Simple, Non-invasive Method For Measuring PUFA Status

haidut

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Aside from a blood test for iodine number of FFA or levels of Mead acid, there are few reliable non-invasive techniques for determining PUFA status of a person. This study claims that intra-ocular pressure is a reliable and sensitive method for for determining the PUFA stores of a person. A person deficient in PUFA will have low pressure and vice versa.

Essential Fatty Acid Deficiency in Total Parenteral Nutrition: Detection by Changes In Intraocular Pressure

"...Intraocular pressure determination seem to be a simple, harmless, inexpensive, reliable and sensitive indicator of EFAD. Moreover, IOP determination represent a functional derangement which in a clinical setting lends functional credence to the biochemical changes of EFAD whose entire significance has not yet been determined. Similarly, serial IOP determinations are sensitive in detecting adequate functional repletion of EFAD. As PG are known to act as intermediaries in a variety of physiological processes it seems reasonable to assume that the change in IOP is only one of many different changes and derangements to occur as a result of PG and EFA deficiency."
 
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johns74

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yerrag

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Aside from a blood test for iodine or Mead acid, there are few reliable non-invasive techniques for determining PUFA status of a person. This study claims that intra-ocular pressure is a reliable and sensitive method for for determining the PUFA stores of a person. A person deficient in PUFA will have low pressure and vice versa.

Essential Fatty Acid Deficiency in Total Parenteral Nutrition: Detection by Changes In Intraocular Pressure

"...Intraocular pressure determination seem to be a simple, harmless, inexpensive, reliable and sensitive indicator of EFAD. Moreover, IOP determination represent a functional derangement which in a clinical setting lends functional credence to the biochemical changes of EFAD whose entire significance has not yet been determined. Similarly, serial IOP determinations are sensitive in detecting adequate functional repletion of EFAD. As PG are known to act as intermediaries in a variety of physiological processes it seems reasonable to assume that the change in IOP is only one of many different changes and derangements to occur as a result of PG and EFA deficiency."
From what I gather from reading the article, the comparison is between subjects given EFA and not given EFA through parenteral means, with those given EFA experiencing higher IOP. Would incorporating another control group of subjects given SFA through parenteral means give the study more data to work with? It would address the question of whether the increase in IOP is driven by EFA in the diet, or mainly by inclusion of fat in the diet, be it EFA or SFA.

Is there a constraint involved that keeps the study from incorporating SFA into the TPN (total parenteral nutrition) formula? I noticed that pretty much all commercial TPN formulas use purified soya oil. This was when I once had to compare the available TPN formulas and found I had little choice but to resign myself to the use of a soya oil-based TPN, knowing that an SFA-based TPN formula would be better (Sure enough, 3 days later my mom had chills, which I attribute to hyperglycemia that lead to hypoglycemia with the attendant insulin reaction. This was with my mom). I wondered then why there is no SFA-based TPN formula. I thought that since the TPN formulas are kept in a refrigerator environment, an SFA-based formula would make the formula solidify, and this would present some risks during the intavenous administration.

As to IOP being sensitive to EFA in the diet, wouldn't blood pressure be sensitive to it as well? Would be interesting to include blood pressure in the study as well, since the IOP is expressing something that is systemic.

While on this subject, I noticed too frequently in the past when I had blood sugar control issues, mainly of the hypoglycemic type, I would sense my eyes feeling uncomfortable, feeling close to tears, and my eyes having a slight tinge of red. Does the condition of low blood sugar affect the IOP? Would it the mechanism of increased IOP due to EFA be possibly attributed to its effect of causing the blood sugar to be left unused, thereby increasing blood sugar, to the point where an insulin reaction causes an abrupt drop in blood sugar, leading to stress conditions? If so, what would you imagine to be the mechanism involved that leads to it being expressed in malaise in my eyes?
 
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haidut

haidut

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From what I gather from reading the article, the comparison is between subjects given EFA and not given EFA through parenteral means, with those given EFA experiencing higher IOP. Would incorporating another control group of subjects given SFA through parenteral means give the study more data to work with? It would address the question of whether the increase in IOP is driven by EFA in the diet, or mainly by inclusion of fat in the diet, be it EFA or SFA.

