Moreless Alkalising & Remineralising Drink

Hi Ya’ll,

Enclosed is the recipe for the drink from the website which is now closed til a new site is up.
The Moreless Alkalizing Drink

Here’s a great alkalizing drink that can help
remineralise you quickly and cheaply!
This is an amazing power packed, mineral and nutrient
dense drink that will not only help to alkalize you, but
will give you loads of electrically charged energy! It may
be taken 2-3 times a day as needed.

Ingredients:
1. 1 tablespoon of blackstrap molasses (it may be Unsulphured )

2. Juice of half a lemon (OR 1 tablespoon apple cider vinegar if you can’t take citrus or get hold of lemons)

3. 1 + tablespoon pickling lime water (how to make pickling lime water : 1 tablespoon of pickling lime powder, aka calcium hydroxide, diluted in 1 gallon (=4 litre) of distilled water) *see safety notes below*

4. Small pinch of Epsom salts

5. Norwegian kelp powder 1 + teaspoons

6. 1 glass of clean water to mix it with

*** you can take a lot MORE pickling lime water and “Kelp”
than is suggested above. Start slow and if things don’t
improve, slowly build up. Some of us use up to 20
tablespoons of pickling lime water and up to 2
tablespoons of kelp powder each time ***

The chemical reaction between the acid in the lemon
juice and the alkaline minerals in the molasses releases
energy into the body and makes the minerals more
bioavailable.

Method:
*Dissolve the blackstrap molasses and epsom salts in
warm water (leave to cool if desired)

*Add 1 (or more) tablespoons of pickling lime water

*Add the lemon or ACV (I sometimes add both) Add these
only when the drink has cooled down, you don’t want to
destroy the enzymes

*Some people like to mix their kelp in with their drink,
some just put the kelp straight into their mouths
Special note on the kelp!: Most people find the taste
absolutely vile ?

it may help to moisten it and your mouth first so you
don’t gag! Some people use a straw to bypass the taste.
But this really is an essential part of the drink and is
packed with loads of minerals and complex carbohydrates,
so do what you need to do to get it down! And yes, kelp
is available in capsules, but the powder is much cheaper.

(This is an edit .. after several months of taking the
kelp powder, it no longer tastes so vile! I am becoming
immune to the taste – hooray!)
… And drink!

If you are chronically ill: I suggest you start with
with just a teaspoon of kelp and a tablespoon of the
pickling lime water along with all the other
ingredients. Over time, start building up on both those
ingredients until you can manage 2-3 teaspoons of kelp
and 2-4 tablespoons of the picking lime water in each
drink. You don’t have to drink it all at once, you can
also sip it over a few hours.

When someone has been chronically ill for a while, a
drink like this might create a powerful reaction and
start to release acids from organs and tissues too
quickly, that is why I am suggesting you start slow.
(Better to aim for minimal discomfort while you begin to
rebuild your health)
Can you make a batch in advance?

You can mix the Blackstrap Molasses, pickling Lime water
and kelp together without the Lemon juice or the ACV and
keep this cool – then add the ACV or Lemon juice just
before drinking. The batch should be ok for a day, but
not longer than two days. Fresh is best!
Heath Notes:

*Blackstrap molasses should be unsulphured. Sulphur is
acid forming.
*If using apple cider vinegar, buy organic and
unpasteurised (*with mother*) so full of active enzymes.
Otherwise, just find a good source of unpasteurised ACV.
*Pickling lime is normally found in the pickling/canning
section of shops. Your alternative is to buy calcium
hydroxide powder and put 1 tablespoon of the powder in 1
gallon of distilled water and use that as your pickling
lime solution.
*Buy food grade epsom salts.
*Kelp is apparently purest from Norway, and it is better
if it is finely powdered.
*If you are very acidic, you can also add a pinch of
epsom salts or a tablespoon of ACV with a tablespoon of
pickling lime water to your normal glasses of water (the
pickling lime provides calcium by the way).

I’ve been happily drinking the above 2-3 times a day.
And it has a buzz to it!
To keep your mineral reserves up, to every glass of
water throughout the day, you may also add a tablespoon
of pickling lime water (plus a dash of lemon or ACV)
The Moreless alkalizing drink is basically a very cheap
and effective method of creating alkalinity and is NOT
meant as a substitue for a wholesome diet with complex
carbs as is found in foods like green veges. The drink
is basically a method to get us more alkaline quicker,
but it is NOT the way to become alkaline totally, that
takes some effort!

What Moreless is presenting people here are various
options. Not everyone is prepared or able to go all the
way with eating right. So he is giving people easy and
cheap ways to kick start their healing whilst finding
their way at improving their diet, which will in turn be
the most important part of their healing. The kelp and
molasses are packed full of minerals that may be
difficult for people to find in the foods that are
available to them right now.
Moreless on the alkalizing drink: HERE
The Epsom salts, pickling lime water, lemon juice or ACV
create the electro-magnetic energy so that our bodies can make
the best use of the minerals.

