Atherosclerosis, Glucorticoids & The Fried Lard Diet

[zkt]

62 yo male
As some of you know, I have a history of atherosclerosis, hypertension and familial hypercholesterolemia which resulted in a bifemoral-aortic bypass some 20 years ago and a thalamic stroke 8 years ago. Lipids and BP are now well controlled, at healthy levels even, by a host of drugs and a low saturated fat diet.
Lifelong smoking has resulted in severe COPD. Interestingly, childhood asthma returned within 2 weeks of smoking cessation 8 years ago, and is currently barely adequately controlled by inhaled glucorticoids (Mometosone 220mcg bid).
In the spring of 2009 I injured my left basal thumb joint resulting in severe pain, lack of mobility and loss of use of my left hand in doing any meaningful work. The best that the medical profession had to offer was to fuse the joint. I found both the situation and their treatment to be unacceptable. So, knowing that inflammation mediated joint remodeling was at the root of the problem, I undertook the responsibility to treat it myself with the minimum effective dose of oral glucocorticoids. I decreased the dose every few months and the Sx reappeared each time until last fall. It appeared that the inflammatory response had given up on it and that the treatment was successful. I am currently taking 2.5mg prednisone eod with the goal of zero in a few weeks, at which point I`ll test serum cortisol.
The most noticable effect in coming off the GCs is greatly increased airway inflammation. I`m not at all sure the current situation is tolerable but will reserve judgement until cortisol level is tested.
I have often wondered if the Medrol hasnt actually been theraputic in terms of atherosclerotic plaque build up. Carotid and renal artery plaque has remained stable for the past two years as evidenced by ultrasounds. GC therapy lasted 18 mts. during the past 2 years.
There are a few studies that GC dosing prior and post stent placement dramatically reduced restenosis. Not sure the current state of research of GC eluting stents.
GC are conventionally thought to exerabate atherosclerosis by way of increasing BP, insulin resistance and calcification.
But then I find this study which finds that they slow the progression of arterial plaque build up.

Reduced carotid atherosclerosis in asthmatic patients treated with inhaled corticosteroids

Then theres the whole Atkins thing POSSIBLY reducing LDL and BP. That would be a major change in itself. Add to that the possibility that I might be doing great harm by stopping exogenous GC and we arrive at the fried lard and dexamethasone diet.
Thoughts ?

 

[vantage108]

As someone with Addison's who eats paleo, I'm all for lard and dexamethasone.

Broadly speaking, paleo-type diets (think Atkins minus processed foods, more or less) are credited with a variety of inflammation-reducing effects. I assume you've read Gary Taubes' books on food and science?

 

[CubbieBlue]

62 yo male
As some of you know, I have a history of atherosclerosis, hypertension and familial hypercholesterolemia which resulted in a bifemoral-aortic bypass some 20 years ago and a thalamic stroke 8 years ago. Lipids and BP are now well controlled, at healthy levels even, by a host of drugs and a low saturated fat diet.
Lifelong smoking has resulted in severe COPD. Interestingly, childhood asthma returned within 2 weeks of smoking cessation 8 years ago, and is currently barely adequately controlled by inhaled glucorticoids (Mometosone 220mcg bid).
In the spring of 2009 I injured my left basal thumb joint resulting in severe pain, lack of mobility and loss of use of my left hand in doing any meaningful work. The best that the medical profession had to offer was to fuse the joint. I found both the situation and their treatment to be unacceptable. So, knowing that inflammation mediated joint remodeling was at the root of the problem, I undertook the responsibility to treat it myself with the minimum effective dose of oral glucocorticoids. I decreased the dose every few months and the Sx reappeared each time until last fall. It appeared that the inflammatory response had given up on it and that the treatment was successful. I am currently taking 2.5mg prednisone eod with the goal of zero in a few weeks, at which point I`ll test serum cortisol.
The most noticable effect in coming off the GCs is greatly increased airway inflammation. I`m not at all sure the current situation is tolerable but will reserve judgement until cortisol level is tested.
I have often wondered if the Medrol hasnt actually been theraputic in terms of atherosclerotic plaque build up. Carotid and renal artery plaque has remained stable for the past two years as evidenced by ultrasounds. GC therapy lasted 18 mts. during the past 2 years.
There are a few studies that GC dosing prior and post stent placement dramatically reduced restenosis. Not sure the current state of research of GC eluting stents.
GC are conventionally thought to exerabate atherosclerosis by way of increasing BP, insulin resistance and calcification.
But then I find this study which finds that they slow the progression of arterial plaque build up.

