"Coconut Oil Is Pure Poison"

[Jon]

But that's naturally discarded. Unfortunately this isn't going to happen because the person who felt invincible due to eating safe fats ended up neglecting teeth care, got a nasty infection that progressed to make the earlier dyings. Still! The person left kids instead of books, and the opportunity for correction was halted when the same habit was passed to them. Over time these families were unselected and became extinct along with the coconut plantations when the ratio of oil bottles to alive customers started to increase.

So the AHA WAS RIGHT? COCONUT OIL KILLS YOU IN MYSTERIOUS WAYS.

 

[Jon]

Waiter: How would you like your canola sir?

Guest: Could you mix-in a little wheat flour and, uh.. . a bit of yeast and, uh.. . lipoperoxidize it at 375°?

Waiter: Oh, well actually: That would be quite similar to our bread option sir. Would you like to order bread since that wouldn't be charged as a 'custom' order?

Guest: Well, I do need alot of canola! I mean, quite a lot. You see, my tumor is shrinking again and I, uh.. . my health insurance plan is getting a bit steep and I, uh.. . my son, well you know.

(Waiter comes back from kitchen):

Sir, this ones on the house. We all just hope to be the AHA poster child you are one day.

(tears of admiration stream to a softly playing violin)

 

[Travis]

Since n-6 fats are in practically everything, how many grams per day do think is the tipping point where things head south? Thanks!

Well our elongation & destaturation enzymes have an inherent preference for ω−3 fatty acids, meaning that a ratio as high as 4∶1 doesn't effect the membrane's lipid profile in a terrible way. The 4∶1 ratio was the '60s Japanese ratio, and today India boasts the highest with about 30∶1. Subcontinental Indians also appear to have the highest rates of hair loss, and cancer is probably more common there than is currently diagnosed. The seed farmers had ruined some otherwise decent foods in America—i.e. pork, chicken, and their eggs—by artificially enriching them with ω−6 fatty acids. Anything grass-fed should certainly be better, and the fractional tipping point for arterial cholesterol ingression could probably be gleaned from the articles of Simopolous the Greek:

[1] Simopoulos, Artemis P. "The importance of the ratio of omega-6/omega-3 essential fatty acids." Biomedicine & pharmacotherapy (2002)
[2] Simopoulos, Artemis P. "The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases." Experimental biology and medicine (2008)
[3] Simopoulos, A. P. "Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases." Biomedicine & pharmacotherapy (2006)​

And of course there are hormonal effects to consider. All prostaglandins are not created equal, and those formed via arachidonic acid have greater potency when compared to those formed via eicosapentaenoic acid. Superficially: the difference is only in one double bond, yet our receptors can discriminate between the two. Perhaps the 2-series prostaglandins are stress signals for increasing latitude and seasonal proccesson? A lipohormal superimposition over temporal and geographic changes in the local food profile? Well maybe so, but maybe not: I suppose it could all be perfectly incidental, merely a coincidence that some peculiarity in our prostaglandin E, prostaglandin D, and leukotriene B receptors all react with increased potency upon binding the respective ω–6-derived eicosanoid.

 

[nwo2012]

Holy smokes! 60/30?? Well luckily I'm not THAT low lol. Thank you for your replies and your compliment :). Honestly this forum has made exercise a healthy thing for me. I'm a much better bodybuilder after the Street Endocrinology/Pharmocology/Biochemistry Peat Style Primer that is offered here lol. Do you still train?

Welcome. Still lift a little with the kids but restricted due to various tendons damaged. Lifted too heavy for too long whilst eating plenty of grains and PUFA!

At least this PUFA loving witch as provided lots of entertainment via this thread.

 

[AretnaP]

one small step back for man, one giant leap backwards for mankind

 

[Suikerbuik]

one small step back for man, one giant leap backwards for mankind

You're going to be famous...unfortunately. But it's inevitable, almost everyone I tried to talk to about health and fats/oils believes these news headlines more than anything - up to the point I just shut up now.

 

[Jon]

Welcome. Still lift a little with the kids but restricted due to various tendons damaged. Lifted too heavy for too long whilst eating plenty of grains and PUFA!

At least this PUFA loving witch as provided lots of entertainment via this thread.

Haha yeah some one should make a B movie about her doctoral studies starring Jane Lynch, seems like a good likeness?

You should look into bfr training. You could still make the gains and save them joints, and time!

https://scholar.google.com/scholar?...=1&oi=scholart#d=gs_qabs&p=&u=#p=TrifQruYBskJ

 

[benaoao]

just an opinion but i think all oils and fats should be limited and not seen as a required health food, rather healthier options with some added benefit of unhealthy fats

I agree with that. I don’t really care about coconut oil because the populations who have a lot of coconut live a vastly different lifestyle and may have adapted to it the same way inuits don’t go into ketosis, or Masai have low cholesterol. Don’t discount genetic pressure in those small populations.