Is there a constraint involved that keeps the study from incorporating SFA into the TPN (total parenteral nutrition) formula? I noticed that pretty much all commercial TPN formulas use purified soya oil. This was when I once had to compare the available TPN formulas and found I had little choice but to resign myself to the use of a soya oil-based TPN, knowing that an SFA-based TPN formula would be better (Sure enough, 3 days later my mom had chills, which I attribute to hyperglycemia that lead to hypoglycemia with the attendant insulin reaction. This was with my mom). I wondered then why there is no SFA-based TPN formula. I thought that since the TPN formulas are kept in a refrigerator environment, an SFA-based formula would make the formula solidify, and this would present some risks during the intavenous administration.

As to IOP being sensitive to EFA in the diet, wouldn't blood pressure be sensitive to it as well? Would be interesting to include blood pressure in the study as well, since the IOP is expressing something that is systemic.

While on this subject, I noticed too frequently in the past when I had blood sugar control issues, mainly of the hypoglycemic type, I would sense my eyes feeling uncomfortable, feeling close to tears, and my eyes having a slight tinge of red. Does the condition of low blood sugar affect the IOP? Would it the mechanism of increased IOP due to EFA be possibly attributed to its effect of causing the blood sugar to be left unused, thereby increasing blood sugar, to the point where an insulin reaction causes an abrupt drop in blood sugar, leading to stress conditions? If so, what would you imagine to be the mechanism involved that leads to it being expressed in malaise in my eyes?

The main reason for not using SFA in TPN formulations is cost. Soy and corn oils are dirt cheap due to subsidies. If the fat used for TPN is MCT then there will be no issue with hardening at low temps. Furthermore, a TPN product with SFA (MCT) would last much longer even without refrigeration due to SFA not spoiling. When they use soy oil or other PUFA not only do they have to add vitamin E but have to refrigerate it to avoid oxidation. So, there is no good medical or even practical rationale for using PUFA, the only reason is cost.
SFA tend to lower both IOP and BP. SFA form a negative feedback with the HPA and usually lower cortisol and adrenaline, which drops BP and blood glucose. The thread on the product DeFibron we have lists a few studies showing methyl palmitate and stearate being potent vasodilators and reducing both BP and IOP. Regular SFA would also work but will probably get oxidized very quickly so the effect would be short-lived, so SFA administration/ingestion would have to be done several times daily in order to get lasting effects.
 

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The main reason for not using SFA in TPN formulations is cost. Soy and corn oils are dirt cheap due to subsidies. If the fat used for TPN is MCT then there will be no issue with hardening at low temps. Furthermore, a TPN product with SFA (MCT) would last much longer even without refrigeration due to SFA not spoiling. When they use soy oil or other PUFA not only do they have to add vitamin E but have to refrigerate it to avoid oxidation. So, there is no good medical or even practical rationale for using PUFA, the only reason is cost.

Wouldn't the main reason be coming from the TPN makers adhering religiously to the mainstream belief that PUFA/EFAs are good and SFAs are bad? The cost would have little to do with it. Given that these TPN formulas are sold at a very lucrative mark-up (Hospital charges $100/liter), the difference in cost between MCT and purified soy oil would not have much of an impact on profit margins.

If the majors are not making TPN, is there anywhere one can buy an MCT-based TPN product?
 
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Wouldn't the main reason be coming from the TPN makers adhering religiously to the mainstream belief that PUFA/EFAs are good and SFAs are bad? The cost would have little to do with it. Given that these TPN formulas are sold at a very lucrative mark-up (Hospital charges $100/liter), the difference in cost between MCT and purified soy oil would not have much of an impact on profit margins.

If the majors are not making TPN, is there anywhere one can buy an MCT-based TPN product?

The very reason for the fraudulent theory behind PUFA being EFA is cost - low cost of production due to subsidies. The cost of MCT production is orders of magnitude higher and if the hospitals around the world were to start using MCT I don't think there will be sufficient supplies. So, yes, the official reason for including PUFA in TPN is to prevent EFA deficiency, but there are TPN without any fat (i.e. pure glucose) and there are plenty of studies on the "surprising" resilience of patients made EFA deficient inadvertently due to these fat-free TPN's. There are also fat-free protein+glucose TPN for special cases that have malfunctioning beta oxidation mechanisms due to inborn metabolic dysfunctions, but those conditions are rare so it is harder to find fat-free protein+glucose TPN than regular PUFA-filled TPN.
 

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Any at home methods to test for intraocular pressure? I could only find the palpation test but it is supposed to be unreliable.
 

yerrag

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The very reason for the fraudulent theory behind PUFA being EFA is cost - low cost of production due to subsidies. The cost of MCT production is orders of magnitude higher and if the hospitals around the world were to start using MCT I don't think there will be sufficient supplies.

