Gyroscopic Investing

Correlation or causation?

A meta-genomic study, conducted as part of the EU-based MetaHIT (Metagenomics of the Human Intestinal Tract) project involving eight countries, reveals a prominent association between the gut bacteria environment and type-2 diabetes.  Oluf Borbye Pedersen, from the University of Copenhagen (Denmark), and colleagues identified that patients with type-2 diabetes have an imbalance in gut bacteria, specifically an excess of harmful strains and a deficit of beneficial strains.  The study authors submit that their findings: “demonstrate that these gut microbial markers might be useful for classifying type 2 diabetes.”?

http://www.nutraingredients-usa.com/Res ... -diabetes/

MEDIA: there is about as much chance of getting an unbiased article on supplements as getting an unbiased article in the NY times on a conservative i.e. slim.

WiseOne:  Your concern about caogulation problems is reasonable given what vit K does, but is not born out.

Here is a review of vit K including the toxicity (coagulation problems are not listed)
http://lpi.oregonstate.edu/infocenter/v ... /vitaminK/

To each his own opinion, but not medical facts. 

MangoMan wrote:

Gumby wrote: There's no real monetary incentive to figure out what's causing the disease. So, the solution to fixing the symptom tends to be pharmaceuticals that only target symptoms. The names of the various diseases reflect this symptomatic-treatment approach. If you have "Heartburn," the fix is to use a drug to stop the burning sensation and the drug tends to cost a lot because it's patented to just do a better job at treating the symptom than the previous drug that was used. Fixing the cause of the disease would end that cycle of lucrative pharmaceutical symptom-treating, but drug companies have little incentive to solve what's causing a disease. (There are practitioners who attempt to fix the cause of things like heartburn, and the treatments tend to be very inexpensive.)

Could you perhaps supply some specific info on that, or direct me where to find it? I have suffered from from brutal heartburn/reflux for years, and I am concerned about the effects of long term use of H2 blockers and proton-pump inhibitors.

You bet..  The solution tends to work with most people in your situation.

I was listening to a Chris Kresser podcast about two weeks ago. He practices acupuncture and "functional medicine" out in San Francisco. Functional medicine attempts to solve symptoms by addressing the underlying problem. I've never been to a functional medicine practitioner, but I've got to say that it is a very interesting approach to dealing with chronic health issues. I might try it as a second opinion if I ever need one. Anyway...

Most doctors will treat digestion issues by recommending you avoid certain foods (such as meat, acidic foods, or FODMAPs) and by prescribing medications to lower the acid in your stomach to prevent indigestion symptoms. The problem with that approach is just treating a symptom — not the cause of the problem.

It turns out that the most people (perhaps as much as 90%) who have GERD or heartburn actually don't have enough acid — since stomach acid and pepsin is required to dissolve and break down meat. If you've ever watched an episode of a TV show or movie where the bad guys dissolve a dead body in acid, you'll know what I mean. Well, your stomach is the same way. If you have low stomach acid, your stomach doesn't break down the food properly and that's when bad things start to happen in your gut. The symptom, in some people, is often a burning sensation in your esophagus as undigested food is backed up in the stomach. So, it's easy to think this means you have too much acid in your stomach, but for most people that isn't the case.

In fact, humans produce less stomach acid as they age. If too much stomach acid was always the cause of heartburn/GERD, there'd be a lot more children with heartburn/GERD. So, having too little stomach acid is the real reason why people tend to get heartburn/GERD as they age.

Unfortunately, doctors will put heartburn/GERD patients on medications to lower stomach acid — making the problem worse since food isn't digested properly on PPIs. Of course, this treatment does lessen the symptoms of acid reflux, but it ends up being a problem because individuals with low stomach acid and poor digestion become Vitamin B12 deficient (and deficient in other nutrients) if they don't treat the cause of the problem (you need stomach acid to absorb B12, which is usually obtained from digesting meat).

Now, I think it's safe to say that not all Heartburn/GERD cases are caused by low stomach acid. Some people do have too much stomach acid or entirely different digestive issues. So, it's important to realize that everyone is different and the following articles will set you in the right direction to discovering the underlying cause of your digestion problems. Keep in mind that this practitioner recommends ancestral diets (high fat, meats, low carbs, etc) so if you've been missing those foods, you may be able to enjoy them. Be sure to comb through the comments as Kresser provides answers to most questions there.

So, how do you attempt to cure Heartburn/GERD?

First, start by reading the series of articles listed here: Heartburn/GERD

The first article in the series on that page is especially interesting: What Everyone Ought to Know About Heartburn and GERD

If it turns out you have low stomach acid (as most people with GERD/heartburn do), it's easily treatable with over-the-counter HCI/pepsin tablets — to generate stomach acid — and a few simple rules explained here…

See: Get rid of heartburn and GERD forever in three simple step

If it's true that most heartburn/GERD sufferers just have low stomach acid, it really makes me wonder if most doctors just get all their solutions directly from pharmaceutical companies who want us to buy drugs for the rest of our lives.

