"Coconut Oil Is Pure Poison"

burtlancast

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Someone else beat her to it.

 

Hairfedup

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They're protecting their lies.

Just like the dentistry profession who will never admit poisoning milliards of people with amalgam fillings.

Not gonna happen.

Too big a crime.

I lost my hair rapidly (after gaining back quite a lot) after I had my first root canal filling with amalgam...surely there is a correlation?
 

burtlancast

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I lost my hair rapidly (after gaining back quite a lot) after I had my first root canal filling with amalgam...surely there is a correlation?

You mean they fill up the cleaned root with mercury ??
Never came across this.
 
D

danishispsychic

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Do you use deodorized coconut oil? Have you tried different brands? Non-deodorized coconut oil also upsets my stomach and I have heard the same from some people when they use coconut cream or milk.

"[...]the main problem with the unfiltered oil is that it's allergenic for many people. It also degrades quicker." Ray


If I remember it correctly, you already had this discussion with haidut and he showed you the studies.



Please provide a reference for your claim that coconut oil is a natural 5AR inhibitor.
No it wasnt that, just an immune response to not being able to digest the fat, And I believe the methyl lysine and other compounds in butter may have some compensating effects
makes total sense. i pretty much go on what i WANT to eat - and butter is a love and coconut oil repels me. i will stick with butter :) but thats just me.
 
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Jon

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Here we go again folks! This is a retort article once again BY HARVARD responding to the scrutiny Karin Michels has come under....

CNN for some reason is blocking the full text of the article from public view but I was able to get ahold of it, and per suggestion avoided linking it :)

Read on for reiteration of Harvard's STUPIDITY:

"The facts behind coconut oil is 'pure poison' claim
Updated 1:38 PM EDT August 22, 2018
Cyanide is a poison. Rattlesnake venom is a poison. Certain household products can be a poison. But coconut oil? One professor seems to think so, colliding head-on with consumers who believe it's good for them.
In her lecture at the University of Freiburg — entirely in German and posted in July — professor Karin Michels, of the university's Institute for Prevention and Tumor Epidemiology, calls the health claims surrounding coconut oil "absolute nonsense" and says it's "pure poison" for its saturated fat content and its threat to cardiovascular health. The video of her lecture has amassed close to a million views and counting.
"Coconut oil is one of the worst things you can eat," Michels said.
While others have taken a more measured view, they hardly buy into the ballyhoo. A 2016 survey in the New York Times suggested that 72% of Americans think coconut oil is healthy, versus only 37% of nutritionists polled.
"There are many claims being made about coconut oil being wonderful for lots of different things, but we really don't have any evidence of long-term health benefits," said Dr. Walter C. Willett, professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, where Michels is also an adjunct professor.
"Coconut oil is somewhere in the middle of the spectrum in terms of types of fats. It's probably better than partially hydrogenated oils, [which are] high in trans fats, but not as good as the more unsaturated plant oils that have proven health benefits, like olive and canola oil," Willett previously told CNN.
Health organizations tend to discourage the use of coconut oil, which is more than 80% saturated fat. The American Heart Association says it's better on your skin than in your food, and it recommends that no more than 5% or 6% of your daily calories come from saturated fats — about 13 grams per day. The association also advocates replacing coconut oil with "healthy fats" such as polyunsaturated fats and monounsaturated fats, like those found in canola and olive oils, avocados and fatty fish.
Coconut oil is "probably not quite as 'bad' as butter but not as good as extra virgin olive oil," Kevin Klatt, a molecular nutrition researcher at Cornell University who is studying the metabolic effects of coconut oil, previously told CNN.
Klatt cautions that we should not develop too strong of an opinion of it without more data. "But at the same time, you have to be evidence-based ... and [currently], the evidence reflects benefits for olive oil, fish, nuts and seeds — so that should be the focus in the diet."
Coconut oil is extracted from the meat of the fruit. It contains mostly saturated fat, which is also found in large quantities in butter and red meat. Like other saturated fats, coconut oil increases LDL cholesterol, commonly known as "bad" cholesterol, which has been associated with increased risk of heart disease.
But coconut oil also raises HDL, the "good" cholesterol, especially when replacing carbohydrates in the diet. This may be due to its high content of a fatty acid known as lauric acid. (This is also noted in Michel's statement summarizing her talk.)
"Coconut oil is half lauric acid, which is a little bit unique," Klatt said, as the acid seems to raise HDL more than other saturated fats and is rarely found in such high amounts in foods.
Still, though the increase in HDL seen with consumption of coconut oil may offset some of the disease risk, it's still not as good as consuming unsaturated oils, which not only raise HDL but lower LDL, according to Willett.
Complicating matters is the fact that we still don't know for sure what exactly a high HDL translates to in terms of health risk. "There's been debate about the role of HDL," Willett cautioned. "Partly because there are many forms of HDL which have different health consequences ... which has made the water murky."
For example, there are different forms of HDL that do different things. One role is to help take LDL cholesterol out of the bloodstream. "But some forms of HDL don't do that," Willett said, "so we don't know for sure that higher HDL is better."
While an elevated LDL level is used as a marker for predicting cardiovascular risk and doesn't always translate to heart attacks, experts say it's still cause for concern.
Research has found a mixed bag when it comes to saturated fats, and coconut oil in particular. A 2015 Cochrane review found that cutting back on saturated fats also lowered the risk of cardiovascular disease by 17% — but it didn't change the risk of dying, and there was no benefit to replacing these fats with protein or starchy foods.
Other research specifically on coconut oil has explored its effects on metabolism, appetite and cognitive function — but "you can't infer from ... studies what coconut oil will and will not do. We need better controlled trials," Klatt said.
"Right now, the internet is jumping the gun and going way beyond the evidence."
Like other oils, coconut oil is calorie-dense, which means consuming large amounts without reducing other calorie sources can lead to weight gain. Just one tablespoon has 120 calories, about the same as a large apple or four cups of air-popped popcorn.
"Oil is a really easy way to increase the energy density of a food. Things like almonds have a lot of fat, but it's easier to overeat pure oil than overeat pure almonds," Klatt said.
In small amounts, however, coconut oil can have a place in one's diet. But for day-to-day use, experts recommend vegetable oils such as olive, canola or soybean oil, along with nuts and seeds, as a primary source of fats in the diet.
"It's not that you have to absolutely avoid coconut oil, but rather limit coconut oil to where you really need that special flavor, like for Thai food or for baking a special dessert," Willett said.
Klatt agreed, saying that coconut oil "is certainly fine to consume occasionally, when a recipe calls for it."
© 2018 Cable News Network, Inc. A Time Warner Company. All Rights Reserved.


