The human body does not require a source of saturated fat.
Then why do you advocate the eating of meat?
Saturated fat from meat or tropical oils is not needed by the body.I am anti heart disease but not anti food.
That really did not answer my question.
By the way, if saturated fats are not needed by the body then why are they produced within the body?
Food is an issue of need from outside the body.
That was not the claim. The claim was that saturated fats are not needed by the body. This does not state internal or external sources, just requirement by the body.
Since the real issue here is inflammation I will focus on the comment from the Wikipedia link you posted:
He also shows that arachidonic acid (AA, 20:4n-6) is an essential Omega-6 (1-6) polyunsaturated fatty acid that is abundant in skeletal muscle membrane phospholipids (figure 2). It is also the body's principal building block for the production of prostaglandins, which are known to have various physiological roles including a close involvement in inflammation.
Inflammatory prostaglandins do not have a close role in inflammation, they cause inflammation. When you injure an area of the body such as sprain your wrist prostaglandins dilate the blood vessels to improve blood flow to the area. But the overdilation of the blood vessels make them permeable and they leak fluids in to the surrounding tissues resulting in the redness, heat and swelling of inflammation. Bradykinin and white blood cells will also play roles in pain and infection fighting. So yes, the arachidonic acid does promote inflammation in part by increasing inflammatory prostaglandins. It also increases levels of inflammatory leukotrienes.
As far as the benefits of arachidonic acid, yes we do need SMALL amounts of arachidonic acid. This is why the body synthesizes what it needs from linoleic acid. But too much arachidonic acid clearly promotes inflammation, which among other things can lead to conditions such as heart disease. It is the same principle as water is essential for so many things in the body but too much can be harmful or deadly.
In addition high intake of arachidonic acid can lower levels of beneficial omega 3 fatty acids. For example:
http://www.ncbi.nlm.nih.gov/pubmed/18710653
In fact the omega 3s help to control inflammation in large part by interfering with arachidonic acid metabolism. So the omega 3s and arachidonic acid are antagonistic to each other. High levels of one will interfere with the other.
Here is my friends counter to your post.
Re: This is why the body synthesizes what it needs from linoleic acid. But too much arachidonic acid clearly promotes inflammation, which among other things can lead to conditions such as heart disease.
I seriously doubt it. China Study showed that if consumption of arachidonic acid were significantly contributing to heart disease then the trend line for all vascular disease on the bottom graph here wouldn't have had a downwards slope! Raw correlation between ischaemic heart disease mortality age 35-69 (tag M063) and dietary animal fat consumption (tag D053) is also strongly negative: -32%, that is statistically significant (marked by * in the doc).
The original document with these correlations can be downloaded from Oxford web site , see page 223. You may notice the same downwards trends if you look at the rheumatoid arthritis (tag M061), and other inflammatory disease statistics. More animal protein or more animal fat equals less disease in China (except for milk!). More plant food especially wheat = more disease! The trend is very clear-cut and hard to miss.
A few studies in relation to arachidonic acid (AA) and heart health:
http://www.ncbi.nlm.nih.gov/pubmed/20435853
"We therefore conclude that arrhythmias following ischemia-reperfusion injury might originate from mitochondrial depolarization mediated by LOX and AA."
http://www.ncbi.nlm.nih.gov/pubmed/20150962
"Atherosclerosis represents an important chronic inflammatory process associated with several pathophysiological reactions in the vascular wall. The arachidonic acid, released by phospholipase A2, is an important substrate for the production of a group of lipid mediators known as leukotrienes, which induce proinflammatory signaling through the activation of specific BLT and CysLT receptors. The interaction of these substances in the vascular wall determines important morphological alterations like the early lipid retention and the accumulation of foam cells, the development of intimal hyperplasia, and advanced atherosclerotic lesions, and it plays an important role in the rupture of atherosclerotic plaque. Many studies regarding myocardial ischemia and reperfusion show that leukotriene signaling may be involved in the development of ischemic injury. For these, reasons both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested for inducing beneficial effects at different stages of the atherosclerosis process and may represent a new therapeutic target in the treatment of atherosclerotic vessel diseases, in particular in acute coronary syndrome."
http://www.nejm.org/doi/pdf/10.1056/NEJMoa025079
"Variant 5-lipoxygenase genotypes identify a subpopulation with increased atherosclerosis.