Reduced carotid atherosclerosis in asthmatic patients treated with inhaled corticosteroids

Then theres the whole Atkins thing POSSIBLY reducing LDL and BP. That would be a major change in itself. Add to that the possibility that I might be doing great harm by stopping exogenous GC and we arrive at the fried lard and dexamethasone diet.
Thoughts ?

I find it interesting that a many times attempted GC taper worked to "heal" your thumb pain. Not sure how that works. I am still unclear as to how inflammatory processes work on healing/pain. A lot of the new stuff says that the inflammation is initially necessary but for how long is unclear before it becomes it starts to become counter-productive.

Obviously, your inflammation (lungs, arteries) needs to be dealt with. I think Atkins or at least Mediterranean diet might help. What are you doing as far as fish oil, herbal anti-inflammatories, NSAIDS, etc.?

 

[zkt]

As someone with Addison's who eats paleo, I'm all for lard and dexamethasone.

Broadly speaking, paleo-type diets (think Atkins minus processed foods, more or less) are credited with a variety of inflammation-reducing effects. I assume you've read Gary Taubes' books on food and science?

Yep, I`m almost a believer. Just not quite how one needs to take the carb restriction yet. Maybe good enought just to shift the insulin-glucagon balance to the glu side by eliminating simple carbs. (sucrose, fructose, short chain carbs)
Born with Addisons or pick it up along the way?

I find it interesting that a many times attempted GC taper worked to "heal" your thumb pain. Not sure how that works. I am still unclear as to how work on healing/pain. A lot of the new stuff says that the inflammation is initially necessary but for how long is unclear before it becomes it starts to become counter-productive.

Obviously, your inflammation (lungs, arteries) needs to be dealt with. I think Atkins or at least Mediterranean diet might help. What are you doing as far as fish oil, herbal anti-inflammatories, NSAIDS, etc.?

Guess I was unclear. Each time I tapered down the Sx returned. Just this last time, 6 mts ago, it didnt to any sig degree. Inflammatory processes seem to operate differently on the young vs older. It is complex and I dont have all the players entirely straight either.
Fish oil cap 3xd, salmon 3-4 times a week, nsaids contraindicated due to renal insufficiencies.
The sat fat appears to decrease inflammtion. Not sure how. do you understand the mechanism?

 

[LW64]

My $0.02:

Have you had a Calcium CT Scan?

Cardiac CT for Calcium Scoring


There are many people on low-carb diets that have their LDL go up and you dont need to have FH for that to happen. Saturated fat increases both HDL and LDL - hopefully HDL will go up more than LDL and improve your ratios, but that doesnt always happen. What will happen is that the LDL size pattern will become predominantly large and bouyant, which is what you want. If your present ratio of TRIGs to HDL is over 3.5, it's very likely you have the small, dense, artherogenic size pattern and it would benefit you to change it.

If you get a Calcium score in your present condition and it's high, you can consider yourself at the same risk level of those who have had a myocardial infarction and continue taking niacin, etc. to keep your LDL down. Even a small dose of a statin could be of benefit - not for the reduction in LDL (I'm a cholesterol skeptic), but for the reduction in inflammation you'll get.

If you're overweight, there's no question your risk level decreases if you drop some pounds.

 

[LW64]

The sat fat appears to decrease inflammtion. Not sure how. do you understand the mechanism?

It doesnt oxidize very much. MUFAs and PUFAs do.

 

[Structure]