i suppose this proves natural selection is real though...have fun drinking your canola oil.
 

Travis

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There are also the leukotrienes, another eicosanoid class, which had been discovered based on their potency for attracting neutrophils. Its an interesting fact, though somewhat incomprehensible, that neutrophils will follow a leukotriene gradient. Yet there are three separate endogenous leukotrienes all having different potencies.They are also all made by a different fatty acid, and their subscripts denote the number of double bonds:

Mead Acid (20∶3ω−9) ⟶ leukotriene B₃

Arachidonic Acid (20∶4ω−6) ⟶ leukotriene B₄

Eicosapentaenoic Acid (20∶5ω−3) ⟶ leukotriene B₅

Based on investigations of neutrophil chemotaxis, it has been found that leukotriene B₄ has the greatest ability to attract neutrophils. The difference is chemotactic potency is substantial, with leukotriene B₄ being fivefold more potent than leukotriene B₃. The omega−3 product is practically inactive, as leukotriene B₅ has been found 5,000× less potent than leukotriene B₄. The absence of immunogenicity displayed by the omega−3 product is intuitive, perhaps a way of signalling to neutrophils they are now in the brain and hence must behave. Mead Acid has a reciprocal relationship with arachidonic acid and is only observed in 'ω−6 deficiency,' yet those in such a state could expect a more tame neutrophil response. Omega−6 fatty acids are produced by yeast and fungi, and since the neutrophil is the inherent neutralizer of this kingdom it should be no surprise that they will follow a leukotriene B₄ gradient. Helminths also synthesize and emit omega−6 fatty acids, and in a similar manner the immune attack cell specific to them—the eosinophil—is also attracted towards leukotriene B₄. These unicellular and multicellular invaders of extracellular spaces are veritable beacons for eosinophils and neutrophils in the absence of interfering dietary linoleic acid, which has the potential to 'white out' the signal with noise.


Leukotriene B₄ is not a highly complex derivative of arachidonic acid, merely a hydroxylated product, and many non-specialized cells do have the capacity to produce it. The hydroxyl groups make it water soluble, so high dietary intakes of omega−6 fatty acids would almost surely increase the circulating leukotriene B₄/(B₃ + B₅) ratio. This could attract neutrophils and eosinophils out of the interstitial spaces where they belong and into the circulation. Dietary antigens and persorbed Aspergillus spores derived from the ingestion of grains could intercalate into the vessel wall, eliciting T-cells and antibodies towards that area. Along with the generalized amplification of neutrophil activity in the circulation, consequent of leukotriene B₄, the stage is set for immunological damage to the vasculature. You may then wonder where saturated fats play a role in this? They don't; they are merely bystanders, residing in lawn chairs and watching this whole sordid affair play out.

