by 3-hydroxytetradecanoic acid. Other fatty acids (usually saturated, unbranched) are ester-linked to hydroxyacids by their hydroxy group. In lipid A of different microorganisms there is a high diversity of fatty acids, from mirystic (tetradecanoic, 14:0) and lauric (dodecanoic, 12:0) acids and their hydroxylated derivatives to such unique structures as cis-11-octadecenoic acid (Rhodospirillum salinarum 40), 3-hydroxy-5-dodecenoic acid (Phenylobacterium immobile), and iso-2,3-dihydroxytetradecanoic acid (Legionella pneumophila). The saccharide core of some bacterial lipid A may consist of sugars different from glucosamine, e.g., 2,3-diamino-2,3-dideoxy-D-glucose. Other substituents of this part of LPS, besides phosphate groups and ethanolamine, are beta -mannopyranose, 4-aminoarabinose, galacturonic acid, and glycine. Therefore, lipid A, though considered the relatively conservative component of endotoxin, reveals relatively large structural diversity, which influences the variety of LPS biological activity.

 

[Cirion]

I had a similar experience when I moved back to olive oil.

First cold press olive oil is quite healthy, especially if you do not cook it. MUFA's are not really suitable for very high heating.

 

[Captain_Coconut]

Fatty Acids Modulate Toll-like Receptor 4 Activation through Regulation of Receptor Dimerization and Recruitment into Lipid Rafts in a Reactive Oxygen Species-dependent Manner


“Lipid A, which possesses most of the biological activities of LPS, is acylated with hydroxy saturated fatty acids. The 3-hydroxyl groups of these saturated fatty acids are further 3-Ο-acylated by saturated fatty acids. Removal of these Ο-acylated saturated fatty acids from Lipid A not only results in complete loss of endotoxic activity, but also makes Lipid A act as an antagonist against the native Lipid A (5, 6). One or more Lipid As containing unsaturated fatty acids are known to be non-toxic and act as an antagonist against endotoxin (7, 8). In addition, deacylated lipoproteins are unable to activate TLR2 and to induce cytokine expression in monocytes (9). Together, these results suggest that saturated fatty acids acylated on Lipid A or bacterial lipoproteins play critical roles in ligand recognition and receptor activation for TLR4 and TLR2. Indeed, it is suggested that the rapid interaction of bacterial lipopeptides with plasma membrane of macrophages occurs via insertion of their acylated saturated fatty acids as determined by electron energy loss spectroscopy and freeze-fracture techniques (10, 11). TLR2 can form a heterodimer with TLR1 or TLR6, which can discriminate the molecular structure of triacyl or diacyl lipopeptides (12–14). So far there is no evidence that microbial ligands for other TLRs are acylated by saturated fatty acids.“

 

[Captain_Coconut]

On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death

 

[Alpha]

“..In contrast, UHT milk, fermented milk and most cheeses only contain low levels or trace amounts (of FBP).”

Folates and dairy products: a critical update. - PubMed - NCBI

Milk drinkers are probably fine with UHT pasteurized milk, which is most milks on the US market today. (Not too sure about Europe.) If not, go for goat milk, which seems to not have the high affinity for atuoantibody formation biovine seems to have, as goat FBP is only about 20% similar to humans.

I believe FBP and folate receptors aren't the same thing. FBP are whey soluble proteins, while folate receptor auto antibodies are formed from exposure to bovine folate receptors reaching their milk.

I don't have the answer for which fraction of milk might or might not contain folate receptors, or if protein denaturing works. Only Travis has really researched it here and can answer that.

 

[Cirion]

So do other saturated fats lower DHT or just coconut oil? I thought MCT's were the healthiest fats? Everything is so confusing. No matter how long I read and post around here I manage to get confused on a daily basis. lol.

Also confusing to me how eating a lower fat diet lowers FFA's and thus supposedly improves metabolism and yet every time I attempt to eat low fat I feel worse and no libido. I think eating a low fat diet increases FFA more than a high fat diet, at least for me, ironically enough.

 

[sebastian_r]

From experimenting and just the feel of it, i would say most fat sources with the exception of butter can have negative effects on DHT.

Tallow I'm not sure, but I like it a lot. Fires up my metabolism nicely. It has quickly become my go to fat source, since I try avoiding dairy.

 

[Cirion]

From experimenting and just the feel of it, i would say most fat sources with the exception of butter can have negative effects on DHT.

Tallow I'm not sure, but I like it a lot. Fires up my metabolism nicely. It has quickly become my go to fat source, since I try avoiding dairy.

If that's true then why do I feel my DHT is highest on high fat diets? (Subjectively by libido and mood, no actual #'s to back it up)

For me fats from ice cream, cheese, butter, chocolate, olive oil are some of the top fats for me mood and libido wise. Beef can be good too. Chocolate ice cream is like almost the ultimate. I've had such a euphoric response from chocolate ice cream sometimes that no other food does for me. There is a reason that the stereotypical woman who is emotional likes chocolate ice cream lol.

 

[sebastian_r]

Could be lower estradiol.
Olive oil can act as aromatase inhibitor.
Dairy has lots of progesterone in it.
I stopped trying to understand the impact of food on hormones. Every week something new pops up.
If I like how I feel eating something, I keep doing so.
If not, I kick it.

 

[tankasnowgod]

So do other saturated fats lower DHT or just coconut oil? I thought MCT's were the healthiest fats? Everything is so confusing. No matter how long I read and post around here I manage to get confused on a daily basis. lol.

Also confusing to me how eating a lower fat diet lowers FFA's and thus supposedly improves metabolism and yet every time I attempt to eat low fat I feel worse and no libido. I think eating a low fat diet increases FFA more than a high fat diet, at least for me, ironically enough.