That’s on top of people being overly sedentary and eating a lot of trash grains and whatnot. I wouldn’t recommend anything that’d lead people to think that fats are fine. Next thing you know they start pouring coconut oil everywhere.

Low fat propaganda is the most adapted to the human genre, and even then people don’t even eat less fat than before, they just buy more fat free industrial BS. High fat on top of industrial food is going to be worth billions for the Big players

 

[Hemo]

I own a treatment center. We are using various testing and compounds. I literally stumble across a means to cause a paradigm shift as related to a very large market that affects teh lives of millions of people. I have two informal cases to give enough creedance to push forward with more testing and to set various controls and test, test, test.

What comes next? Outcome study possible IRB. However, at the end of the day, most everything is questionable, even if not for intentional disinformation. By example, a nattokinease study has been put on hold for 7 years in San Diego. You can bet they are getting paid not to engage the study when you consider WARFIN, which stands for Wisconsin Alumni Research Fund, thats right the University of Wisconsin profits from warfarin scripts, and others who have skin in the game, probably have paid off I believe USC to not engage the study, so it just sits out there.

My way around it: I am having the test subjects sign HIPPA waivers, remove their names and critical ID information, serialize them, and literally publish videos and actual test results. We will engage the other conventional means of outcome and IRB, but I know what I can see and feel and repeat...the rest of it is literally just a political volleyball.

Take the Yale guy on NAD. He pushes NR and was referring to the precursor as NAD+. I called him out on facebook. They no longer refer to their elisium product as NAD. Same thing with Patch MD, look at their NAD patch, it is void of NAD. I wanted to use the PAtch MD Ubiquinol, no ubiquinol in it, fish oil and he admitted it in writting.

Boards and forums like this one give me more insight into reality that 100 studies. I still use studies as a general means of getting a "possible" investigative framework, but I trust no one and test everything. When a bedridden man walks for the first time in 1.5 years. When lab results return time and time and time again as improved, then the empirical meets the actual and reality can proceed.

 

[Hemo]

pissing myself.....i use vegetable oil to lube my garbage disposal!

 

[Jon]

I own a treatment center. We are using various testing and compounds. I literally stumble across a means to cause a paradigm shift as related to a very large market that affects teh lives of millions of people. I have two informal cases to give enough creedance to push forward with more testing and to set various controls and test, test, test.

What comes next? Outcome study possible IRB. However, at the end of the day, most everything is questionable, even if not for intentional disinformation. By example, a nattokinease study has been put on hold for 7 years in San Diego. You can bet they are getting paid not to engage the study when you consider WARFIN, which stands for Wisconsin Alumni Research Fund, thats right the University of Wisconsin profits from warfarin scripts, and others who have skin in the game, probably have paid off I believe USC to not engage the study, so it just sits out there.

My way around it: I am having the test subjects sign HIPPA waivers, remove their names and critical ID information, serialize them, and literally publish videos and actual test results. We will engage the other conventional means of outcome and IRB, but I know what I can see and feel and repeat...the rest of it is literally just a political volleyball.

Take the Yale guy on NAD. He pushes NR and was referring to the precursor as NAD+. I called him out on facebook. They no longer refer to their elisium product as NAD. Same thing with Patch MD, look at their NAD patch, it is void of NAD. I wanted to use the PAtch MD Ubiquinol, no ubiquinol in it, fish oil and he admitted it in writting.

Boards and forums like this one give me more insight into reality that 100 studies. I still use studies as a general means of getting a "possible" investigative framework, but I trust no one and test everything. When a bedridden man walks for the first time in 1.5 years. When lab results return time and time and time again as improved, then the imperical meets the actual and reality can proceed.

Thank you @Hemo for being on team good guys :)

 

[General Orange]

Zinc only inhibits 5-AR at high concentrations (human dose 50+ mg) perhaps signifying testicular toxicity. It potentiates 5-AR, testosterone, luteinizing hormone, androgen receptors and lowers estrogen receptors in normal concentrations compared to deficiency.

You are right, my bad. I looked it up, zinc is pro androgen after oral administration. And inhibiting 5AR at high concentrations in vitro.

 

[General Orange]

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.

I take back what I said earlier, coz in retrospect, DHT is more beneficial for performance hehe.

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

Maybe it was a poor choice of words, but Enzymes are "receptors" in the sense that they receive a molecule and chop 'm up or convert it into something. Finasteride does have influence on the 5AR enzyme expression so that it decreases them on tissue long term. But this "receptor" expression is indeed (also according to Peat) not a good term.

