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  #46   ^
Old Wed, Jul-22-15, 02:36
SilverEm SilverEm is offline
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Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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Eliminating most plants cleared up many symptoms for me. Making my own yoghurt from grass-fed/pastured cream helped a great deal, too.

Eliminating hard cheeses took some gumption, but helped dramatically. Sour cream got tossed out, too. Tested again recently. Don't know if it is due to amines or inferior cream source, but it got tossed.

Reducing amines helps as much as avoiding the phytotoxins in plants. (Phenols, polyols, salicylates, goitrogens, oxalates, solanaceae from nightshades, alkaloids, fungi, etc.)

Here is the page on Elimination Protocol for "Gluten and Casein Responders".

Here is The Introduction to the FailSafe Diet for those new to elimination protocols, and would like to find out which foods might be causing the troubles.

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  #47   ^
Old Wed, Jul-22-15, 02:47
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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Today's food:

Black tea, some w/ cream, butter, and salt
CLO/Flaxseed oil
A few freshly picked herbs and tiny leaves

Chicken livers braised in unsalted Kerrygold and homegrown green onions
Tea gelatin and yoghurt made from Org. Valley hwc/hh

Wild salmon, unsalted Kerrygold and HB yolks
Tea or vinegar-&-sea salt gelatin w/ homemade yoghurt

Gelatin cream made w/ Great Lakes Grass-fed Beef Gelatin and Org. Valley hwc, and PG Tips black tea.

HB yolks and butter w/ herbed sea salt

Seltzer water
Purified water w/ sea salt, as wished

----

Some information on Kerrygold butter, the unsalted one:

All Kerrygold butter comes from the milk of grass-fed cows that are free of growth hormones. Our Unsalted version is an all-natural, cultured-cream Irish butter with a complex, nuanced flavor.

Kerrygold Unsalted Butter has a higher butterfat content and is a perfect butter for baking. You’ll notice its grass-fed cow’s milk richness when you bake for the first time and find your pie crusts are flakier and your cookies are more delectable thanks to Pure Irish Butter.

Ingredients: Cultured pasteurized cream


The unsalted butter has 12 grams of lovely FAT per Tablespoon. (The salted only 11 grams.) Here is the link to the Kerrygold page.

Last edited by SilverEm : Fri, Jul-24-15 at 02:46.
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  #48   ^
Old Fri, Jul-24-15, 02:49
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
Default

Food prep yesterday:

Yoghurt made from Homestead Creamery heavy cream and half-n-half.

Homestead Creamery isn't 100% grass-fed/pastured, but they put their milk and cream into glass bottles, and use 160-165 degree pasteurizing. Organic Valley is grass-fed/pastured, but uses UHT pasteurization, and uses those cartons with some kind of waxy "plastic" inside, and the cartons smell like cheap, gas station, bathroom deodorizer. Some kind of fungicide in the packaging I guess. Homestead Creamery gives the cows grain when milking them. A farmer told me it makes them calmer. (Do grains anesthetize, tranquilize through the opioids or through changing FIAF or ???, or, would the cows be calm at milking time if they were fed grass or silage???)

After reading more about UHT, I am even more leery of Organic Valley.... It'd be nice to have a neighbor with Guernsey cows.

HB eggs. Whites tossed. Yolks in tiny canning jars. As well as buying eggs which are from cage-free chickens which eat feed which is non-soy, non-GMO, I also smell the cartons and eggs to see if they reek of fungicides or petro-chemical fragrances. First choice would be to have chicken which run around eating bugs and worms.

Gelatins: one w/ tea, one w/ vinegar and sea salt. The canning jars are really nice, but the standard two-cup peanut butter jars work fine, too. I got some of those jars from folks who eat peanut butter.

Today's food prep:

Chicken livers
perhaps a gelatin cream or rennet custard

Last edited by SilverEm : Fri, Jul-24-15 at 03:39.
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  #49   ^
Old Mon, Jul-27-15, 03:28
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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I like reading about pastoral peoples, and the Sami are one of my strongest inspirations for my food plan.

