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Vegetable Oils Make You Fat And Cause Disease

obesity chronic disease pufa omega 6

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#1 matisvijs

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Posted 02 September 2017 - 09:45 AM


For anyone who’s looked into and reasearched the health effects of different omega-6 containing vegetable oils, you’ll quickly find that there’s a strong connection between all of them and the major degenerative diseases such as diabetes, cancer, heart disease, alzheimer’s and even obesity.

Here are a couple of excerpts from the full text studies that I found particularily interesting:

 

On obesity from https://www.ncbi.nlm...pubmed/23249760:

 

‘Recent studies have emphasized the proadipogenic properties of the omega-6 PUFA, and provided evidence that rodents fed on diets with omega-6 PUFA contents similar to the typical US diet (6–8% energy) have an increased fat mass. Importantly, recent studies have shown that perinatal exposure to a high omega-6 PUFA diet results in a progressive accumulation of body fat across generations.’

 

On chronic disease from https://www.ncbi.nlm...pubmed/18408140:

 

Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today’s Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases...’

 

On chronic disease from https://www.ncbi.nlm...ubmed/22570770:

 

‘...high intake of n-6 PUFA, along with low intakes of n-3 PUFA, shifts the physiological state to one that is proinflammatory and prothrombotic with increases in vasospasm, vasoconstriction, and blood viscosity and the development of diseases associated with these conditions.

So if you HAVE to cook with oil (which I don’ t recommend) using something like MCT oil or adding olive oil to salad might be less harmful compared to n-6 oils. Even then, fats in general, also those in olive oil have been connected to diabetes and MCT oil/coconut oil has some pretty potent cholesterol raising effects.

 

This is certainly common knowledge around here but I find that researching these connections on my own gives me a more complete understanding rather than just taking somebody’s word for it. I find it’s also easier to stay on a diet and avoid the harmful foods if you are constantly reading studies and seeing evidence everywhere on their negative effects yourself.

 

If you have more reaserch to add, I’d appreciate it.

 


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#2 joelcairo

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Posted 02 September 2017 - 04:50 PM

I don't completely disagree but the title of this thread is misleading because the research is specifically about vegetable oils which have an excess of omega-6 fatty acids. The 3:6 ratio might be useful shorthand for making dietary decisions, but vegetable oils contain other types of fatty acids as well which have their own positive/negative biological effects, not to mention various polyphenols which usually turn out to be healthful.


Edited by joelcairo, 02 September 2017 - 04:51 PM.

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#3 Darryl

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Posted 02 September 2017 - 08:20 PM

Artemis Simopoulos is not a researcher, and has her critics within nutrition academia.
 
In general, only premenopausal women have significant EFA elongation activity, so for the rest of us, the ratio of the long-chain EFAs is probably paramount. It appears that when diets are replete in arachidonate from grain-fed animal products, rather little linoleate undergoes elongation to arachidonate. We know long term adherence to vegetarian diets reduces arachidonate status somewhat, while red meat increases it. I suspect grain-fed tallow has an unusually high content of arachidonate in the sn2 position of its triglycerides, which would account for the disproportunate effect of red meat on arachidonate status.
 

It remains possible that for those on vegan diets, the balance between arachidonate and eicosapentanoate could be a function of the dietary linoleate/α-linolenate ratio, but there hasn't been a study. 
 
Personally, I avoid dietary arachidonate and most refined oils, and supplement with algal eicosapentanoate. My main cooking oils, which I use sparingly, are canola and mustard, which have attractively low linoleate/α-linolenate ratios. I don't worry about the linoleate in whole foods like nuts and sesame.
 
 

 


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#4 Chupo

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Posted 06 September 2017 - 03:14 AM

This is an interesting read. It talks about the metabolites of O6.  http://breaknutritio...s-civilization/


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#5 misterE

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Posted 08 September 2017 - 05:27 PM

I find this fascinating. For anyone else interested in polyunsaturated-fats and the balance between omega-3 and omega-6, watch the following video; it comes from one of the leading researchers on omega-3/omega-6: Bill Lands, who shares his research findings and unconventional views on diet... enjoy!!

 


Edited by misterE, 08 September 2017 - 05:34 PM.

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#6 misterE

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Posted 08 September 2017 - 08:14 PM

Isr J Med Sci. 1996 Nov;32(11):1134-43.
Diet and disease--the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet.
 