62 yo male
As some of you know, I have a history of atherosclerosis, hypertension and familial hypercholesterolemia which resulted in a bifemoral-aortic bypass some 20 years ago and a thalamic stroke 8 years ago. Lipids and BP are now well controlled, at healthy levels even, by a host of drugs and a low saturated fat diet.
Lifelong smoking has resulted in severe COPD. Interestingly, childhood asthma returned within 2 weeks of smoking cessation 8 years ago, and is currently barely adequately controlled by inhaled glucorticoids (Mometosone 220mcg bid).
In the spring of 2009 I injured my left basal thumb joint resulting in severe pain, lack of mobility and loss of use of my left hand in doing any meaningful work. The best that the medical profession had to offer was to fuse the joint. I found both the situation and their treatment to be unacceptable. So, knowing that inflammation mediated joint remodeling was at the root of the problem, I undertook the responsibility to treat it myself with the minimum effective dose of oral glucocorticoids. I decreased the dose every few months and the Sx reappeared each time until last fall. It appeared that the inflammatory response had given up on it and that the treatment was successful. I am currently taking 2.5mg prednisone eod with the goal of zero in a few weeks, at which point I`ll test serum cortisol.
The most noticable effect in coming off the GCs is greatly increased airway inflammation. I`m not at all sure the current situation is tolerable but will reserve judgement until cortisol level is tested.
I have often wondered if the Medrol hasnt actually been theraputic in terms of atherosclerotic plaque build up. Carotid and renal artery plaque has remained stable for the past two years as evidenced by ultrasounds. GC therapy lasted 18 mts. during the past 2 years.
There are a few studies that GC dosing prior and post stent placement dramatically reduced restenosis. Not sure the current state of research of GC eluting stents.
GC are conventionally thought to exerabate atherosclerosis by way of increasing BP, insulin resistance and calcification.
But then I find this study which finds that they slow the progression of arterial plaque build up.

Reduced carotid atherosclerosis in asthmatic patients treated with inhaled corticosteroids

Then theres the whole Atkins thing POSSIBLY reducing LDL and BP. That would be a major change in itself. Add to that the possibility that I might be doing great harm by stopping exogenous GC and we arrive at the fried lard and dexamethasone diet.
Thoughts ?

That's got to feel pretty good, knowing that you have yourself to thank for fixing your thumbs. Pretty inspiring... Congratulations on weaning yourself off of GCs, by the way.

That study certainly does seem to fly in the face of conventional wisdom. I don't really know what to make of it. I'll have to think about it for a bit...

My opinion on low carb dieting is this: if you don't think you are likely to exercise adequately (1 hr a day of hard exercise), then I think it is a good idea. I still think that exercise and a low glycemic diet in combination is the best approach, but you have to be pragmatic: if you don't see yourself doing the exercise, then you should plan for it. In that case, go for the low carb diet. You will lose weight.

My only caveat is this: monitor your cortisol levels to make sure they are well controlled. And I still think that saturated animal fats should be avoided, even when on Atkins. Chicken and vegetables, man. Make them your friends. And keep yourself on a short leash, at least at first: irritability may rear its ugly head...

 

[zkt]

My $0.02:

Have you had a Calcium CT Scan?

Cardiac CT for Calcium Scoring


There are many people on low-carb diets that have their LDL go up and you dont need to have FH for that to happen. Saturated fat increases both HDL and LDL - hopefully HDL will go up more than LDL and improve your ratios, but that doesnt always happen. What will happen is that the LDL size pattern will become predominantly large and bouyant, which is what you want. If your present ratio of TRIGs to HDL is over 3.5, it's very likely you have the small, dense, artherogenic size pattern and it would benefit you to change it.

If you get a Calcium score in your present condition and it's high, you can consider yourself at the same risk level of those who have had a myocardial infarction and continue taking niacin, etc. to keep your LDL down. Even a small dose of a statin could be of benefit - not for the reduction in LDL (I'm a cholesterol skeptic), but for the reduction in inflammation you'll get.

If you're overweight, there's no question your risk level decreases if you drop some pounds.

It doesnt oxidize very much. MUFAs and PUFAs do.

Not so much concerned with improving my lipids.
06/29/10
Tot Chol=185
TG=57
HDL=93
VLDL=11
LDL=81
LDL/HDL ratio= 2.0

If you can believe these labs CHL accumulation is actually reversed. which brings up the issue of if it aint broke why fix it? Answer is because my older sister lived on beans and olive oil for the last 20 years of her life and finally died from heart failure. Not firmly convinced that SF is the bad guy.
Good point re the statins and inflammation. Not everyone knows this.
Calcium is actually a two sided sword. One one hand it is an indicator of the extent of lesions, but on the other it stabilizes the arterial plaque. For instance my left subclavian artery near the aortic branch is hard as a rock and the plaque there isnt going anywhere. Colaterals grew up to the vertebral artery and feeds my left arm. The A-gram clearly shows the flow going up the carotid and then back down and into the arm. This may be why the renal artery stenosis hasnt fucked up kidney function more than it already has.
BMI=19. Not a concern, but when I do put on weight it tends to accumulate in the midsection- a good reason to decrease insulin I think.
I think a lipids profile every 3 mts would be a very good idea if I go with it.
But aside from the diet the real wild card is the GCs.
BTW the wife has downed half a liter of the MCT since we first discussed the subject. She seems sharper. Hope your mother is doing well.
Oh, got any further info on SF metabolism? You know how I like the biochemistry. I still get a hard on when I watch Lustig go thru the fructose metabolism.