Here is a lovely site, translated into English, with some basic information about the Sami: The Sami Homeland.

A short (unedited) excerpt:

The reindeer in the Sami culture.

Long before recorded history the Sami's developed an almost symbiotic relationship with the reindeers. During the long wintermonths food and other useful commodities could get scarce, the Sami's therefore always made the maximum use of the reindeers. Aside from the use as a transport animal, the reindeers used to be milked. All parts of a butchered animal that could be used for food was eaten, inluding the intestines, something that provided the Sami's with vitamines that would have been impossible to obtain in other ways for the largest part of the year.


Tendons and sinews where -and still are- used for sewing, both for putting together the coneshaped "tents" Laitok/Lavvu as well for creating shoes and clothing. Whereas the Sami tents nowadays are made of bought fabric, reindeer skin is still used for clothes and shoes -even such items that are used in daily life. Reindeer are marked with a set of marks cut in the ears, such marks shows ownership but also makes identification easier for the owner who can be an individual, a family or a community.
....
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  #50   ^
Old Wed, Jul-29-15, 02:17
SilverEm SilverEm is offline
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Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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There is a very nice article about Dr. Russell Wilder, "A Line in the Sand", at the Mayo Clinic site. Dr. Wilder worked with Dr. Frederick Banting, and Dr. Frederick Allen. If you are interested in the history of the use of insulin for diabetics, or ketogenic diets for those with diabetes or epilepsy, it is a lovely article to read. Pioneering doctors working to help. This must have been at the top of the news headlines in the 1920s.

Here is the link to the article at the Mayo Clinic, "A Line in the Sand".
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  #51   ^
Old Wed, Jul-29-15, 02:40
SilverEm SilverEm is offline
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Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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Some interesting things about brain food:

Here is the link to the paper.

Using positron emission tomography to study human ketone body metabolism: A review

Here is the abstract. (The full-text is only available with payment.)

Abstract

Ketone bodies – 3-hydroxybutyrate and acetoacetate – are important fuel substrates, which can be oxidized by most tissues in the body. They are synthesized in the liver and are derived from fatty acids released from adipose tissue. Intriguingly, under conditions of stress such as fasting, arterio-venous catheterization studies have shown that the brain switches from the use of almost 100% glucose to the use of >50–60% ketone bodies.

A similar adaptive mechanism is observed in the heart, where fasting induces a shift toward ketone body uptake that provides the myocardium with an alternate fuel source and also favorably affects myocardial contractility.

Within the past years there has been a renewed interest in ketone bodies and the possible beneficial effects of fasting/semi-fasting/exercising and other “ketogenic” regimens have received much attention. In this perspective, it is promising that positron emission tomography (PET) techniques with isotopically labeled ketone bodies, fatty acids and glucose offer an opportunity to study interactions between ketone body, fatty acid and glucose metabolism in tissues such as the brain and heart.

PET scans are non-invasive and thus eliminates the need to place catheters in vascular territories not easily accessible. The short half-life of e.g. 11C-labeled PET tracers even allows multiple scans on the same study day and reduces the total radiation burden associated with the procedure.

This short review aims to give an overview of current knowledge on ketone body metabolism obtained by PET studies and discusses the methodological challenges and perspectives involved in PET ketone body research.


I added some lines spaces and the bold type.
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  #52   ^
Old Wed, Jul-29-15, 02:56
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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Here is a link, at archive.org, for the main page for Dr. Russell Wilder's, Primer for Diabetics, the first edition, 1921. The dietary recommendations included a version for those who could not tolerate more than 40g/CHO/d.

Before insulin, Dr. Elliott Joslin, 1869-1962, helped diabetics with having them on a strict diet and exercise. He continued helping patients to help themselves, working until he was 92. Here is a short video about his work. In that short film, there is a small bit of Dr. Joslin talking about insulin, how it was a great help, a miracle, but that the patients still needed to keep tight control of their diet and exercise.