 

[Jon]

I take back what I said earlier, coz in retrospect, DHT is more beneficial for performance hehe.



Maybe it was a poor choice of words, but Enzymes are "receptors" in the sense that they receive a molecule and chop 'm up or convert it into something. Finasteride does have influence on the 5AR enzyme expression so that it decreases them on tissue long term. But this "receptor" expression is indeed (also according to Peat) not a good term.

Pastured Butter for life now.

 

[General Orange]

Maybe the reasoning behind the claim that "coconut oil being like a poison" is that for it's metabolism:

• Does not need bile acid or pancreatic lipase
  
• Travels directly to the liver, by using portal vein and not lymphatic
• Does not need Cholesterol for transport, in contrast to long chain fatty acids
  
• Does not need Carnitine to enter mitochondria to function as fuel

 

[Jon]

Maybe the reasoning behind the claim that "coconut oil being like a poison" is that for it's metabolism:

• Does not need bile acid or pancreatic lipase
  
• Travels directly to the liver, by using portal vein and not lymphatic
• Does not need Cholesterol for transport, in contrast to long chain fatty acids
  
• Does not need Carnitine to enter mitochondria to function as fuel

So all the reasons it's...good? Lol

 

[jb116]

Maybe the reasoning behind the claim that "coconut oil being like a poison" is that for it's metabolism:

• Does not need bile acid or pancreatic lipase
  
• Travels directly to the liver, by using portal vein and not lymphatic
• Does not need Cholesterol for transport, in contrast to long chain fatty acids
  
• Does not need Carnitine to enter mitochondria to function as fuel

Haha my reminders to people why coconut oil is remarkable

 

[Mito]

Dr Aseem Malhotra slams professor who claimed coconut oil is POISON

 

[Jon]

Dr Aseem Malhotra slams professor who claimed coconut oil is POISON

Finally someone with credentials calls her a moron.

 

[LeeLemonoil]

Coconut Oil 'Pure Poison' or 'Superfood'? These 2x5x PRO vs. CON Human Studies Will Help You to Form an Opinion - SuppVersity: Nutrition and Exercise Science for Everyone


among the valubale blog-post from suppversity this gem, a recent study:

And last, but not least, fifth, a very recent study by Oliveira-de-Lira et al. (2018) that compared the effects of 8 weeks on hypocaloric diets supplemented (pre-meal) with coconut oil (CO | here 93% SFA), safflower oil (SAF | here 5% SFA), and chia oil (CHIA | here 14% SFA) and compared them to a control condition, in which the subjects, seventy-five overweight/obese women consumed soybean oil (SOY | here 20% SFA), instead. The subjects' weight, anthropometric parameters, and body fat (%BF), as well as their lean mass percentages (%LM), were evaluated along with biochemical parameters related to lipid and glycemic profiles before and after the 8-week intervention.

Figure 3: Relative changes (%) in body weight (left) and body fat (right) over the course of the 8-week study by Oliveira-de-Lira et al. according to type of fatty acid suppl.; * p<0.05 vs. CHIA & SOY; ** p<0.05 for SOY.
And guess what, the subjects who consumed 3x2g of CO 30 minutes before meals (a) lost the most weight and body fat (p < 0.05 vs. CHIA and SOY for both, %weight and %body fat | see Figure 3) and gained the highest amount of %lean mass (2.61% ± 1.40 kg, p < 0.001 for pre- vs. post and p < 0.05 vs. CHIA and SOY).

Cool? Well, the improvements in body composition are nice, but the results that will bother Prof. Michels are different ones: the scientists also found that the coconut supplement had the most pronounced beneficial effect on the long-term glucose gauge HbA1c (-0.86% vs. -0.49%, -0.53%, and -0.36% in the SAF, CHIA, and SOY group, respectively). With elevated HbA1c being in itself a risk factor for cardiovascular disease (Singer 1992; Selvin 2005 & 2006), this could be interpreted as yet another indicator of health-benefits of coconut oil - one that has been observed in direct comparison to high MUFA and PUFA oils, of which Michelsen is convinced that they are much healthier than coconut oil.

As far as the mechanism is concerned, we can by the way, exclude that the benefits were a mere results of the ~100kcal greater reduction in energy intake in the coconut group (−612.69 kcal/day in the CO group vs. -500.49, -532.59, and -532.50 kcal/day in the SAF, CHIA, and SOY group respectively). Accordingly, something else must be responsible for the observed benefits on body composition and glycemia, and the scientists' observation that total cholesterol, LDL, VLDL, and triglycerides changed in response to CO to the same extent as they did in the SAF and SOY treatments, while HDL increased just as much in the CO group as it did in the CHIA group, which produced the highest reductions in total and LDL cholesterol.