It is possible to transition from PPIs to over-the-counter acid pills over a short period of time, but the longer you've been on PPIs, the more likely you may need to be on acid pills indefinitely. But, for most people, the ability to eat high quality/pastured fatty foods is worth it.

Good luck!

it might also be worth looking through the forum's saturated fat, paleo diet, nutrition threads, a number of low carb followers here (myself included) found low carb diets made a significant  improvement in the frequency and severity of acid reflux problems.

MangoMan wrote: Gumby,

Thanks for that tremendous post. I will start looking into this immediately, and post results in the future.

You're welcome!

For the most part, you should be able to determine if you have low stomach acid by following the advice in the articles. But, if you run into any difficulties, you may want to consider seeing a functional medical practitioner near you — at least for a second opinion — since their primary goal is to find the real underlying cause of your health issues.

You can search for a practitioner near you here: http://www.functionalmedicine.org

But, you should be fine with those articles, and some simple experimentation, if you have typical heartburn/GERD.

Benko wrote:Here is a review of vit K including the toxicity (coagulation problems are not listed)
http://lpi.oregonstate.edu/infocenter/v ... /vitaminK/

You gotta love the Linus Pauling Institute's review of Vitamin K. It briefly explains the difference between Vitamin K1 and Vitamin K2 and then proceeds to just recommend sources of Vitamin K1, implying that some K2 is synthesized by bacteria in a healthy large intestine.

But, then they acknowledge the human body's inability to convert much Vitamin K1 into Vitamin K2...

Linus Pauling Institute at Oregon State University wrote:"Bacteria that normally colonize the large intestine synthesize menaquinones (vitamin K2), which are an active form of vitamin K. Until recently it was thought that up to 50% of the human vitamin K requirement might be met by bacterial synthesis. However, research indicates that the contribution of bacterial synthesis is much less than previously thought, although the exact contribution remains unclear"
Source: http://lpi.oregonstate.edu/infocenter/v ... /vitaminK/

And then they make the following recommendation...

Linus Pauling Institute at Oregon State University wrote:"Although the AI for vitamin K was recently increased, it is not clear if it will be enough to optimize the gamma-carboxylation of vitamin K-dependent proteins in bone (see Osteoporosis). Multivitamins generally contain 10 to 25 mcg of vitamin K, while vitamin K or "bone" supplements may contain 100 to 120 mcg of vitamin K. To consume the amount of vitamin K associated with a decreased risk of hip fracture in the Framingham Heart Study (about 250 mcg/day), an individual would need to eat a little more than 1/2 cup of chopped broccoli or a large salad of mixed greens every day. Though the dietary intake of vitamin K required for optimal function of all vitamin K dependent proteins is not yet known, the Linus Pauling Institute recommends taking a multivitamin-mineral supplement and eating at least 1 cup of dark green leafy vegetables daily. Replacing dietary saturated fats like butter and cheese with monounsaturated fats found in olive oil and canola oil will also increase dietary vitamin K intake and may also decrease the risk of cardiovascular diseases."
Source: http://lpi.oregonstate.edu/infocenter/v ... /vitaminK/

They really do a terrible job of explaining the difference between Vitamin K1 and Vitamin K2. Their roles are so different that many believe they should be considered completely different vitamins.

Here's a different perspective on Vitamin K1 and K2:

Chris Kresser wrote:New evidence, however, has confirmed that vitamin K2's role in the body extends far beyond blood clotting to include protecting us from heart disease, ensuring healthy skin, forming strong bones, promoting brain function, supporting growth and development and helping to prevent cancer – to name a few. In fact, vitamin K2 has so many functions not associated with vitamin K1 that many researchers insist that K1 and K2 are best seen as two different vitamins entirely.

A large epidemiological study from the Netherlands illustrates this point well. The researchers collected data on the vitamin K intakes of the subjects between 1990 and 1993 and measured the extent of heart disease in each subject, who had died from it and how this related to vitamin K2 intake and arterial calcification. They found that calcification of the arteries was the best predictor of heart disease. Those in the highest third of vitamin K2 intakes were 52 percent less likely to develop severe calcification of the arteries, 41 percent less likely to develop heart disease, and 57 percent less likely to die from it. (Geleijnse et al., 2004, pp. 3100-3105) However, intake of vitamin K1 had no effect on cardiovascular disease outcomes.

While K1 is preferentially used by the liver to activate blood clotting proteins, K2 is preferentially used by other tissues to deposit calcium in appropriate locations, such as in the bones and teeth, and prevent it from depositing in locations where it does not belong, such as the soft tissues.(Spronk et al., 2003, pp. 531-537) In an acknowledgment of the different roles played by vitamins K1 and K2, the United States Department of Agriculture (USDA) finally determined the vitamin K2 contents of foods in the U.S. diet for the first time in 2006. (Elder, Haytowitz, Howe, Peterson, & Booth, 2006, pp. 436-467)

Another common misconception is that human beings do not need vitamin K2 in their diet, since they have the capacity to convert vitamin K1 to vitamin K2. The amount of vitamin K1 in typical diets is ten times greater than that of vitamin K2, and researchers and physicians have largely dismissed the contribution of K2 to nutritional status as insignificant.