In Dr. Wilder's "Primer", the diet recommendations include Hepco cakes. I found a recipe for them in Dr. Joslin's book. Apparently Hepco flour was some kind of soy flour and it was believed that the soy flour would not raise the blood sugar in the same way that wheat flour would. There are also recipes for something called Cellu-flour, which seems to have been cellulose fiber. There are meal plans for 40 grams of carbs per day, 60, and 100. His book is based on Dr. Joslin's, and includes some of Dr. Allen's recipes, and is easier to read than Dr. Joslin's. There are methods given in this, as well as Dr. Joslin's Manual for testing the amount of sugar in the urine.

Here is the link to archive.org for "A Diabetic Manual for the Mutual Use of Doctor and Patient", from 1918, by Dr. Joslin.

Dr. Joslin's Manual explains how to calculate a low carb diet for oneself. He includes helpful photographs, explains what a calorie is, how to use the metric system. It's an amazing book on Low Carb. 1918!!!! this was in print and given to his patients.

From page 77, in Dr. Joslin's 1918 Manual:

The Eskimos live largely upon fat. Diabetic patients
should be very thankful that there is a race of Eskimos
through which proof is afforded that it is perfectly possible
to maintain life on a diet in which carbohydrate is largely
replaced by fat.


Dr. Joslin however, as much wonderful help as he gave, was one of those early researchers who believed that high levels of dietary fat somehow caused trouble for diabetics. He quotes a study by Williams and Dresbach, which I have yet to find, and also some work by Dr. Allen, and his tests on diabetic dogs. I have not yet read through Dr. Allen's paper. Who knows what one can find without access to the old medical journals.

The Rockefeller University Hospital Centennial has a short bio about Frederick Allen and his research of diabetic dogs, his strict dietary protocol (starvation diet of 75g/PRO/d) which kept diabetics alive, until insulin was discovered and became available. Here is the link to the article. That Centennial section of the site is fascinating. There are one-page histories/biographies of advances in medicine and science over the last century. It's a bit of glorious time travel to read it.

Thank goodness, Dr. Richard Bernstein has debunked all that old nonsense about fat being bad for diabetics. But, at least those early doctors had their patients on low carb and good protein and real fat.

----

It wasn't until Dr. Pennington came along, that it was shown how obesity is a defect in glucose metabolism, too.

----

Will edit and add info, if I find good things.

Last edited by SilverEm : Wed, Jul-29-15 at 13:47.
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  #53   ^
Old Thu, Jul-30-15, 03:37
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
Default

Lovely new batch of yoghurt cooling. Was able to mix my own half-n-half proportions from the Homestead Creamery brand. One half-gallon of not-homogenized whole milk and one quart of not-homogenized heavy cream gives, according to the individual macronutrient stats for each of those, reckoned together: .9P: 3.5F: 1.3C per ounce. Yeah! Homestead Creamery pasteurizes at 160-165 degrees for 15-20 seconds. (Pasteurization info via telephone call to company.)

Some info on the evils of homogenization:

From an article at Natural News, by Jo Hartley


Homogenization is a more recently invented process and it has been called "the worst thing that dairymen did to milk." When milk is homogenized, it is pushed through a fine filter at pressures of 4,000 pounds per square inch. In this process, the fat globules are made smaller by a factor of ten times or more. These fat molecules then become evenly dispersed throughout the milk.

Milk is a hormonal delivery system. When homogenized, milk becomes very powerful and efficient at bypassing normal digestive processes and delivering steroid and protein hormones to the human body (both your hormones and the cow's natural hormones and the ones they may have been injected with to produce more milk).

Homogenization makes fat molecules in milk smaller and they become "capsules" for substances that are able to bypass digestion. Proteins that would normally be digested in the stomach are not broken down and instead they are absorbed into the bloodstream.