Also , youre are right about the vldl.
Could you reiterate, with labs if possible, what your pre and post Adkins data were?

 

[zkt]

That's got to feel pretty good, knowing that you have yourself to thank for fixing your thumbs. Pretty inspiring... Congratulations on weaning yourself off of GCs, by the way.

That study certainly does seem to fly in the face of conventional wisdom. I don't really know what to make of it. I'll have to think about it for a bit...

My opinion on low carb dieting is this: if you don't think you are likely to exercise adequately (1 hr a day of hard exercise), then I think it is a good idea. I still think that exercise and a low glycemic diet in combination is the best approach, but you have to be pragmatic: if you don't see yourself doing the exercise, then you should plan for it. In that case, go for the low carb diet. You will lose weight.

My only caveat is this: monitor your cortisol levels to make sure they are well controlled. And I still think that saturated animal fats should be avoided, even when on Atkins. Chicken and vegetables, man. Make them your friends. And keep yourself on a short leash, at least at first: irritability may rear its ugly head...

BMI=19: not anissue. Chicken, veggies and olive oil have been more than friends. Just wondering if I havent been hanging with the wrong crowd. The sat fat is the other wild card. It somehow reduces inflammation. You gotta admit that inflammation is at the root of atherosclerosis. This paper brings it all together:
http://www.pasteur.edu.uy/publico/cayota/Bibliografia%20Dis%20End/DE%20y%20aterosclerosis/Atherosclerosis%20Inflamatory%20disease%20NEJM%202005.pdf

 

[cvictorg]

Not so much concerned with improving my lipids.
06/29/10
Tot Chol=185
TG=57
HDL=93
VLDL=11
LDL=81
LDL/HDL ratio= 2.0

If you can believe these labs CHL accumulation is actually reversed. which brings up the issue of if it aint broke why fix it? Answer is because my older sister lived on beans and olive oil for the last 20 years of her life and finally died from heart failure. Not firmly convinced that SF is the bad guy.
Good point re the statins and inflammation. Not everyone knows this.
Calcium is actually a two sided sword. One one hand it is an indicator of the extent of lesions, but on the other it stabilizes the arterial plaque. For instance my left subclavian artery near the aortic branch is hard as a rock and the plaque there isnt going anywhere. Colaterals grew up to the vertebral artery and feeds my left arm. The A-gram clearly shows the flow going up the carotid and then back down and into the arm. This may be why the renal artery stenosis hasnt fucked up kidney function more than it already has.
BMI=19. Not a concern, but when I do put on weight it tends to accumulate in the midsection- a good reason to decrease insulin I think.
I think a lipids profile every 3 mts would be a very good idea if I go with it.
But aside from the diet the real wild card is the GCs.
BTW the wife has downed half a liter of the MCT since we first discussed the subject. She seems sharper. Hope your mother is doing well.
Oh, got any further info on SF metabolism? You know how I like the biochemistry. I still get a hard on when I watch Lustig go thru the fructose metabolism.

Also , youre are right about the vldl.
Could you reiterate, with labs if possible, what your pre and post Adkins data were?

You should do an essential fatty acid profile blood test to see if the omega6/omega3 ratio is correct - should be around 3-1 or so. High levels of omega 3 are pro inflamatory and on fish oild supps should be taken

 

[LW64]

zkt,
You CLEARLY dont need to change a thing re your lipids. It's amazing how effective niacin is! IMHO, however, what you might like to do is have your lipids be more reflective of your diet rather than just manipulations due to taking supplements that are adjusting liver metabolism.

My labs before and three months into the diet
Before

TC 235
HDL 47
LDL 150
TRIG 191

After 3 months

TC 202
HDL 68
LDL 118
TRIG 59


Importance of Saturated Fats

Dr. Mary Enig is an authority on this subject:

http://www.westonaprice.org/know-your-fats/528-importance-of-saturated-fats-for-biological-functions.html

Her book "Know Your Fats" is very comprehensive.

SFA's resistance to oxidation because they lack a reactive double bond between carbon atoms is one of the main reasons why they need to be preferred over PUFAs, particularly Omega-6s aka industrial vegetable and seed oils.