 
Abstract

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet, a diet that until recently was widely recommended. Despite such national habits, there is paradoxically a high prevalence of cardiovascular diseases, hypertension, non-insulin-dependent diabetes mellitus and obesity-all diseases that are associated with hyperinsulinemia (HI) and insulin resistance (IR), and grouped together as the insulin resistance syndrome or syndrome X. There is also an increased cancer incidence and mortality rate, especially in women, compared with western countries. Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.

 



#7 aza

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Posted 12 September 2017 - 02:13 PM

Now, this in quite interesting. I've known about a few issues with the polyunsaturated fat trails for a while. But i learned quite a lot of new information from this recent meta analysis, which as far as i can tell is fairly well done.

I recommend reading the whole thing.

Essentially, previous meta analysis's used inadequately controlled trials, such as trials with multifactoral interventions for example.

Even many of the better controlled trials are positively biased towards the polyunsaturated groups. Because they often ended up with lower trans fat intakes or received health advice the controls did not, such as avoiding fried food, pastry, cakes ect.

As a result the negative effect of vegetable oil is likely greater then the results currently show.

Moreover, we have no idea just how bad the effects are over a long period of time, if the negative effect compounds further after 10 years or so then thats quite a large oversight.

 

I'm also not quite sure if total pufa or the omega ratio is more important. For now i limit my omega 6 intake to 3-4% of calories and eat 1-1.5% from omega 3

 

https://nutritionj.b...2937-017-0254-5

The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials

When pooling results from only the adequately controlled trials there was no effect for major CHD events (RR = 1.06, CI = 0.86–1.31), total CHD events (RR = 1.02, CI = 0.84–1.23), CHD mortality (RR = 1.13, CI = 0.91–1.40) and total mortality (RR = 1.07, CI = 0.90–1.26). Whereas, the pooled results from all trials, including the inadequately controlled trials, suggested that replacing SFA with mostly n-6 PUFA would significantly reduce the risk of total CHD events (RR = 0.80, CI = 0.65–0.98, P = 0.03), but not major CHD events (RR = 0.87, CI = 0.70–1.07), CHD mortality (RR = 0.90, CI = 0.70–1.17) and total mortality (RR = 1.00, CI = 0.90–1.10).

 

Available evidence from adequately controlled randomized controlled trials suggest replacing SFA with mostly n-6 PUFA is unlikely to reduce CHD events, CHD mortality or total mortality. The suggestion of benefits reported in earlier meta-analyses is due to the inclusion of inadequately controlled trials.

 

 

 


Edited by aza, 12 September 2017 - 02:16 PM.


#8 misterE

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Posted 13 September 2017 - 08:04 PM

 

 

I'm also not quite sure if total pufa or the omega ratio is more important. For now i limit my omega 6 intake to 3-4% of calories and eat 1-1.5% from omega 3

 

 

 

I think it's both. Currently in the USA the percentage calories from PUFA is 8% with an omega-6/3 ratio of 25, whereas in 1909 the percentage of calories from PUFA was 1% with a ratio of 8. 

 

So it's probably best to reduce the total amount, while providing a 1:1 ratio


Edited by misterE, 13 September 2017 - 08:05 PM.


#9 Kalliste

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Posted 14 September 2017 - 06:19 AM

What happens if you have a high intake of both.

 

Example

Breakfeast: Can of sardines, some walnuts.

Later that day: Potato chips made with sunflower oil.

 

Does this oily balancing act do me any good?



#10 aza

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Posted 14 September 2017 - 02:53 PM

No one knows... *rainbow hands*.

However the sardines, as well as walnuts (in moderation) should be positive.

potato chips in sunflower oil, not so much.

The only issue with the meta analysis in regards to polyunsaturated fat is that it may not apply to whole foods.

 

if you do have a high intake, its probably a good idea to balance it out.


Edited by aza, 14 September 2017 - 02:53 PM.


#11 What-a-Riot

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Posted 15 September 2017 - 12:59 PM

 Honest question: is it not completely absurd to shoot for a 1:1 ratio of omega 6:3? Can anyone name a single food that has such a low ratio (ok, maybe mustard seed) let alone a well rounded diet? What is actually reasonable?



#12 pamojja

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Posted 15 September 2017 - 01:20 PM

 Honest question: is it not completely absurd to shoot for a 1:1 ratio of omega 6:3?

 

For me a dietary 2:1 omega-6:3 ratio wasn't that difficult. Just left out grains (actually for blood sugar issues) and added fish 1-2 times a week. And of course, no industrial processed food full of omega-6 oils.