The observed diet–gene interactions further suggest that dietary n¡6 polyunsaturated
fatty acids promote, whereas marine n¡3 fatty acids inhibit, leukotriene-mediated
inflammation that leads to atherosclerosis in this subpopulation."
Re: study #1 - AA and arrhythmia (http://www.ncbi.nlm.nih.gov/pubmed/20435853 )
There is probably something wrong, either with their conclusion or with other studies of similar kind.
The same could be said about the study your friend supplied. Especially since it does not take in to account other factors such as the high level of anti-inflammatory herbs the Chinese consume.
There must exist a state of disagreement among scientists regarding the role of AA in arrhythmia.
Arrhythmias are primarily caused by lack of blood flow to the heart setting up ectopic pacemakers that cause the arrhythmia. So it is very easy to manipulate studies claiming AA has no effect on arrhythmias since it still takes a great deal of time for the AA induced inflammation to create enough plaque to induce the arrhythmias.
Other studies using real animals (not in-vitro) showed the opposite effect, such as this:
Effects of arachidonic, linoleic, linolenic and oleic acid on experimental arrhythmias in cats, rabbits and guinea-pigs
You need to post the actual abstract, not just the title so it can be reviewed.
I am not sure which is correct, but since the wiki article does point out that AA plays multiple role in many processes, thus multiple, even contrary outcomes aren't surprizing.
(I will reply about the second paper later)
Quote: Many studies regarding myocardial ischemia and reperfusion show that leukotriene signaling may be involved in the development of ischemic injury.
They are probably wrong about the "development" part.
Probably is not evidence, it is a guess.
Leukotrienes are most likely the response to atherosclerotic injury rather than the cause of it.
Again this is a guess.
If leukotrienes are not the cause then AA isn't either.
More on leukotrienes in cardiovascular disease:
http://www.nature.com/nrd/journal/v4/n8/full/nrd1796.html
http://ajrccm.atsjournals.org/cgi/reprint/161/2/S1/S112.pdf
http://www.pnas.org/content/102/48/17501.abstract?cited-by=yes&legid=pnas...
This paper showed that people with genetic anomaly (6% of the study group)
Genetic anomalies are not the norm. The question is not about the effects of AA and leukotrienes on a small fragment of the population but rather the population in general. And as the research has shown arteriosclerosis is caused by inflammation, and AA and leukotrienes are involved in arterial inflammation.
Antiarrhythmic effects of the Prostaglandin (PG) precursors arachidonic and Linoleic acid were demonstrated on three models of experimental arrhythmias, whereas the fatty acids linolenic and oleic acid proved to be ineffective in these models. In ouabain-induced arrhythmias infusions of arachidonic acid (1,0 mg/kg/min) caused a strong antiarrhythmic effect in 80 percent of the animals.
Actually this is easily explained. As they mentioned the AA is a prostaglandin precursor. And as I have pointed out many times the most common cause of arrhythmias is a lack of blood flow to the heart leading to ectopic pacemakers that throw the rhythm off. Prostaglandins though dilate the blood vessels and thus increase blood flow going to the heart and reducing ectopic pacemakers.
Although the real question was whether or not AA increased the rick of atherosclerosis, not arrhythmias. Atherosclerosis is more likely to lead to death than most arrhythmias. So getting back to the original claims does AA contribute to heart attack and strokes? The answer is yes. It is those same prostaglandins that contribute to arterial inflammation. Arterial inflammation in turn leads to cholesterol deposition on the arterial walls over time increasing the risk of heart attack and stroke.