However, although animals can convert vitamin K1 to vitamin K2, a significant amount of evidence suggests that humans require preformed K2 in the diet to obtain and maintain optimal health. The strongest indication that humans require preformed vitamin K2 in the diet is that epidemiological and intervention studies both show its superiority over K1. Intake of K2 is inversely associated with heart disease in humans while intake of K1 is not (Geleijnse et al., 2004, pp. 3100-3105), and vitamin K2 is at least three times more effective than vitamin K1 at activating proteins related to skeletal metabolism. (Schurgers et al., 2007) And remember that in the study on vitamin K2's role in treating prostate cancer, which I mentioned at the beginning of this article, vitamin K1 had no effect.

All of this evidence points to the possibility that vitamin K2 may be an essential nutrient in the human diet. So where does one find vitamin K2 in foods? The following is a list of the foods highest in vitamin K2, as measured by the USDA:

Foods high in vitamin K2

- Natto
- Hard cheese
- Soft cheese
- Egg yolk
- Butter
- Chicken liver
- Salami
- Chicken breast
- Ground beef

Unfortunately, precise values for some foods that are likely to be high in K2 (such as organ meats) are not available at this time. The pancreas and salivary glands would be richest; reproductive organs, brains, cartilage and possibly kidneys would also be very rich; finally, bone would be richer than muscle meat. Fish eggs are also likely to be rich in K2.

It was once erroneously believed that intestinal bacteria are a major contributor to vitamin K status. However, the majority of evidence contradicts this view. Most of the vitamin K2 produced in the intestine are embedded within bacterial membranes and not available for absorption. Thus, intestinal production of K2 likely makes only a small contribution to vitamin K status. (Unden & Bongaerts, 1997, pp. 217-234)

On the other hand, fermented foods, however, such as sauerkraut, cheese and natto (a [fermented] soy dish popular in Japan), contain substantial amounts of vitamin K2. Natto contains the highest concentration of K2 of any food measured; nearly all of it is present as MK-7, which research has shown to be a highly effective form. A recent study demonstrated that MK-7 increased the percentage of osteocalcin in humans three times more powerfully than did vitamin K1. (Schurgers & Vermeer, 2000, pp. 298-307)

It is important to note that commercial butter is not a significantly high source of vitamin K2. Dr. Weston A. Price, who was the first to elucidate the role of vitamin K2 in human health (though he called it “Activator X”? at the time) analyzed over 20,000 samples of butter sent to him from various parts of the world. As mentioned previously in this paper, he found that the Activator X concentration varied 50-fold. Animals grazing on vitamin K-rich cereal grasses, especially wheat grass, and alfalfa in a lush green state of growth produced fat with the highest amounts of Activator X, but the soil in which the pasture was grown also influenced the quality of the butter. It was only the vitamin-rich butter grown in three feet or more of healthy top soil that had such dramatic curing properties when combined with cod liver oil in Dr. Price’s experiments and clinical practice.

Therefore, vitamin K2 levels will not be high in butter from grain-fed cows raised in confinement feedlots. Since the overwhelming majority of butter sold in the U.S. comes from such feedlots, butter is not a significant source of K2 in the diet for most people. This is yet another argument for obtaining raw butter from cows raised on green pasture.
Source: Vitamin K2: The Missing Nutrient

So, if you were to follow the Linus Pauling Institute's recommendations, you might be led to believe that Vitamin K1 and K2 were generally the same thing and you'd basically be avoiding all of the important natural sources of the vital Vitamin K2 that are typically found in pastured animal products, like grassfed butter.

Clearly the Linus Pauling Institute wants to give 'politically correct' advice for avoiding saturated fats — unfortunately few people seem to realize that saturated fat is actually only a fraction of most animal fats. (I'm guessing if they didn't make politically correct recommendations, they probably wouldn't receive much funding from the food industry.) But, it really is something to see as each year more and more evidence mounts to support the health benefits of grassfed/pastured animal food and all they can do is steer people towards plants that are difficult to digest and tend to lack the bioavailable nutrients found in animal foods. Then again, I suppose few people really have access to grassfed/pastured animal foods these days.

This has some really interesting and referenced background on bone broth and its components.

http://www.townsendletter.com/FebMarch2 ... th0205.htm

MachineGhost wrote: This has some really interesting and referenced background on bone broth and its components.

http://www.townsendletter.com/FebMarch2 ... th0205.htm

Quite an in-depth overview of bone broth. Who knew it had so many nutrients in it? Speaking of glycine...