 

After adding supplemental fish-oil I ended up at about 1.5:1
 


Edited by pamojja, 15 September 2017 - 01:21 PM.


#13 What-a-Riot

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Posted 15 September 2017 - 02:00 PM

ok i dont know what i've looked at before that i thought that was so undoable.  thanks for making me look it over again



#14 joelcairo

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Posted 15 September 2017 - 03:55 PM

To get that low you basically have to rely on fish and flax/chia seeds. Some vegetables are good if you eat them in large quantities, but they don't really have a lot of fatty acids of any kind so they probably wouldn't have a huge impact on the 3:6 ratio in your overall diet.


Edited by joelcairo, 15 September 2017 - 04:00 PM.


#15 Kalliste

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Posted 17 September 2017 - 04:01 PM

There are people who consume 5 cans of Sardines a day and they claim good ratios. However I wonder about all the aluminium in the can, but I guess you can get glass cannisters.



#16 misterE

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Posted 17 September 2017 - 07:32 PM

What happens if you have a high intake of both.

 

Example

Breakfeast: Can of sardines, some walnuts.

Later that day: Potato chips made with sunflower oil.

 

Does this oily balancing act do me any good?

 

 

I don't think so personally because the higher the TOTAL amount of polyunsaturated fat in the diet requires much more vitamin-E to regulate their actions and oxidation.



#17 misterE

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Posted 17 September 2017 - 07:35 PM

 

However the sardines, as well as walnuts (in moderation) should be positive.

 

 

The problem with walnuts is that they are (i think) 55% O-6 with 7 fold more O-6 than O-3, so they do nothing in terms of tipping the balance back in favor of a 1 to 1 ratio. The ratio is harder to control if the absolute amount of O-6 is high.

 

The problem with sardines is that they contain PCBs and dioxins.


Edited by misterE, 17 September 2017 - 07:37 PM.


#18 misterE

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Posted 17 September 2017 - 07:43 PM

 Honest question: is it not completely absurd to shoot for a 1:1 ratio of omega 6:3? Can anyone name a single food that has such a low ratio (ok, maybe mustard seed) let alone a well rounded diet? What is actually reasonable?

 

 

Pinto-beans and kidney-beans have a perfect ratio and a low total fat content. Leafy-greens like kale and spinach are 1:1, white-rice and potatoes have a 1:3 ratio, many fruits have balanced ratios. You can combine foods like grains (1:15 ratio) with some beans and leafy-green to get not only a low total PUFA amount but a good ratio. Flaxseed actually has a 4:1 ratio and is great to help balance things out. Oatmeal for instance has a 1:15 ratio, but add some ground flaxseed on top and the ratio drops to 1:2


There are people who consume 5 cans of Sardines a day and they claim good ratios. However I wonder about all the aluminium in the can, but I guess you can get glass cannisters.

 

 

With fish, aluminium is probably the least of your worries. 


Edited by misterE, 17 September 2017 - 07:47 PM.


#19 Nate-2004

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Posted 18 September 2017 - 05:49 PM

The title of this thread is a bit misleading, I agree with the earlier reply to the same point. Extra Virgin Olive Oil is a vegetable oil but it only contains 1g per serving of PUFA in the form of linoleic acid. The rest is monounsaturated fat and some saturated fat. The important bits are the polyphenols. If you're going to use a vegetable oil, EVOO should be the only one, find a good source and don't cook it. As for MCT oil, it's derived from coconut and is different from plain coconut oil in that it leaves out other cholesterol increasing fatty acids such as lauric acid.

 

I agree about people's balance of Omega 6 to 3 being totally off. It doesn't help that we're poor ALA converters. However, ground flaxseed and flaxseed oil as well as spinach and kale are high in omega 3 ALAs. You can find sites out there that list the balances of various veggies. Carrots are high in omega 6, so is chard. My smoothies lean heavily towards ALA over LA. 

 

You can also very strongly shift the balance towards omega 3 by adding Viva Fish Oil to your supps, or Krill oil which is more bioavailable. I take both. Why Viva? Check out Labdoor.com to see for yourself. Refrigerate your fish oil!!

 

Stearic and capric acid is good, it's in coconut oil but so is lauric acid. I add plain stearic acid to my smoothies, it's derived from palm oil. I'm not sure what the case is with palm oil.