The homogenization process breaks up an enzyme in milk which in its smaller state can then enter the bloodstream and react against arterial walls. This causes the body to protect the area with a layer of cholesterol. If this only happened once in a while it wouldn't be of big concern, but if it happens regularly there are long term risks.

Proteins were created to be easily broken down by digestive processes. Homogenization disrupts this and insures their survival so that they enter the bloodstream. Many times the body reacts to foreign proteins by producing histamines, and then mucus. Sometimes homogenized milk proteins resemble a human protein and can become triggers for autoimmune diseases such as diabetes or multiple sclerosis.

Two Connecticut cardiologists have demonstrated that homogenized milk proteins did in fact survive digestion. It was discovered that Bovine Xanthene Oxidase (BXO) survived long enough to affect every one of three hundred heart attack victims over a five-year time period. Even young children in the U.S. are showing signs of hardening of the arteries.


Photographs at great magnification of different types of milk: raw; pasteurized and not homogenized, pasteurized and homogenized, ultra-pasteurized.... Here is the link to the page, at realmilk.

On the benefits of yoghurt:

From this article on butter, at realmilk.

Here a very important point is touched on: Lactic-acid-producing germs — very helpful for our digestion — are able to suppress all other unwanted, even pathogenic, germs. Lactic-acid fermentation is far superior to the heating of milk (pasteurization) in suppressing pathogenic germs. The pasteurization of the milk dramatically changes the fine composition of the raw milk. Even warming to 120 degrees Fahrenheit alters this fine composition that includes various proteins, vitamins, sugars and enzymes. Homogenization destroys the butterfat globules so much that the cream can no longer rise in the milk. The milk is denaturalized.

Last edited by SilverEm : Thu, Jul-30-15 at 03:46.
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  #54   ^
Old Sun, Aug-09-15, 01:37
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
Default

Stan Bleszynski's post at his blog, Heretic, "Is Type II Diabetes Result of Mitochondrial Destruction?", from Tuesday, October 4, 2011, has been one of my favorites.

Excerpt:

1. A hypothesis:

- Metabolic syndrome and diabetes t2 results from mitochondrial destruction caused by overfeeding with glucose (and fructose but only in the liver), taking place over many years. An individual mitochondrion has (hypothetical assumption!) a fixed maximal total energy yield out of the two main energy sources: glucose (or glucose+fructose in the liver) plus fatty acids.

There is a self-clamping regulatory mechanism preventing mitochondrial overfeeding by fatty acids, by means of Malonyl-CoA/CPT1 feedback (see Peter’s discussion), but there are no very effective self-regulation feedbacks for glucose, only a partial mechanism reducing the glucose transport into in the cells! This partial mechanism is mediated by insulin regulating the transport of glucose into a cell through the cellullar membrane. This regulatory mechanism is not always effective or fast because the insulin secretion is not local to the cell, rather it is produced in the pancreas whose rate of secretion is regulated by the autonomous nervous system and pancreating glucose concentration involving many factors other than some particular mitochondria overload. Furthermore, the insulin regulation (blocking) of glucose can be overriden by high glucose concentration.

2. Conclusions.

A straight conclusion would be that a high carbohydrate diet can indeed be healthy and avoid diabetes as long as it restricts calories to prevent mitichondrial overfeeding. What is the limit? In my guesstimate (based on published literature) - probably around 25kcal/kg for women and 30kcal/kg for men.

A second straight conclusion is that a high fat low carb diet automatically avoids mitochondrial deterioration and thus diabetes among other degenerative diseases, by its built-in biochemical overfeeding protection mechanism. (note: my daily caloric intake on a high animal fat diet, is and has been around 20-25kcal/kg since 1999).