What's also fascinating is that our ancestors made a real effort to consume foods made from from all parts of the animals: skin, bones, liver, etc. They probably didn't realize how important it was to consume those nutrients — most people were just trying to make sure food never went to waste.

But, it turns out that if you only ate muscle meat — and avoided beans, bones, skin and offal — you'd really wreak havoc on your body over time by not getting the right balance of nutrients...

Chris Masterjohn wrote:Muscle meats and eggs are very rich in methionine, which increases our need for homocysteine-neutralizing nutrients (vitamins B6, B12, folate, betaine, and choline), and also increases our need for the amino acid glycine, found most abundantly in skin and bones.

[...]

While the metabolism of methionine uses up glycine, betaine and folate can generate glycine in addition to neutralizing homocysteine, although the effect of betaine is restricted primarily to certain tissues such as the liver and kidney.

But where's all the folate?  Liver and beans.  You can get lots of folate if you eat liver, and you can get lots by eating lentil soup, but if you're eating a bean-free diet and you can't stand the taste of liver, you're going to have to eat the quantities of green vegetables that Joel Fuhrman recommends in order to obtain a comparable amount of folate.

And where's the betaine?  We can make betaine from the choline obtained from egg yolks and liver, but the best source is spinach and the most common source is wheat.  Again, the utility of choline and betaine in neutralizing homocysteine and generating glycine is limited to the liver and kidney, so folate is more important.

Glycine itself is most abundant in skin and bones.
Source: http://blog.cholesterol-and-health.com/ ... bones.html

It's actually pretty amazing to think about, but our ancestors were supplementing themselves pretty well if they were just eating typical ancestral foods: grass fed butter, cheese, liver, beans, bone broths, marrow, etc.

I've been doing my best to eat liver once or twice a week when I can. And, though I never thought it was possible, I actually discovered a few recipes that actually make liver taste good!

In trying to explain the difference in results regarding lifespan extension between the NIA and WNPRC studies, the NIA scientists noted that the diets fed to the two groups of monkeys differed significantly. The WNPRC monkeys received a diet containing 28% sucrose, compared to only 4% in the diet given to the monkeys at NIA. The NIA diet, which has a natural ingredient base, also contains fish oil and phytochemicals, including flavonoids, and protein derived from wheat, corn, soybean, fish, and alfalfa. In contrast, the WNPRC diet is a “purified”? diet with no added fish oil or phytochemicals, and protein from a single source called lactalbumin. Hence, the authors suggested that the WNPRC monkeys on caloric restriction lived longer than their non-restricted counterparts because they got less of a bad diet that caused the ad libitum-fed (without restraint) control monkeys to die prematurely. In contrast, the NIA monkeys got a healthier diet and lived longer, and under these circumstances, caloric restriction did not extend lifespan.

...


Q. What do you think about the recently published study by scientists at the NIA that reported that long-term caloric restriction for about 25 years in monkeys did not affect lifespan?

A. It doesn’t surprise me! Dietary restriction works in organisms ranging from yeast to mice. The question is whether it will work in our closest biological relatives, the primates. A previous study done in monkeys in Wisconsin had published results different from those we observed in this study from NIA. Why? Well, I think there are several possible reasons. For example, the diet used in the Wisconsin study was high in sucrose, which can be considered a metabolic stress. Also, the genetic background of the monkeys used in the NIA study is diverse compared to the homogenous genetic background of monkeys used in the Wisconsin study, and we know from previous studies done in mice that the benefits of dietary restriction depend on the genetic background of the animal. For example, it was observed that dietary restriction had a deleterious effect in some animals. The “ad libitum”? control monkeys in the NIA study were not really fed without restraint; there were some restrictions. So there are differences, including diet, genetic background, and other factors, between these two studies—and, therefore, they produced different results.

Source: Linus Pauling Institute, Research Newsletter-Fall/Winter 2012

I finally got my EPA/DHA test results in.  Apparantely, the first blood sample was invalid so I had to send in another (not like they contacted me or anything!).  Unfortunately, I intentionally started taking fish oil right after the first sample (I've already been taking flaxseed meal and krill oil for 5+ years), so who knows how much worse the values were originally.  I eat a low-carb, balanced fat diet restricted in inflammatory AA so its rather interesting that AA is bad as I was suspecting, but I can't see how or why it would be so high unless it is genetic?  The thing is I've experimented with different fish oil capsules or liquids over the years and have never seen a reduction in inflammation sensitivity.

Here's how to interpret the scores: https://www.lef.org/magazine/mag2010/ma ... tus_01.htm

Pugchief, I was just thinking about your quest the other day. That's amazing. Chalk one up for functional medicine, I guess!

Wow. Truly amazing. Congrats!

MachineGhost wrote:I eat a low-carb, balanced fat diet restricted in inflammatory AA so its rather interesting that AA is bad as I was suspecting, but I can't see how or why it would be so high unless it is genetic?  The thing is I've experimented with different fish oil capsules or liquids over the years and have never seen a reduction in inflammation sensitivity.