 

Let's not forget pecan and other nut oils. Pecan oil is largely omega 9 fatty acids, however its second most abundant PUFA is omega 6, so I don't know if they tested pecan oil but it's probably not nearly as bad as others.

 

There are also other potential nut oils that are healthier, with more balanced omega 6:3 profiles AND omega 9s and 7s. The guy in the video is totally wrong about phytates being an anti-nutrient though. Phytates are quite good for you.

 

If you're not vegan, then substituting vegetable oils with butter is fine. There is nothing wrong with saturated fat and the myth about it needs to be squashed. 

 

See these videos for more details:

 

 

 

 

 

 


Edited by Nate-2004, 18 September 2017 - 06:05 PM.


#20 misterE

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Posted 18 September 2017 - 09:01 PM



It doesn't help that we're poor ALA converters. However, ground flaxseed and flaxseed oil as well as spinach and kale are high in omega 3 ALAs. You can find sites out there that list the balances of various veggies. Carrots are high in omega 6, so is chard. My smoothies lean heavily towards ALA over LA.



Let's not forget pecan and other nut oils. Pecan oil is largely omega 9 fatty acids, however its second most abundant PUFA is omega 6, so I don't know if they tested pecan oil but it's probably not nearly as bad as others.



The reason we are "bad converters" is because too much LA interfers with ALA conversion, we are actually good converters and reaearch by Lands and Innis show this quite well, but the more LA the less ALA gets converted into EPA. In terms of vegetables like carrots and chard, despite being high in O-6, their total amount of fat is so little, that it can be easily managed and balanced with other foods. In regards to nuts: macadamia is the only nut with relatively low amounts of total PUFA and a (if I can remember correctly) 1:6 ratio. Almonds and peanuts for instance have ratios of 1:2000 and 1:5000 respectively.
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#21 aza

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Posted 20 September 2017 - 02:36 AM

When people say vegetable oils, they primarily mean polyunsaturated oils.


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#22 misterE

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Posted 21 September 2017 - 04:59 PM

Another way researches think that omega-6 causes obesity is by inhibiting the conversion of white adipose-tissue into brown adipose-tissue, and also by increasing the levels of endocannabinoids (anandamide and 2-AG) which stimulate hunger, increase laziness and decrease energy expenditure.

 

Not to mention: fat is just so calorie-dense, 9-calories per gram of fat compared to 4-calories per gram of carbohydrate. Oil is 9-calories per gram compared to potatoes which are 1 calorie per gram.  


Edited by misterE, 21 September 2017 - 05:12 PM.

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#23 Nate-2004

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Posted 21 September 2017 - 05:16 PM

Fat is also satiating though and studies show that people have trouble eating more than a certain amount when the diet is high in fat. Where do they talk about omega-6 inhibiting the browning of fat?



#24 misterE

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Posted 21 September 2017 - 07:03 PM

Fat is also satiating though and studies show that people have trouble eating more than a certain amount when the diet is high in fat. Where do they talk about omega-6 inhibiting the browning of fat?

 

 

Actually fat doesn't satiate since it does not stimulate insulin release, neither does fructose, this is why (besides being hyperpalatable and calorie-dense) high-fat/high-sugar diets lead to obesity, whereas low-fat/high-fiber diets based around starch are less palatable and calorie-dense and increase insulin sensitivity and secretion, leading to correct weight and metabolic management. Insulin is the most powerful satiety hormone in the body; so being "resistant" to insulin basically means you are resistant to satiety signaling (among  many other functions insulin has control over).

 

 

 

https://www.ncbi.nlm...41/pdf/main.pdf

 

https://www.ncbi.nlm...pubmed/27159788

 

 


Edited by misterE, 21 September 2017 - 07:13 PM.

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#25 Nate-2004

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Posted 21 September 2017 - 09:26 PM

 

Fat is also satiating though and studies show that people have trouble eating more than a certain amount when the diet is high in fat. Where do they talk about omega-6 inhibiting the browning of fat?

 

 

Actually fat doesn't satiate since it does not stimulate insulin release, neither does fructose, this is why (besides being hyperpalatable and calorie-dense) high-fat/high-sugar diets lead to obesity, whereas low-fat/high-fiber diets based around starch are less palatable and calorie-dense and increase insulin sensitivity and secretion, leading to correct weight and metabolic management. Insulin is the most powerful satiety hormone in the body; so being "resistant" to insulin basically means you are resistant to satiety signaling (among  many other functions insulin has control over).