I don't even know that Coconut Oil does. There was one study that showed that one of the isolated fats found in coconut oil could affect DHT in vitro, or something, but to my knowledge, it has never been shown in vivo in any animal. There are quite a few wild extrapolations out there, and the idea that coconut oil negatively impacts DHT is certainly one of them.

 

[Broken man]

I would like to see a well designed, reputable study on humans that clearly demonstrates that starch and NOT sfa is to blame for postprandial serum lps. I haven't found one yet, have you? When is the last time you consumed a starch only meal, without any SFA in the same window, and experienced endotoxemia??

SFA is the major dietary factor which contributes to increased intestinal permeability, sure starch can feed bad bacteria, but it only becomes a problem when the permeability is compromised, what compromises it according to RP?

Perceive, think, act.

I think that member "tyw" found answer for this, its something like saturated fat is detoxifying organism.

 

[TeaRex14]

Also confusing to me how eating a lower fat diet lowers FFA's and thus supposedly improves metabolism and yet every time I attempt to eat low fat I feel worse and no libido. I think eating a low fat diet increases FFA more than a high fat diet, at least for me, ironically enough.

Well the randle cycle is only half of the equation from what I understand about it. When Kyle Mamounis gave his 2016 AHS talk I think he summed up the randle cycle about as perfect as one could get. It's a switch, and when you flood your body with heavy amounts of one energy substrate (i.e carbohydrate), while restricting the other substrate (i.e fat), you start burning the glucose more efficiently.

However, this is only 50% of the process. There's several negative, stress induced, feedback loops that can prevent the proper usage of the glucose. What we want is the conversion of glucose into pyruvate. Several things can go wrong here which forces glucose conversion into lactate. B1 deficiency, biotin deicency, and endotoxin are some of the most common things that interfere with glucose pyruvate conversion. There's several other things though, and I'm really not the best at explaining any of this, lol.

 

[Cirion]

Well the randle cycle is only half of the equation from what I understand about it. When Kyle Mamounis gave his 2016 AHS talk I think he summed up the randle cycle about as perfect as one could get. It's a switch, and when you flood your body with heavy amounts of one energy substrate (i.e carbohydrate), while restricting the other substrate (i.e fat), you start burning the glucose more efficiently.

However, this is only 50% of the process. There's several negative, stress induced, feedback loops that can prevent the proper usage of the glucose. What we want is the conversion of glucose into pyruvate. Several things can go wrong here which forces glucose conversion into lactate. B1 deficiency, biotin deicency, and endotoxin are some of the most common things that interfere with glucose pyruvate conversion. There's several other things though, and I'm really not the best at explaining any of this, lol.

So how does one break the stress cycle? And I mean practically and not theoretically. There is way too much theory, most of which I've tried, but none of it really works. And I am burned out on supplements. I no longer think supplementation is the answer. I am just tired of being serotonin dominant it is so annoying.

The only things that seem to work for me do NOT include supplementation. One of the most effective strategies for me is sleep 12-13 hrs a day, but it's so hard to do that during the workweek. I guess that just means from now on going to bed the moment I get back from work I guess.

 

[TeaRex14]

So how does one break the stress cycle? And I mean practically and not theoretically. There is way too much theory, most of which I've tried, but none of it really works. And I am burned out on supplements. I no longer think supplementation is the answer. I am just tired of being serotonin dominant it is so annoying.

The only things that seem to work for me do NOT include supplementation. One of the most effective strategies for me is sleep 12-13 hrs a day, but it's so hard to do that during the workweek. I guess that just means from now on going to bed the moment I get back from work I guess.

It's really hard to say, because I think every individual has a different "trigger" that's keeping them in the stress state. If that weren't the case, then the same protocol should work for everyone, which we know it doesn't. All I know is you should definitely know when it's working and when it's not. When the oxidative metabolism is firing like it should, you'll be very warm and relaxed. You can generate heat very efficiently. For me, the game changer seemed to be reworking my macros, focusing mostly on sugar and low fiber starches, while not totally neglecting dietary fats (about 15% fat, mostly non-hydrogenated coconut oil). Also niacinamide seems to be really helpful to me for processing the huge carbohydrate load, about 1,000mgs total each day, divided doses. I do take energin, which gives me the B1 and biotin. And some anti-serotonin drugs when needed, like cypro, charcoal, and theanine.

 

[Cirion]

My main problem is that getting restful sleep is super super hard for me. No matter how 100% perfect my nutrition was for the day, it doesn't seem to give me better sleep. And if my sleep was bad, it throws the whole next day off regardless of what food or supplements or sunlight or anything that I do. That's my current stress cycle I am stuck in.

Only thing that seems to break the cycle like I say is sleep upwards of 13 hrs. Which I know isn't normal, but if it's the only way to break the cycle, then that's what I shall do.... thing is I can never do it for more than two nights in a row thanks to having to work during the week. I start to recover during the weekend then start feeling bad as lack of sleep creeps up during the workweek.

 

[TeaRex14]

My main problem is that getting restful sleep is super super hard for me. No matter how 100% perfect my nutrition was for the day, it doesn't seem to give me better sleep. And if my sleep was bad, it throws the whole next day off regardless of what food or supplements or sunlight or anything that I do. That's my current stress cycle I am stuck in.

Only thing that seems to break the cycle like I say is sleep upwards of 13 hrs. Which I know isn't normal, but if it's the only way to break the cycle, then that's what I shall do.... thing is I can never do it for more than two nights in a row thanks to having to work during the week. I start to recover during the weekend then start feeling bad as lack of sleep creeps up during the workweek.

Are you having problems getting to sleep? Or are you having issues of waking up periodically? Bag breathing can really help people dealing with insomnia. Waking up periodically throughout the night might suggest you're running out of liver glycogen before morning.