Just curious, but which edible oils are you using in food preparation and how much of them would you say you use on a typical day?

Gumby, I wanted to thank you as well for recommending Crowdtilt to me.

Reub wrote: Gumby, I wanted to thank you as well for recommending Crowdtilt to me.

You bet, Reub! And congrats on tilting. Hope your dad is doing better.

Gumby wrote:

Reub wrote: Gumby, I wanted to thank you as well for recommending Crowdtilt to me.

You bet, Reub! And congrats on tilting. Hope your dad is doing better.

Yeah, I hope things get better for you, Reub.  Crowdtilt is pretty interesting.

MG, I have two thoughts....

My initial thought is that you may be taking too much olive oil. I seem to remember that was one of the oils you tolerated. Your Linoleic Acid levels are quite high and olive oil tends to be a high source of Omega-6 — especially Linoleic Acid. The word "Linoleic" is actually derived from "oleic" (i.e. "olive").

Chris Masterjohn sums it up this way...

Chris Masterjohn wrote:"An excess of linoleate from vegetable oil will interfere with the production of DHA while an excess of EPA from fish oil will interfere with the production and utilization of AA"
Source: http://www.cholesterol-and-health.com/P ... eport.html

Take a look at the following sources of Linoleic acid...

See: http://en.wikipedia.org/wiki/Linoleic_a ... ry_sources

As you will notice in that Wikipedia link, Olive Oil is relatively high compared to coconut oil, which has much less LA in it.

So, Coconut oil is low in Omega-6, and has no Omega-3 (a good thing when using heat). From Dr. Mary Newport (the Alzheimer's coconut-research doc):

Dr. Mary Newport wrote:"Olive oil is about 10% omega-6 and has a 13:1 ratio,and by the way, olive oil is not all mono-unsaturated fat and has about 14% long chain saturated fats. My favorite, coconut oil, is about 4% omega-6 and has no omega-3."
Source: http://coconutketones.blogspot.com/2009 ... acids.html

My second thought is that the Flax Oil did you absolutely no good. Supposedly less than 5% of ALA gets converted to EPA, and less than 0.5% (one-half of one percent) of ALA is converted to DHA.

See: http://chriskresser.com/why-fish-stomps ... of-omega-3

So, my guess is that when you use olive oil and flax oil together, the olive oil competes with the flax oil for the same enzymes and the olive oil ends up being more efficient at converting to AA than the flax oil is at converting to EPA and DHA.

What do you think? Sound plausible?

I'd be willing to bet that the switch to Fish Oil is helping a lot. But, my sense is that you don't want to take too much fish oil for fear of it oxidizing. I believe Chris Masterjohn only recommends something like 1 gram per day at most for maintenance and low oxidation. His findings are in his PUFA report that is probably worth reading (for a fee):

See: http://www.cholesterol-and-health.com/P ... eport.html

Gumby wrote: Just curious, but which edible oils are you using in food preparation and how much of them would you say you use on a typical day?

Just EVOO, about 1-3T.  I use nothing else since it is too inflammatory or toxic.  Additional sources of LA would be the 1/4 cup of raw almonds, 2T of raw flaxseed meal and more recently, 1T of non-GMO lecithin.

I am not sure yet but I may be able to tolerate pasteurized grass-fed butter, unlike the grass-fed ghee.  I will have to do a food challenge test to be 100% sure.

I don't really see a realistic solution other than ingesting some seriously large amounts of fish oil for a very long time.  I wonder what the average Japanese daily intake of EPA/DHA is.

Gumby wrote: What do you think? Sound plausible?

Hmm it's plausible, but I'm not sure if its applicable.  For me, unrefined EVOO is inert, but there is a clear threshold where too much LA or AA from any source causes inflammation, whether that be refined or unrefined.  I don't take the flaxseed meal for the ALA, but for the lignans.

Here's the problem though.  The RDA for LA is 17 grams a day, so the almonds, the lecithin, the flaxseed meal, a krill oil capsule, and 3T of EVOO:

Lipids (51%)
===========================================
Saturated            |    8.4 g      42%
  Omega-3            |    4.0 g      252%
  Omega-6            |    10.4 g      61%
Cholesterol          |    0.0 mg      0%

...don't even get me to it.  Now add in 15 grams (3x a serving) of cod liver oil:

Lipids (57%)
===========================================
Saturated            |    11.5 g      57%
  Omega-3            |    6.9 g      434%
  Omega-6            |    10.5 g      62%
Cholesterol          |    30.2 mg      10%

...before solid food increases the Omega-6 even more.  1 gram of unconcentrated fish oil just isn't going to cut it (1.3 grams of that Omega-3 is ALA).  I only take 550mg EPA/DHA now since krill oil is worthless for raising serum levels and I'm skeptical spending a lot on fish oil that has no detectable benefit.

The almonds contain almost as much LA in just 1 ounce as in 3T of EVOO.  But again, we're not talking about high levels of intake here to begin with.