 

 

 

https://www.ncbi.nlm...41/pdf/main.pdf

 

https://www.ncbi.nlm...pubmed/27159788

 

 

This flies against everything I just posted above. Insulin is not satiating, leptin is.  Also, fat does not lead to obesity. Sugar, yes, possibly PUFA imbalances, yes, but not fat in general. Neither of those links support anything you just said.

 

https://youtu.be/zcMBm-UVdII?t=7m20s


Edited by Nate-2004, 21 September 2017 - 10:02 PM.

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#26 misterE

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Posted 22 September 2017 - 03:05 AM

Are you one of those Gary Taubes followers who doesn't believe in The Law of Thermodynamics? 

:|?


Edited by misterE, 22 September 2017 - 03:05 AM.

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#27 Darryl

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Posted 22 September 2017 - 06:31 PM

The brain does monitor insulin, as well other homones leptin, ghrelin; blood leucine, glucose, triglycerides; and gastrointestinal nerve signalling, in determining appetite. Leptin seems the most important satiety hormone, but by no means the only input.

 

 


Edited by Darryl, 22 September 2017 - 06:33 PM.

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#28 misterE

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Posted 23 September 2017 - 03:19 AM

The brain does monitor insulin, as well other homones leptin, ghrelin; blood leucine, glucose, triglycerides; and gastrointestinal nerve signalling, in determining appetite. Leptin seems the most important satiety hormone, but by no means the only input.

 

 

True. When the fat-cells are undergoing lipolysis (as in starvation or diabetes), their production of leptin decreases. Insulin is the main hormone that puts a stop on lipolysis and lowers FFA's, which do two things for leptin: it stimulates it's production and increases it's sensitivity because FFA's decreases leptin-sensitivity (as well as insulin-sensitivity of course). So insulin and leptin are closely connected hormones.



#29 Darryl

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Posted 23 September 2017 - 04:48 AM

For whomever wanted references on how leptin is but one of many inputs to central energy sensing and satiety, some reviews to get you up to date:

 

Blouet and Schwartz, 2010. Hypothalamic nutrient sensing in the control of energy homeostasisBehavioural brain research209(1), pp.1-12.

Hypothalamic nutrient sensing of glucose, leucine, and oleic acid.

Grill and Hayes, 2012. Hindbrain neurons as an essential hub in the neuroanatomically distributed control of energy balanceCell metabolism16(3), pp.296-309.

The nucleus tractus solitarius integrates nutrient sensing from the nearby hypothalamus, vagus nerve signalling of gastric stretching as well as intestinally produced satiety hormones (5-HT, peptide YY, glutamate, and enterostatin), glucose, the hunger hormone ghrelin, as well as satiety hormones cholecystokinin, melanocortin, leptin, amylin, and glucagon like peptide-1.

Filippi et al, 2013. Insulin and glucagon signaling in the central nervous systemReviews in Endocrine and Metabolic Disorders14(4), pp.365-375.

Both suppress food intake.

 

I erred above in indicating the CNS detects triglycerides directly. Their packaging in chylomicrons or VLDL can't cross the blood brain barrier. However oleic acid, the most common nonesterified fatty acid released by adipose tissue, does seem to play an active role in the hypothalamus. 


Edited by Darryl, 23 September 2017 - 04:56 AM.

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#30 Batambob

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Posted 21 January 2018 - 11:15 AM

Ray Peat has been saying for decades that ALL polyunsaturated oils (PUFAs - Poly Unsaturated Fatty Acids) cause inflammation at a cellular level. That includes Omega 3 as well as Omega 6 based PUFAs, including fish oil. He says the positive effects of Vitamin E observed by the Shute family, is a measure of how well E protects us from the damage caused by the PUFAs stuck in our cells. Peat says that the term "Essential" Fatty Acids (EFA) was coined by erroneous observations made by George and Mildred Burr, back in the 1920s.

 

Peat says that the concept of feeding meat animals an unnatural diet of PUFA rich rape, cottonseed, soy and corn was  promoted post WW2  by oilseed grower lobbyists, who had lost their main market, the paint industry. Meat animals fed coconut products got lean; when fed oilseeds they got fat and sick.

 

Those ugly age spots we see on our skin are made of PUFA-containing lipofuscin, an excess of which our cells cannot properly metabolize... and therefore "stores" in the body. 

 

EFAs don't exist, except in our minds.


Edited by Batambob, 21 January 2018 - 11:22 AM.

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