Eating is a zero-sum game: if you think SFAs are bad, you have to replace them with something and that something has been PUFAs. While PUFAs have their place in a healthy diet. if they become dominant - as in a low saturated fat diet - they compete with Omega-3s for an enzyme that O-3 metabolism needs and this affects eicosanoid ratios in the body and that's what brings on the inflammation. Both O-6 and O-3 fatty acids are more susceptible to oxidation due to their multiple unsaturated carbon-carbon double bonds and this is known to contribute to atherosclerosis.

If you try to do low-carb AND low SFA, you will definitely increase your PUFA intake and essentially defeat the whole purpose of eating a whole foods diet. Eating excess PUFAs is at least as bad for you as sugar and wheat. In fact, it could be worse because of the connection between oxidized fats and heart disease.

I know there's epi data showing how heart disease rates have gone up as SFA consumption went down and PUFA consumption went up. When I find it, I'll post it.

I'm very happy to hear the MCT is helping your wife! It has made my mother more alert, at the very least, and that's an improvement. We'll see how it goes! I have a few more tricks up my sleeve now thanks to you. Have you looked at "The Brain Trust" book yet? McCleary is an interesting doctor. He originally studied Physics and worked with Roger Penrose (worked with Stephen Hawking) but went into neurosurgery.

He has a bunch of other recommendations in addition to the MCT/Flax/EPA cocktail.

E.g.:

Krill Oil: 2 to 4 caps/day
B Vitamins: 25 mg/day supplement
Magnesium (Calcium channel blocker analogous to Namenda): 600 mg/day
Taurine (reduces blood platelet stickiness and increases acetylcholine): 2 gm/day
Acetyl-L-Carnitine (enhances shuttling into brain cells): 100 to 500 mg/day
Alpha-Lipoic Acid (improves blood sugar metabolism): 50 to 300 mg/day
Co-Q10 (I'm not surprised. EVERYONE over the age of 50 needs this): 25 to 100 mg/day
Vitamin D: 400 to 2,000 IUs/day (she's already on 5,000IUs'day)
Huperzine A: 75 to 100 mg 2x/day
Vinpocetine: 5 to 10 mg/2x/day

 

[Structure]

BMI=19: not anissue. Chicken, veggies and olive oil have been more than friends. Just wondering if I havent been hanging with the wrong crowd. The sat fat is the other wild card. It somehow reduces inflammation. You gotta admit that inflammation is at the root of atherosclerosis. This paper brings it all together:
http://www.pasteur.edu.uy/publico/cayota/Bibliografia%20Dis%20End/DE%20y%20aterosclerosis/Atherosclerosis%20Inflamatory%20disease%20NEJM%202005.pdf

It's certainly intriguing, but you have to wonder why so many studies have been published that say otherwise. I'm still a bit traditional in my views regarding corticosteroids and saturated fats (i.e. that both are bad for cardiovascular health). However, you're a smart guy, so I'm not worried about you getting taken in by a fringe theory unless there's good reason to do so.

 

[LW64]

Case Closed

Here's the consumption data I mentioned in my last post:

http://wholehealthsource.blogspot.com/2009/05/coronary-heart-disease-epidemic_19.html

and part 1, for completeness

Whole Health Source: The Coronary Heart Disease Epidemic

 

[LW64]

It's certainly intriguing, but you have to wonder why so many studies have been published that say otherwise. I'm still a bit traditional in my views regarding corticosteroids and saturated fats (i.e. that both are bad for cardiovascular health). However, you're a smart guy, so I'm not worried about you getting taken in by a fringe theory unless there's good reason to do so.

Have you read "Good Calories, Bad Calories" [Taubes, 2007]?

 

[zkt]

You should do an essential fatty acid profile blood test to see if the omega6/omega3 ratio is correct - should be around 3-1 or so. High levels of omega 3 are pro inflamatory and on fish oild supps should be taken

Yes, the ratio going in would be very interesting, essential really, to know.
Got a link to where?

 

[cvictorg]

Yes, the ratio going in would be very interesting, essential really, to know.
Got a link to where?

where what? to take the test or about the ratio?