A third conclusion concerns a situation of the cells with the insufficient number of or worn-out mitochondria. Having lower total mitochondrial energy throughput, such cells may be forced to over-rely upon and and over-utilize the Penthose Phosphate Pathway (PPP) (also called the Penthose Shunt) which takes place in the cytosol volume outside of the mitochondria. This has originally been proposed by Dr. Jan Kwasniewski, the author of Optimal Diet in the 1970-ties. I found his idea fascinating, largely because there was no easy or obvious way of proving it at the time, and last but not least - it flew right against the medical dogma! Interestingly the PPP is mainly a synthesis pathways resulting in lipids and lipoproteins manufactured inside the cells, in-situ. Such as the infamous "cholesterol" plaque perhaps? Out of glucose? Like suggested by R.W. Stout in his 1968 and 1969 Lancet papers?

--- Part 2 (9-Oct-2011) ---

3. Declining energy syndrome and carbo-loading trap.

More conclusions can be drawn out of this simple hypothesis. If t2 diabetes is the results of mitochondrial decline caused by overfeeding (carbs or by a combination of carbs and fats) then it should be accompanied by a steadily declining energy yield.

Suppose for the sake of discussion that a healthy individual consumes 30kcal/kg/day, leading active live. If he looses 10% of his mitochondria he would be able to process only 27kcal/kg/day. Less energy to work, more lethargic, getting tired sooner. What do we do when that happens? I was in that situation 15 years ago. Falling energy level at work, especially after 3pm. I snacked! I snacked on carbs! Why on carbs? Because I couldn't snack on fat! (even if I didn't believe that fat is harmful...) Fats don't work if you have mitochondrial deficiency because of the Malonyl-CoA/CPT1 feedback(*). A mitochondrion can only process a certain maximum amount of energy out of fat and that's it! If your total mitochndrial yield declined from 30 to 27 during the first 20 years of dietary abuse, then 27 is all what you can get out of fat! But you can still push your partially worn-out "engine" into overdrive by flooding it with extra glucose! It will sputter and spew out lots of smoke polluting your cells with free radicals, AGE's etc but it would allow you to bring your yield back to the previous level of 30. At least for a time being because the process of mitochondrial decline has accelerated due to the pushing them over the limit and the ensuing end product toxicity. So instead of 27kcak/kg/d, now the maximum available yield drops by another 10%, this time over 2 years. You can now safely draw 24kcal/kg/d out of fat or carbs or a combination of both. However if you want to stay awake at work you have got to load up on carb snack now by 20% not 10% over your maximum limits creating more problems, requiring a lot more insulin to overcame the natural barrier that your body cells have enacted against your plan. It also requires maintaining a high blood glucose level to speed up diffusion across cellular boundaries. Which particular cells of your body will be the first in line to see the high glucose and high insulin? Your arterial endothelium! Your liver!

This appears to be a run-away process where your tissues cells would keep enacting more and more barriers agaisnt excessive metabolism, your conscious brain will make you snack like crazy on carbs to maintain the same energy level, your pancreas will try keeping up with that pumping your insulin, your immune system will work overtime trying to clean up the mess after glucose and eventually it will also try saving your body tissue by attacking the source of the excessive insulin - pancreating beta cells, in some cases it will try even to sequester the excessive insulin floating in your bloodstream, and last but not least your poor mitochondria will keep dying! Eventually one of more of the players described above will give up. If you stop snacking and keep below your maximum metabolic yield, you will feel hungry and lethargic. Especially if you have to work 9-5. If you don's stop snacking your blood glucose would go up until you develop kidney failure. If you force you blood glucose below renal dumping threshold (about 160mg/dl) by injecting insulin you will develop heart failure or arteriosclerosis (or both). What to do? This will be the next subject.


4. The way out - what exactly happens (and when) if you start curing yourself of diabetes using a high fat low carb diet.


------
More references, links and thoughts are in this file.

Footnote:

*) I am speculating but there seems to be cases when the fat-clamp mechanism may also be defeated, leading to fatty acids overload(+). This condition is also harmful creating large amount of toxins that require a massive cleanup operation my the immune system (see Masterjohn's article, in my reference file above). I suspect that this is one reason behind the so-called "low-carb flu" syndrome sometimes reported by inexperienced diabetic low carb dieters. It is interesting that fat overload (if that does happen, however unlikely) may be as unpleasant as glucose overload!