In addition the AA was used in what is suspected to be relatively healthy animals. Long term exposure to the high levels of AA though again leads to arterial plaque build up from arterial inflammation. As arterial plaque builds up though, blood flow to the heart actually decreases leading to an increased risk of arrhythmias. So the study can actually be considered misleading since it fails to take in to account the long term adverse effects of AA. That would be like doing a study on the effects of caffeine on the adrenals and starting out with healthy individuals. But they only give small doses of caffeine for a few days and come to the conclusion that caffeine has no adverse effects on the adrenals. Of course caffeine does adversely affect the adrenals, but this goes to show how easy it is to manipulate studies to show what a person wants to show. Just like that study failed to take in to account the long term effects of AA on the arterial lining and arrhythmias.
There are as many theories as research grant-giving bodies. AA as the causative factor is one of many, so is (was until recently) dietary cholesterol, microbial injury, excess iron, hyperinsulinemia, hyperthyroidism, genetics, saturated fat, transfats, polyunsaturated fat, chlamydia, stress, animal fat, plant oils, lack of fat, hyperglycemia, wheat (very recently), too much arterial exercize, too litle exercize, etc etc. Some of them explained some of the cases some of the time. Some better than the other. None of them explain all cases all of the time.
Nobody claimed that AA was the ONLY cause of cardiovascular disease from atherosclerosis. If you check my older posts and you will see that I mentioned various causes including bacterial infection, xanthine oxidase, hypertension, diabetes, etc. But all of these have one common denominator, which is arterial inflammation. And what else causes arterial inflammation? Arachidonic acid from animal fats.
Even if that hypothesis were true then there is a question what is causing the immune system to become overactive? Are humans built such that some increase in the immune activity caused by some dietary change (i.e. more animal fat) were supposed to kill us by heart diesease where as a decrease were supposed to kill us by infections? I doubt! If they want to prove that atherosclerosis is caused by the immune system gone amok then they must find out what exactly does cause the immune system and the ensuing endotheliarl repair to go amok! Immune system is homeostatic - it stabilizes itself.
So when you want to know how sugar provides energy to the body do you also want to know each and every chemical process in the body that allows the sugar to be utilized by the body starting with digestion? Or do you accept the fact that sugar provides energy to the cells? Or do you want to debate that even further that it is really not the sugar but rather the ATP generated that is providing the energy to the cells involving numerous other reactions that must be verified before you accept it?
On top of that where is the evidence that there is even an overreaction by the immune system to begin with? So I guess since you want to claim that the process involves an overactive immune system that is where your evidence needs to start.
This is from Dr. Rick Dina. I read Hv´s answer just now and remembered when I was studying that. This quote came to my mind. It is another way of explaining what Hv said bellow:
"Too many Omega-6 fats, which are pro-inflammatory, actually inhibit the conversion process of converting alpha-linoleic acid into the longer Omega-3 fats. Now we find Omega-6 fats in animal products; there's an Omega-6 fat called arachidonic acid. We have arachidonic acid in our cell membranes; we talked about the cell membranes that are made largely out of fat. We need some of it in there. So do animals. So when we eat the tissue of an animal, muscle, liver, whatever it may be, we're consuming arachidonic acids. So that's a source because arachidonic acid is an Omega-6 fat.
Then we look at corn oil, soybean oil, cottonseed oil, like when you read the junk food label - partially hydrogenated corn, cottonseed, soybean - those are also very high in Omega-6 fats. What's the average American eating out there? Domesticated animals and processed junk food. So the ideal ratio of Omega-6 to Omega-3 fats is about 1 to 1. You can go up to about maybe four times Omega-6's than Omega-3's and still be within a range where everything stays in balance. The average American though eats about 20 times more Omega-6's than Omega-3's. So even if you have enough alpha-linoleic acid, you have so many Omega-6's that the enzymes are so busy working on the Omega-6's they don't have the opportunity to act on the Omega-3's. They call that "competitive inhibition." It's the same enzymes that work on the Omega-3 family also work on the Omega-6 family. So that's one thing to consider.
When they take standard people who eat a totally altered ratio and they give them some of that alpha-linoleic acid, yeah, they'll find that maybe they don't make enough DHA. But if they were to clean up their diet and have a healthier ratio it's at least hypothesized, and there's some good evidence to support that, the conversion process actually works a lot better."