The quest labs test

http://www.questdiagnostics.com/hcp/testmenu/jsp/showTestMenu.jsp?fn=11254X.html&labCode=QTE (FATTY ACID PROF,C12-C22 - (11254X))

82426 Clinical: Fatty Acid Profile, Essential (C12-C22), Serum

http://www.metametrix.com/test-menu/profiles/fatty-acids/fatty-acids-erythrocytes

Increased Consumption of Fatty Acid Supplements

Evidence of the adverse effects of fatty acid deficiencies has led to sharply increased consumption of essential fatty acid supplements. When incorporated into the cell membranes of the body, these omega-3 and omega-6 fatty acids function as precursors for eicosanoids that control a host of cellular functions and responses. The balance between the pro-inflammatory and anti-inflammatory eicosanoids is influenced in large part by the balance of fatty acids we consume. Since inflammation has now been shown to be integral to so many disease processes, nutrients which counteract inflammation can have profound health benefits. But your patients need an answer to a critical question about their fatty acid supplementation- are they taking too little to be effective to such an excess that they are causing other health problems?

Anti-inflammatory and Pro-inflammatory Eicosanoids

Cold water fish oils contain high concentration of the omega-3 fatty acids EPA

(eicosapentaenoic acid) and DHA (Docosahexaenoic acid). EPA is the precursor for the Series 3 eicosanoids, which have potent anti-inflammatory effects. The oil from certain plant seeds, particularly borage, evening primrose, and black currant, have high concentrations of the omega-6 fatty acid GLA (gamma linolenic acid), the precursor to the anti-inflammatory Series 1 eicosanoids. The omega-6 fatty acid AA (arachidonic acid) is found in high concentration in the fat of red meats. AA is converted to the pro-flammatory Series 2 eicosanoids, increasing the risk for various disease and inflammatory processes in the body. The Bloodspot Fatty Acid Profile can guide patients to the right balance of FA intake.

Statins Negatively Impact Fatty Acid Status

Recent research has shown that HMG-CoA reductase inhibitors ("statins") can increase the relative amounts of AA in the blood, resulting in an increase in the AA:EPA ratio (1). "High fish oil consumption is now recommended for individuals at high risk for heart disease, and our findings suggest that increased dietary n-3 FAs---LNA, EPA, and DHA---may result in a more favorable FA profile during statin treatment." Routine monitoring of the AA:EPA ratio---an early marker of inflammation---would be particularly important for patients on these cholesterol-lowering drugs.

Excessive Intake of PUFAs Induces Free Radical Production

The free radical pathology induced by excessive intake of polyunsaturated fatty acids (PUFAs) develops insidiously. Researchers found that PUFA-induced lipid peroxidation is common among patients who supplement high doses of fatty acids without adequate antioxidant protection (2). Clinical management of fatty acid and antioxidant supplementation is aided by testing for fatty acid balance and measuring markers of oxidant damage.

Immunosuppressive Effects of Omega-3 Fatty Acids

As a result of all the positive research on the health benefits of fish oil and/or GLA rich oils, the nutrition industry has seen an explosive growth in consumption of these supplements. But taking too much and in the wrong balance is potentially dangerous, a fact not well appreciated or understood. The anti-inflammatory effects of omega-3 fatty acids can actually suppress immune function, leading to increased infections, poor wound healing, and possible tumor growth (3). The EPAGLA ratio in the Bloodspot Fatty Acid Profile can help fine tune intake of these Series-1 and -3 eicosanoid precursors.

Research is revealing the long-term health benefits of consumption of fish oils and/or GLA-rich oils on...
Cardiovascular Health
Endocrine influence
Glucose maintenance
Lipids and triglycerides
Metabolic parameters
Primary prevention
Secondary prevention
Children's Health and Development
Adolescent and teen health
ASD - Autism spectrum disorders
Attention, learning, and behavior
Disease prevention
Neurological development
Intelligence
Vision
Female Health and Reproduction
Peri-and post-menopause
Pregnancy & breastfeeding
Puberty and menstrual years
Immune Health
Acute infections
Allergies
Chronic immune deficiencies
Joint and Tissue Inflammation
Intestinal health
Joint flexibility & mobility
Lifestyle and Healthy Living
Alcohol and tobacco use
Body fat/weight
Fitness
Healthful living
Stress
Mental/Neurological Health
CNS Developement
Cognitive function/agent
Depression and mood
Mental balance

(1) Harris JI, Hibbeln JR, Mackey RH, Muldoon MF, Statin treatment alters serum n-3 and n-6 fatty acids in hypercholesterolemic patients. Prostaglandins, Leukotrienes and Essential Fatty Acids Volume 71, Issue 4, October 2004, Pages 263-269
(2) Lord, RS and Bralley, JA, Polyunsaturated Fatty Acid-Induced Anti-oxidant Insufficiency, Integrative Medicine Vol. 1, No. 1 Dec 2002/Jan 2003.
(3) Rees D, Miles EA, Banerjee T, Wells SJ, Roynette CE, et al., Dose-related effects of eicosapentaenoic acid on innate immune function in healthy humans: a comparison of young and older men. AM J Clin Nutr, 83:331 42, 2006

http://www.tsimtsoum.net/yyijjournal/100620-RBS-Inflm,Athero,osteoporosis-KK.pdf

 

[zkt]

where what? to take the test or about the ratio?