Footnote to a footnote:

+) Indeed it does happen! Peter just posted an interesting discussion about this issue here. A must read! It appears that when the adipose tissue develops insulin resistance, it is then capable of releasing fat into triglyceride particles and into the bloodstream under the condition of falling but still higher than normal insulin level! Fatty acids are then forced into the cells and a smaller fraction are then forced into mitochondria. The free fatty acids left-over inside the cell (but outside of the mitochondria) become the main cause of the insulin resistance and the cause of major cellullar cleanup operation. I have a mental picture of my old sputtering "Komar" motorbike with its carburator overflooded with gasoline...


This makes a fascinating fork in the metabolic failure modes under overfeeding. On one hand, the overfeeding with glucose may be wearing off the mitochondria and also forcing the excess fuel into adipocytes. On the other hand releasing those excessive fats from the adipocytes into the bloodstream may be setting up the physiological insulin resistance and still damaging the cells even more through the high free fatty acids level in the cytosol. Interestingly this excessive fatty acids may as likely (if not more so) come from the internal source (adipose tissue) than from a diet! It also explains why many obese people experience a health breakdown only AFTER they undergo a weight loss, especially after a repeatable weight loss and weight gain cycling.


A weight loss diet is therefore ALWAYS a HIGH FAT diet even if a person eats nothing but lean veggies!


.... [The information represented by the ellipsis is fascinating. I recommend going to Stan's blog and reading.]

After some comments, Stan posted this:

- It seems that the problems some (but not all) diabetics experience on an Atkins-like diet stem from the fact that they attempt to increase their metabolic yield through overfeeding!.

If they overfeed using fat it brings the symptoms like I described above. If they try overfeeding with protein it brings other problems, one of them being conversion of excessive protein into glucose and then the body having to deal with excess fat, protein and glucose at the same time.

I realize that a high fat low carb diet is easy for me but it may be quite difficult for a diabetic patient. It requires a certain amount of determination to maintain a discipline because one of the diabetic symptoms is an incessant hunger. There is no easy "fix"! For a type 2 diabetic, the easiest way is perhaps the scenario (a) - the road to "hell". From my own observation of diabetic people than I know, the second easiest path is (c) because of the hunger-quenching property of fat, although it does require an acceptance of low energy level (if you are diabetic). I believe that (b) is actually the hardest.
H.


More on mitochondria in next post....

Last edited by SilverEm : Sun, Aug-09-15 at 01:53.
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  #55   ^
Old Sun, Aug-09-15, 01:49
SilverEm SilverEm is offline
Senior Member
Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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Dr. Chris Masterjohn, the biochemist, posted about "When SAMe Helps, Consider Magnesium and Your Metabolic Rate", at WAPF, on July 15th.

Excerpt:


I have written quite a bit recently about the methylation cycle and its relation to nutrient balance. At Wise Traditions this November in Anaheim, one of my three talks will expand these ideas to include targeting methylation nutrition to individual needs based on genetics and health status. Here, I’d like to chip away at one small piece of the puzzle that I have not written about yet: why benefits from SAMe supplementation should cause one to look not only at the most commonly discussed methylation nutrients (e.g., B12, folate, choline, betaine, methionine) and genetic polymorphisms (e.g., MTHFR) but also at issues that are more commonly neglected when discussing methylation: magnesium and the metabolic rate.


In my previous posts and articles, I have simplified the methylation cycle in order to make the nutritional topics I was discussing easier to understand. One thing I have left out (e.g., here and here) is that before methionine can be used for methylation it must be activated to S-adenosyl-methione, which is sold as a supplement and in the supplement market generally abbreviated as SAMe.


...