If there is some formula for determining the "potency" of Omega-3 vs Omega-6 on a weight basis, I'm all eyes.

What I can do eventually is replace the flaxseed meal with a lignan supplement (oh joy, another freakin' pill!) and see if I can replace the EVOO with refined coconut oil for cooking and grass-fed butter for veggies, etc..  For now I will double or triple up the concentrated, elephant-sized fish oil gelcap, but my gag reflex won't tolerate that for the long-term.  So, I'll be trying the expensive LEF version when I run out; they've apparantely reduced the size by using regular capsules instead of gelcaps, plus they're still the only brand including sesame seed extract to prevent oxidization.  Not sure its worth the money, but a smaller capsule size and no corresponding increase in the quantity to take would be a huge win.  Actually, I should try it out now using that $25 credit and member pricing!

Speaking of which, if anyone would like a free 1-month membership (discount pricing but is not as good as Amazon, etc.) and a $25 product credit at LEF, enter this contest:

https://mycart.lef.org/Sweeps/E/Entry.a ... gn=SWH203W

Ah, ok. So, eating lots of LA isn't supposed to raise AA, since the tissues levels of AA plateau at low levels of LA according to Masterjohn. (Again, purchase his report if you want to read more about this).

So, it seems clear that the Flax Oil is what screwed up your numbers. Humans — especially those who have compromised digestive systems — are pretty much unable to convert any ALA into DHA/EPA. So, you have to assume that the fish oil will help significantly. Check your numbers again in 6 months from when you started taking fish oil.

As I'm sure you are aware, the best way to improve the Omega 3:6 ratio is to eat less Omega 6...

How much omega-3 is enough? That depends on omega-6

And, then there is eating fish to consider — as well as its absorption...

The fish vs. fish oil smackdown

MachineGhost wrote:What I can do eventually is replace the flaxseed meal with a lignan supplement (oh joy, another freakin' pill!)

Isn't Lignan a phytoestrogen? ALA does you no good as far as I can see (beyond some unproven cancer reduction). Our bodies really can't convert any ALA to DHA/EPA. Studies have shown that ALA consumption doesn't raise serum levels of DHA/EPA. This is why many researchers now believe that the largest health benefits we get from omega-3 fats come from the longer chain derivatives, such as EPA/DHA.

MachineGhost wrote:I can replace the EVOO with refined coconut oil for cooking and grass-fed butter for veggies, etc.

If you want to try eating less LA, you should seriously think about Pharmaceutical Grade MCT oil (sold by Dr. Bernd Friedlander). It's the same MCT oil that Dave Asprey sells. The oil is just a high-quality filtered coconut oil where they filter coconut oil down to the capric & caprylic acids. You should definitely be able to tolerate that if you start with teaspoon doses and it's amazing brain food (as explained by Dr. Mary Newport). Many people swear by MCT oil, not only for its affect on the brain, but for the way it enhances the flavor of food. On its own, it has no taste. I just ordered my first bottle the other day (new shipments expected in the next two weeks). People say you can drizzle it on a salad and it makes the salad taste amazing. Brush it on top of sushi and you won't believe how good it tastes. And you can cook with it up to ~350º. You can also rub it onto scars and it will heal them quite quickly. Now Foods also makes a good MCT oil, but I don't know if it's pharmaceutical grade and I don't think it's as high in capric & caprylic acids as the pharmaceutical grade MCT oil.

MachineGhost wrote:For now I will double or triple up the concentrated, elephant-sized fish oil gelcap, but my gag reflex won't tolerate that for the long-term.

Your body won't tolerate that long term either (due to oxidation), so only use it to adjust your levels. Your best bet seems to be to reduce n-6 during this time as well and avoid ALA for its inefficiency.

Gumby wrote: How much omega-3 is enough? That depends on omega-6

Good article.  So essentially, 1T of fish oil is necessary to get a 60% tissue concentration of EPA/DHA equivalent to the Japanese, and even that is not as ideal as old-school Eskimos or Greenlanders which is really extreme (they do tend to die of hemmorhaging-type deaths).  1T also appears enough to offset the typical S.A.D. LA intake.  Considering I'm even higher than that, I feel more confident about such a dosage now.

Gumby wrote: The fish vs. fish oil smackdown

Leaving aside taste considerations, I think eating that much fish is neither fun nor affordable.  But he does bring up a good point of absorption.  I would never take an esthyl ester form of fish oil as it is unstable and not the natural state found in fish (triglycerides).  The latter is not as common in the marketplace nor necessarily inexpensive or concentrated, but it can be found.  I haven't updated it in a year or more, but I maintain a spreadsheet comparing many different forms and brands of fish oil as to the net absorption kinetics of EPA/DHA vs its cost.