The quest labs test

http://www.questdiagnostics.com/hcp/testmenu/jsp/showTestMenu.jsp?fn=11254X.html&labCode=QTE (FATTY ACID PROF,C12-C22 - (11254X))

82426 Clinical: Fatty Acid Profile, Essential (C12-C22), Serum

http://www.metametrix.com/test-menu/profiles/fatty-acids/fatty-acids-erythrocytes

Increased Consumption of Fatty Acid Supplements

Evidence of the adverse effects of fatty acid deficiencies has led to sharply increased consumption of essential fatty acid supplements. When incorporated into the cell membranes of the body, these omega-3 and omega-6 fatty acids function as precursors for eicosanoids that control a host of cellular functions and responses. The balance between the pro-inflammatory and anti-inflammatory eicosanoids is influenced in large part by the balance of fatty acids we consume. Since inflammation has now been shown to be integral to so many disease processes, nutrients which counteract inflammation can have profound health benefits. But your patients need an answer to a critical question about their fatty acid supplementation- are they taking too little to be effective to such an excess that they are causing other health problems?

Anti-inflammatory and Pro-inflammatory Eicosanoids

Cold water fish oils contain high concentration of the omega-3 fatty acids EPA

(eicosapentaenoic acid) and DHA (Docosahexaenoic acid). EPA is the precursor for the Series 3 eicosanoids, which have potent anti-inflammatory effects. The oil from certain plant seeds, particularly borage, evening primrose, and black currant, have high concentrations of the omega-6 fatty acid GLA (gamma linolenic acid), the precursor to the anti-inflammatory Series 1 eicosanoids. The omega-6 fatty acid AA (arachidonic acid) is found in high concentration in the fat of red meats. AA is converted to the pro-flammatory Series 2 eicosanoids, increasing the risk for various disease and inflammatory processes in the body. The Bloodspot Fatty Acid Profile can guide patients to the right balance of FA intake.

Statins Negatively Impact Fatty Acid Status

Recent research has shown that HMG-CoA reductase inhibitors ("statins") can increase the relative amounts of AA in the blood, resulting in an increase in the AA:EPA ratio (1). "High fish oil consumption is now recommended for individuals at high risk for heart disease, and our findings suggest that increased dietary n-3 FAs---LNA, EPA, and DHA---may result in a more favorable FA profile during statin treatment." Routine monitoring of the AA:EPA ratio---an early marker of inflammation---would be particularly important for patients on these cholesterol-lowering drugs.

Excessive Intake of PUFAs Induces Free Radical Production

The free radical pathology induced by excessive intake of polyunsaturated fatty acids (PUFAs) develops insidiously. Researchers found that PUFA-induced lipid peroxidation is common among patients who supplement high doses of fatty acids without adequate antioxidant protection (2). Clinical management of fatty acid and antioxidant supplementation is aided by testing for fatty acid balance and measuring markers of oxidant damage.

Immunosuppressive Effects of Omega-3 Fatty Acids

As a result of all the positive research on the health benefits of fish oil and/or GLA rich oils, the nutrition industry has seen an explosive growth in consumption of these supplements. But taking too much and in the wrong balance is potentially dangerous, a fact not well appreciated or understood. The anti-inflammatory effects of omega-3 fatty acids can actually suppress immune function, leading to increased infections, poor wound healing, and possible tumor growth (3). The EPAGLA ratio in the Bloodspot Fatty Acid Profile can help fine tune intake of these Series-1 and -3 eicosanoid precursors.