Indeed, any problems recycling methionine from homocysteine should be fully investigated because if these are the real problems then an expensive supplement like SAMe is a waste of money. These conditions would tend to be associated with elevated levels of homocysteine and they could include deficiencies of B12 or folate, especially in the context of a diet that is not rich in choline or betaine, or genetic polymorphisms in the pathways of these nutrients. They could also result from a deficient intake of methionine itself, which would be most likely on a very low-protein vegan diet or a diet that is outright deficient in protein, and this may not (necessarily) be associated with any elevation of homocysteine.

There is another possibility, however, that is strongly suggested by the biochemistry: some people may not be efficiently activating methionine to SAMe. In order for this activation to take place, the enzyme methionine adenosyltransferase (MAT, also known as S-adenosyl methionine synthetase) breaks apart ATP to harvest from it a molecule of adenosine and then activates methionine by sticking adenosine onto it.

People who have severe genetic deficiencies of the MAT enzyme are unable to use methionine, even when adequately present, for the methylation process. This is because that methionine is never activated to SAMe. Thus, they are deficient in methylation, they have little risk of depleting glycine by consuming excess methionine if the problem isn’t fixed (though they still may have inadequate glycine for other purposes, such as detoxification and synthesizing collagen), and since they never use up the methionine to make homocysteine, their methionine becomes elevated rather than their homocysteine, and their homocysteine is actually low.

The biochemistry suggests that people with a normally functioning MAT gene could have two other reasons for poor activation of methionine: poor magnesium status, or a low metabolic rate. Since ATP is the source of the activating molecule, the reaction is, quite clearly, ATP-dependent. Since ATP is always utilized as a chelate with magnesium, the reaction is also magnesium-dependent. The presence of a magnesium deficiency, a low metabolic rate, or both conditions together, could prevent methionine from being activated.

It is important to realize, however, that a low metabolic rate or a magnesium deficiency will compromise thousands of bodily processes, and that either condition would be likely to coexist with multiple nutrient deficiencies. Thus, such a person will not necessarily replicate the presentation of someone with a genetic deficiency of the MAT enzyme. They will not, for example, necessarily have low homocysteine. If the recycling of homocysteine is also being compromised, then homocysteine could be normal or elevated even while methionine is failing to be utilized properly and is thereby generating homocysteine at a much lower rate.

In my opinion, if someone benefits from SAMe supplementation or suffers from any of the conditions for which SAMe supplementation has shown to be beneficial, and it can be ruled out that simply ensuring adequacy of dietary methionine and relevant B vitamins would fix the problem, magnesium status and metabolic rate should be evaluated.

Magnesium concentrations in serum, plasma, red blood cells, and urine can be useful in assessing magnesium status, but probably should not be used to rule out the possibility that magnesium supplementation could be helpful. In addition to supplementation, proper stress and sleep management as well as eating a wide variety of unrefined plant foods can help with magnesium status.

Ensuring a normal basal body temperature is, in my current opinion, probably the most cost-effective and helpful way to address the metabolic rate. However, addressing why the metabolism may have slowed may be more complicated. Managing stress and sleep, ensuring adequacy of most nutrients, and eating enough total food and carbohydrate are probably the key factors to consider.




To me, Dr. Masterjohn's emphasis on eating for optimal nourishment underlines Stan's point that we need to live a lifestyle which strengthens the mitochondria, in content and proportions of what we eat, in how we exert ourselves and rest.

For me, that means our whole approach to nourishment and balance. It means conscious choice of that for which we exert ourselves, conscious choice of what we eat, how much, and why, having conscious parameters and keeping those parameters.
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  #56   ^
Old Mon, May-07-18, 08:50
SilverEm SilverEm is offline
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Posts: 964
 
Plan: VLC Pastoral
Stats: 137/136/136 Female 67"
BF:
Progress: 100%
Location: Maintenance since 2001
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I have fiddled around with eating some things not on this plan, and I am coming back to this.

Simple is nice.
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