Gumby wrote: Isn't Lignan a phytoestrogen? ALA does you no good as far as I can see (beyond some unproven

Yes, but its not a bad phytoestrogen.  It helps detoxify harmful estrogens to protect the prostate.  Since prostate BPH/cancer starts in men in their 30's, its not something to only worry about only when it becomes a serious problem 35+ years later (by which time its too late!).  Aside for helping to thicken my smoothies a bit, I don't think I'll miss it.  I'll keep the remaining on hand to continue to use as an egg replacer.

Gumby wrote: If you want to try eating less LA, you should seriously think about Pharmaceutical Grade MCT oil (sold by Dr. Bernd Friedlander). It's the same MCT oil that Dave Asprey sells. The oil is just a high-quality filtered coconut oil where they filter coconut oil down to the capric & caprylic acids. You should definitely be able to tolerate that if you start with teaspoon doses and it's
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I'm familiar with MCT oil since it provides ketones for a glucose-intolerant brain -- very useful for ameliorating Alzheimer's Disease.  I am hypersensitive to tiny amounts of MCT though, get liver pain and/or naseua.  However for sake of the argument, why would I want to give up the medium-chain saturates that make coconut oil healthy and temperature stable for cooking?  And what about the missing lauric acid which is a large part of coconut oil's benefits?  AFAIK, caprylic acid is just useful against candida overgrowth in the vagina or intestine.

Gumby wrote: amazing brain food (as explained by Dr. Mary Newport). Many people swear by MCT oil, not only for its affect on the brain, but for the way it enhances the flavor of food. On its own, it has no taste. I just ordered my first bottle the other day (new shipments expected in the next two weeks). People say you can drizzle it on a salad and it makes the salad taste amazing. Brush it on top of sushi and you won't believe how good it tastes. And you can cook with it up to

Are you sure there's no MSG/umami involved with this?  Foodstuffs does not just normally "taste better" without that kind of neurotoxin involved.

Gumby wrote: Your body won't tolerate that long term either (due to oxidation), so only use it to adjust your levels. Your best bet seems to be to reduce n-6 during this time as well and avoid ALA for its inefficiency.

Yessir!  But, you do realize how very little LA I'm already eating to begin with?  Sheesh.

MachineGhost wrote:Considering I'm even higher than that, I feel more confident about such a dosage now.

Yes. Should be fine as you even things out over the short term.

Btw, in 2010, Masterjohn wrote a great piece on the dangers of too much fish oil...

Chris Masterjohn: Precious Yet Perilous

Kresser gets a lot of his EFA recommendations from Masterjohn, and Kresser passed the info along to his readers here a few weeks later...

Chris Kresser: When it comes to fish oil, more is not better

Definitely read the piece from Masterjohn, but keep in mind that he's updated some of his findings in his PUFA report this year (which I haven't read).

MachineGhost wrote:Leaving aside taste considerations, I think eating that much fish is neither fun nor affordable.

In terms of affordability, wild fish is certainly more expensive. But, I've recently become a fan of Faroe Island farmed salmon. It's much more affordable, but it's nothing like other farmed salmon. Definitely worth researching as it is sustainable and about as good as farmed can be. Eat fish two or three times a week and you're in good shape.

In terms of taste, well you need to make it taste good. One really needs to find a way to incorporate more seafood in the diet in order to balance Omega 3:6 in today's high n-6 world without overdosing on fish oil. Personally, I've really enjoyed Rick Stein's Complete Seafood cookbook. Great photos, steps and relatively easy recipes.

MachineGhost wrote:But he does bring up a good point of absorption.  I would never take an esthyl ester form of fish oil as it is unstable and not the natural state found in fish (triglycerides).  The latter is not as common in the marketplace nor necessarily inexpensive or concentrated, but it can be found.  I haven't updated it in a year or more, but I maintain a spreadsheet comparing many different forms and brands of fish oil as to the net absorption kinetics of EPA/DHA vs its cost.

He has a great post on the top fish oils he recommends...

Chris Kresser: The definitive fish oil buyer’s guide

MachineGhost wrote:Yes, but its not a bad phytoestrogen.  It helps detoxify harmful estrogens to protect the prostate.  Since prostate BPH/cancer starts in men in their 30's, its not something to only worry about only when it becomes a serious problem 35+ years later (by which time its too late!).  Aside for helping to thicken my smoothies a bit, I don't think I'll miss it.  I'll keep the remaining on hand to continue to use as an egg replacer.

Got it. Good to know.

MachineGhost wrote:I'm familiar with MCT oil since it provides ketones for a glucose-intolerant brain -- very useful for ameliorating Alzheimer's Disease.  I am hypersensitive to tiny amounts of MCT though, get liver pain and/or naseua.

I've heard that some MCT oils are derived from canola oil. Not sure how they could do that (since canola oil doesn't really have MCTs in it, afaik). Anyway, a good MCT oil should be only derived from coconut oil. And whether you buy MCT oil or coconut oil, they need to be "Direct Micro Expelling" (DME) coconut oils. DME is a cold process and requires fresh coconuts that aren't dried and stored in moldy warehouses.