Research is revealing the long-term health benefits of consumption of fish oils and/or GLA-rich oils on...
Cardiovascular Health
Endocrine influence
Glucose maintenance
Lipids and triglycerides
Metabolic parameters
Primary prevention
Secondary prevention
Children's Health and Development
Adolescent and teen health
ASD - Autism spectrum disorders
Attention, learning, and behavior
Disease prevention
Neurological development
Intelligence
Vision
Female Health and Reproduction
Peri-and post-menopause
Pregnancy & breastfeeding
Puberty and menstrual years
Immune Health
Acute infections
Allergies
Chronic immune deficiencies
Joint and Tissue Inflammation
Intestinal health
Joint flexibility & mobility
Lifestyle and Healthy Living
Alcohol and tobacco use
Body fat/weight
Fitness
Healthful living
Stress
Mental/Neurological Health
CNS Developement
Cognitive function/agent
Depression and mood
Mental balance

(1) Harris JI, Hibbeln JR, Mackey RH, Muldoon MF, Statin treatment alters serum n-3 and n-6 fatty acids in hypercholesterolemic patients. Prostaglandins, Leukotrienes and Essential Fatty Acids Volume 71, Issue 4, October 2004, Pages 263-269
(2) Lord, RS and Bralley, JA, Polyunsaturated Fatty Acid-Induced Anti-oxidant Insufficiency, Integrative Medicine Vol. 1, No. 1 Dec 2002/Jan 2003.
(3) Rees D, Miles EA, Banerjee T, Wells SJ, Roynette CE, et al., Dose-related effects of eicosapentaenoic acid on innate immune function in healthy humans: a comparison of young and older men. AM J Clin Nutr, 83:331 42, 2006

http://www.tsimtsoum.net/yyijjournal/100620-RBS-Inflm,Athero,osteoporosis-KK.pdf

The paper lends more support to the of the role of inflammation in atherosclerosis and particularily the importance of the W3/W6 FA ratio. Thanks.
These test will be out of pocket for me. Do you know the ~ cost(s)?

 

[Claude Monnet]

Have a look at this:

The Great Cholesterol Con

 

[Structure]

Have a look at this:

The Great Cholesterol Con

You've got to watch out for this kind of stuff. The next time you encounter a site that seems to be a very long, single web page that is building up to something: do yourself a favor, and just click on the "page dn" button to see what is at the bottom (or better yet, just click the "end" button). You'll find out what the punch line always is: "CLICK HERE NOW TO ORDER"

Frequently, I find myself disagreeing with some of the fringe theories that get discussed on these forums, but in general, I just keep it to myself. It's a free internet after all. I'm making an exception this time because this web site is such a prime example of the modern version of a snake-oil sale.

Here is a succinct algorithm to reproduce a site like this (from Quackwatch: Index to "Fad" Diagnoses)

Recipe for a New Fad Disease

1. Pick any symptoms—the more common the better.
2. Pick any disease—real or invented. (Real diseases have more potential for confusion because their existence can't be denied.)
3. Assign lots of symptoms to the disease.
4. Say that millions of undiagnosed people suffer from it.
5. Pick a few treatments. Including supplements will enable health food stores and chiropractors to get in on the action.
6. Promote your theories through books and talk shows.
7. Don't compete with other fad diseases. Say that yours predisposes people to the rest or vice versa.
8. Claim that the medical establishment, the drug companies, and the chemical industry are against you.
9. State that the medical profession is afraid of your competition or trying to protect its turf.
10. If challenged to prove your claims, say that you lack the money for research, that you are too busy getting sick people well, and that your clinical results speak for themselves.

I'm a bit skeptical, but I too have been taken in a few times. The first time was when I believed the hype behind the Atkins diet (I still think part of their claims are true, but I was such a believer that I thought the Atkins diet was a superior diet for everyone, and that all could reap countless health benefits by following it). The second time was with the adrenal fatigue holistic nonsense (I didn't have adrenal fatigue). I still think that adrenal hypofunction is real, but I think that real adrenal hypofunction can be tested for by directly measuring HPA hormones just like hypogonadism can be tested for by directly measuring HPT hormones.

 

[cvictorg]

The paper lends more support to the of the role of inflammation in atherosclerosis and particularily the importance of the W3/W6 FA ratio. Thanks.
These test will be out of pocket for me. Do you know the ~ cost(s)?

You could contact

http://www.greatplainslaboratory.com/home/eng/fattyacid.asp

http://www.metametrix.com/test-menu/profiles/fatty-acids/fatty-acids-bloodspot

The mayo clinic charges $423.00

82426 Overview: Fatty Acid Profile, Essential (C12-C22), Serum

Another article for you to look at

http://www.csuchico.edu/grassfedbeef/research/documents/sources/Simopoulos%20omega3%20review%202004.pdf