This is a sad state in as far as TPN usage goes. This is a typical example of the medical profession and industry using cost above more relevant criteria in determining treatment modalities. If cost-effectiveness were to be the yardstick, this puts the medical industry as one that produces duds for products they force feed on patients. This industry operates on a different plane. If Apple were to make products on the same level of quality as the medical industry, it would have been out of business long ago. But Apple is a company that listens to the market's needs. The medical industry forces its dictates on its patients, and doesn't have to answer for the willful harm it does out of habit and design, which it conveniently covers up.

If MCT is the oil that has to be used, they should do the obvious right thing. They can worry about whether the MCT supply would be sufficient later on. Just cross the bridge when they get there, so to speak. The market will take care of it. If demand increases, production will follow suit to meet the demand eventually. Using soya oil to make the US agribusiness lobby happy while causing untold suffering and death is not a conscientious choice. But then, corporations and hatchet men have no conscience.

I've personally seen what the PUFA (purified soya oil) did to a patient. It causes a patient to suffer chills from the hyperglycemic/hypoglycemic effect from 3 days of PUFA-TPN. To add insult to injury, the patients was then given "black-box warning" level fluoroquinolone antibiotics. The TPN-induced hypoglycemia amplified the excitotoxic side effects of the antibiotic, and the patient suffered damage to her nerves. It upended her state of balance. She was awae for 3 whole days, and then when she went to sleep, she was left in stupor for 3 more days. What saved her was home-made formula with magnesium, VCO, honey, eggs, colostrum, and whey. Using commercial meal replacement formulas like Ensure and Glucerna would have led her to kingdom come.

but there are TPN without any fat (i.e. pure glucose) and there are plenty of studies on the "surprising" resilience of patients made EFA deficient inadvertently due to these fat-free TPN's. There are also fat-free protein+glucose TPN for special cases that have malfunctioning beta oxidation mechanisms due to inborn metabolic dysfunctions, but those conditions are rare so it is harder to find fat-free protein+glucose TPN than regular PUFA-filled TPN.

I wasn't given the choice of fat-free TPN. The hospital and medical staff made sure I had no choice but to choose from three brands of TPN that are all similar. They all have PUFA purified soya oil. What's wrong anyway with fat-free TPN?

For what it's worth, it's good to know that there is a relationship between IOP and PUFA usage from the TPN study. A study that links PUFA usage in TPN to patient deterioration would be as useful, or even more, to bring home the point that PUFA should be banned from TPN .

Sorry if it's off-topic. But TPN "triggered" me.
 
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Andman

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so any specific number to be shooting for? my guess would be lower = better?
 

yerrag

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I should pay an ophthalmologist a visit to take a tonometry test. I think I will do well given how long I've been PUFA-free. I got rid of my glasses for a long time already, even when I was myopic, with left eye being 150, and right eye being 75. I managed to drive with it, and perhaps my eyes are improving. At my age, 56, I can still read books and small type easily.

I should expect an intraocular pressure of around 10mm Hg, if I'm really PUFA-free.
 

postman

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Aside from a blood test for iodine number of FFA or levels of Mead acid, there are few reliable non-invasive techniques for determining PUFA status of a person. This study claims that intra-ocular pressure is a reliable and sensitive method for for determining the PUFA stores of a person. A person deficient in PUFA will have low pressure and vice versa.

Essential Fatty Acid Deficiency in Total Parenteral Nutrition: Detection by Changes In Intraocular Pressure

"...Intraocular pressure determination seem to be a simple, harmless, inexpensive, reliable and sensitive indicator of EFAD. Moreover, IOP determination represent a functional derangement which in a clinical setting lends functional credence to the biochemical changes of EFAD whose entire significance has not yet been determined. Similarly, serial IOP determinations are sensitive in detecting adequate functional repletion of EFAD. As PG are known to act as intermediaries in a variety of physiological processes it seems reasonable to assume that the change in IOP is only one of many different changes and derangements to occur as a result of PG and EFA deficiency."
When my metabolic rate ramps up I get increased pressure behind my eyes. It's visible to other people, and I can feel it myself with my fingers. For example if I eat a good meal and take some aspirin and my body temperature rises, the eye pressure will increase with it. Are you saying this is because my tissues are saturated with PUFAs? If so then what can be done about it, other than waiting out 4 years of an EFAD diet

I once asked Ray about eye pressure and he said pregnenolone should fix it. It fixed it for a short while but then it stopped working completely.
 
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