My sense is that you just needed to start with a smaller dose of coconut oil or MCT oil and work your way up to whatever amount you want to tolerate. Dr. Mary Newport explains in her FAQ on Alzheimers...

Dr. Mary Newport wrote:If you take too much oil too fast, you may experience indigestion, cramping or diarrhea.  To avoid these symptoms, take with food and start with 1 teaspoon coconut oil or MCT oil per meal, increasing slowly as tolerated over a week or longer. If diarrhea develops drop back to the previous level. For most people, the goal would be to increase gradually to 4-6 tablespoons a day, depending on the size of the person, spread over 2-4 meals.  Mixing MCT oil and coconut oil could provide higher levels and a steady level of ketones. One formula is to mix 16 ounces MCT oil plus 12 ounces coconut oil in a quart jar and increase slowly as tolerated, starting with 1 teaspoon.  This mixture will stay liquid at room temperature.

Source: http://www.coconutketones.com/

MachineGhost wrote:However for sake of the argument, why would I want to give up the medium-chain saturates that make coconut oil healthy and temperature stable for cooking?  And what about the missing lauric acid which is a large part of coconut oil's benefits?  AFAIK, caprylic acid is just useful against candida overgrowth in the vagina or intestine.

I only recommended MCT oil in the off chance that the pharmaceutical grade MCT oil is high enough quality to avoid a reaction to whatever was in the last batch of coconut oil you tried. People use one or the other for different effects. For instance, Dr. Newport recommends a combination of MCT oil and coconut oil for Alzheimer's.

MachineGhost wrote:Are you sure there's no MSG/umami involved with this?  Foodstuffs does not just normally "taste better" without that kind of neurotoxin involved.

Yeah. I'm 99% sure. It's an odd phenomenon with those medium chains. Nobody seems to know why it happens just yet. And some people have noticed flavor enhancing properties with coconut oil as well. The people who recommend MCTs are well aware of the dangers of MSG — particularly those with brain problems who rely on the benefits of MCTs.

MachineGhost wrote:

Gumby wrote: Your body won't tolerate that long term either (due to oxidation), so only use it to adjust your levels. Your best bet seems to be to reduce n-6 during this time as well and avoid ALA for its inefficiency.

Yessir!  But, you do realize how very little LA I'm already eating to begin with?  Sheesh.

Yeah, and I'm no longer worried about your LA after realizing that too much LA shouldn't raise AA levels. My mistake. I was thrown by the blood test saying your LA was high. I guess high LA doesn't really matter in terms of AA, but maybe it matters in terms of oxidation? No idea. I suppose, for all we know, the test could have been inaccurate.

Anyway, I really believe it was the inefficiency of Flax oil to EPA/DHA that screwed up your numbers. My guess is you'll be fine in a few months now that you're on the right track.

Gumby wrote: Synthetic triglyceride oil. This form occurs when natural triglycerides are converted to ethyl esters for concentration (as above), but then re-converted into synthetic triglycerides. The original position of the triglyceride’s carbon bonds change and the molecule’s overall structure is altered, which impacts the bioavailability of the oil.

Do you have any references to evidence to back up this opinion from Kessler?

MachineGhost wrote:

Gumby wrote: Synthetic triglyceride oil. This form occurs when natural triglycerides are converted to ethyl esters for concentration (as above), but then re-converted into synthetic triglycerides. The original position of the triglyceride’s carbon bonds change and the molecule’s overall structure is altered, which impacts the bioavailability of the oil.

Do you have any references to evidence to back up this opinion from Kessler?

Kresser doesn't cite a reference, but I found a pharmacy website that states references on that...

http://www.whitmanpharmacy.com/nutriceuticals.php

MachineGhost wrote:Here's the problem though.  The RDA for LA is 17 grams a day, so the almonds, the lecithin, the flaxseed meal, a krill oil capsule, and 3T of EVOO

Just curious, but why do you try to get the "RDA" of LA? The Omega-6 chains are in practically everything these days, so I just assume that there's no point trying to get more of it beyond what's already in our everyday foods.

Gumby wrote:

MachineGhost wrote:

Gumby wrote: Synthetic triglyceride oil. This form occurs when natural triglycerides are converted to ethyl esters for concentration (as above), but then re-converted into synthetic triglycerides. The original position of the triglyceride’s carbon bonds change and the molecule’s overall structure is altered, which impacts the bioavailability of the oil.

Do you have any references to evidence to back up this opinion from Kessler?

Kresser doesn't cite a reference, but I found a pharmacy website that states references on that...

http://www.whitmanpharmacy.com/nutriceuticals.php

None are relevant.  I'm not concerned with triglycerides vs free fatty acids vs ethyl esters as I already have that data, but specifically his claim that re-esterified triglycerides are inferior to natural triglycerides.  Since the body cleaves the EFA's off the glycerol backbone during digestion only to reassemble the whole enchilada later on, I find his unsupported claim to be baseless.  But I could be wrong.