The association of saturated fats with cardiovascular disease had been a consequent of the proposed role of cholesterol. Unsaturated fatty acids have a greater propensity for immediate liposomal formation, quickly leaving the intestines as all-lipid chylomicrons with low density. Saturated fatty acids have a proclivity for the portal vein, going towards the liver to be incorporated into circulating lipoproteins—roughly equal parts proteins and lipid. Since a good amount of cholesterol is synthesized in the liver, you have immediate basis for a statistical association right there. However, as mentioned above, sterols have greater solubility in saturated fatty acids than unsaturated ones. Since the unsaturation index also determines lipid volume, and hence density, it's easy to see why high density lipoproteins (HDL) have the most cholesterol. Based on their heavier and cholesterol-rich nature they'd been assigned a reverse-transport function and thus are often moronically-termed 'good cholesterol,' yet somehow paradoxically—to the 'Keys Hypothesis'—it had been the lower cholesterol LDL found most associated. Linus Pauling tells us that this is because LDL has more lipoprotein(a)—not to be confused with lipoprotein A—a hoop-like protein that corrals lipids yet also has a lysine-kringle domain. This lysine rich region is similar to one found on fibrinogen, lending them both substantial affinity towards damaged collagen. This functions somewhat like a 'patch,' a way of maintaining vascular integrity under low-collagen conditions—a molecular MacGyver if you will, called to the scene only during subclinical scurvy. Linus Pauling maintains that lp(a) is upregulated in low ascorbate conditions, and studies since his time verify that lp(a) is the single apoprotein most correlated with cardiovascular disease.
 
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Fractality

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Now the fanbois of Ancel Keys would have us believe that they'd be clogged silly with beaded strings of 16∶0 cholesterol conjugates and lipoprotein(a), yet they'd been entirely free of that concern. 'Cardiovascular disease' appears more like an umbrella term invoked to describe vascular pathology in general, one encompassing at least two main forms having distinct etiologies. Linus Pauling fully describes one of them, highlighting the organism's necessity to maintain high collagen synthesis rates in high-pressure arteries. The Pauling Paradigm is well-supported and highly logical, and also synergizes well with the sodium connection as blood pressure will increase vascular stress and collagen wear. Immunological mechanisms that damage collagen, such neutrophil attack, also overlay nicely and without conflict. This paradigm also best explains the small yet consistent epidemiological connection with cigarettes, and not cigars, as smokestream nitric oxide—from cigarettes' added ammonia—will reliably oxidize vitamin C into dehydroascorbate. Ascorbic acid has been shown to increase collagen synthesis rates in vitro by a factor of seven.

If vitamin c levels are sufficient, is one protected from the mechanical stress of high blood pressure due to stimulants? Or more broadly, is there any mechanism by which CVD could be induced that is NOT dependent on vitamin c levels?
 

michael94

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back when I played runescape coconut milk was an ingredient for weapon poison... maybe these "game designer" are giving use clues we arent aware of. world is strange...
 
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Jon

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back when I played runescape coconut milk was an ingredient for weapon poison... maybe these "game designer" are giving use clues we arent aware of. world is strange...

Subliminal messaging at its finest.

"He alone, who owns the youth, gains the future" -Adolf Hitler
 

Tenacity

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back when I played runescape coconut milk was an ingredient for weapon poison... maybe these "game designer" are giving use clues we arent aware of. world is strange...
It was also an ingredient in antipoison, apparently.
 

Ron J

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Natural 5AR are usually non-competitive for receptor binding, drugs are very competative and highly downregulating. This natural mild downregulating of 5AR will trigger other enzymes to upregulate conversion of DHT metabolites back into DHT eventually to compensate for a net loss of DHT.
During this window you can profit from increased androgens for performance.
So we should only worry about drugs? Flavonoids in chocolate/lycopene aren't a problem either? Basically any food source, unless it's extracted to a concentrated form?
 
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Jon

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So we should only worry about drugs? Flavonoids in chocolate/lycopene aren't a problem either? Basically any food source, unless it's extracted to a concentrated form?

Eh I'm sure they're still a problem, probably just like pufa best to avoid or minimize them. Coconut oil isn't even a for sure 5AR inhibitor as to my knowledge the study that shows that activity was in vitro. In vivo it may act very different, but I was curious if the effect may be utilized for a good purpose.
 
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5AR is an enzyme. Never heard of it having receptors or finasteride binding to androgen receptors.
You could easily have raised estrogen, some people are resistant to gyno and it takes massive estrogen to get here.
Let’s not forget that not only is it DHT but neurosteroids that come from the 5AR
My errors a meant to stimulate discussion and research.
 
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So we should only worry about drugs? Flavonoids in chocolate/lycopene aren't a problem either? Basically any food source, unless it's extracted to a concentrated form?
Yess, that is right.

Unless you can calculate the net balance or trend, you have towards, pro-whatever :P
 
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