** SAFETY NOTES ON CALCIUM HYDROXIDE ** (For those who
can’t get hold of the pickling lime water.)
CALCIUM HYDROXIDE (also known as – pickling lime
water/Ca(OH)2/slaked lime/biocalc/lime water etc.)

In concentrated powdered form, this stuff is a skin, eye
and respiratory irritant. It is CORROSIVE and causes
burns. Should you be using this concentrated form to
dilute with water before use, please protect yourself by
wearing safety glasses, gloves and minimize your
exposure to the dust itself.
There are no safety issues if you buy the pre made
pickling lime water.

Remember, the drink asks for 1 (to 4) tablespoon of the
diluted lime water – you take 1 tablespoon of the powder
and add it to a gallon of water. You do NOT add the
powder directly to your drink!

This powder is also incompatable with strong acids!

Start small and slow, and add more after checking your
response. We are all unique, so someone else’s ideal
doseage may not be the same as yours.

My suggestion is to make up your solution outdoors. This
powder is very fine and fluffy, it’d be easy to
accidently spill some on your kitchen or bathroom floor
for unsuspecting kids and pets to walk on.

More useful information about Calcium Hydroxide here:

http://en.wikipedia.org/wiki/Calcium_hydroxide

The following is as good a description of calcium
hydroxide as I can find (albeit it relating to use in
aquariums, but surely applicable when considering human
consumption):

“A preferred method of calcium supplementation comes in
the form of calcium hydroxide, known as “kalkwasser” to
reef aquarists. Calcium hydroxide has a chemical formula
of Ca(OH)2, in other words, it supplies one Ca+2 ion for
every two OH- ions. Calcium hydroxide can be mixed at
approximately 2 teaspoons [5.7g Ca(OH)2] per gallon (or
1.5g/L) of filtered freshwater to attain approximately
800mg/L calcium solution to be dripped slowly into the
reef aquarium. A beneficial side effect of using calcium
hydroxide is that the OH- (hydroxide) ions maintain the
pH of the aquarium by neutralizing acids present in the
aquarium, thereby helping to maintain (but not build)
the alkalinity in the aquarium. One could use pickling
lime, which is also calcium hydroxide.

Smile Tis your choice.

Chooselife Notes : Moreless is not talking third person here, there are somewhat un-obvious replies to forum questions mixed into this post. Website = http://www.sicknesshope.com

Glycemic Load Chart

Care of : https://www.glycemic-index.org/glycemic-load-chart.html

Glycemic load chart below should be used as a guide to make wiser food choices to perform better all day long and feel better generally by keeping your blood glucose levels relatively constant.

If there is a sudden spike in your blood sugar, your pancreas secretes more insulin, bringing your blood sugar down by transforming the excess sugar to fat. The higher the rate is, the lower your blood sugar will go. Blood glucose being too low means increased hunger and fatigue.

Glycemic index and glycemic load are both about the impact of carbohydrate rich foods on your blood glucose levels or in other words how quick or slow they cause a rise and a fall.

The difference is that glyemic load is based on the idea that a small serving of a high GI food will have the same kind of effect as a big serving of a low GI food. Foods that are mostly water, for instance, will not cause a sudden rise in your blood sugar even if they have high GI values.

 

That’s how they’ve come up with the glycemic load- GL. GL takes into account both the GI value and the quantity of carbohydrate in that food. So it provides a more accurate picture than glycemic index, as you will see on the glycemic load chart below.

Glycemic Load = (Quantity of carbohydrate content x GI ) / 100.

• GL of 20 or more is high, a GL of 11 to 19 is medium and a GL of 10 or less is low.

• A food with a GI of 70 and a carb content of 10g has a GL value of 7.

• A food with a GI of 10 and a carb content of 70g has also a GL value of 7.

Glycemic Load Chart:

Dairy Products:

• Full cream milk — 250ml — 3

• Soy milk — 250ml — 4

• Skimmed milk 250ml — 4

• Semi skimmed milk — 250ml — 4

• Low fat ice cream — 50g — 6

• Low fat fruit yogurt — 200g — 7

• Banana smoothie — 250ml — 8

• Mars flavoured milk — 250ml — 15

Fruits:

• Grapefruit — 120g — 3

• Cherries — 120g — 3

• Peach — 120g — 4

• Watermelon —120g — 4

• Pear — 120g — 5

• Plum — 120g — 5

• Orange — 120g — 5

• Apricot — 120g — 5

• Apple — 120g — 6

• Grapes — 120g — 8

• Banana — 120g — 12

• Sultanas — 60g — 25

• Raisins — 60g — 28

Glycemic load chart below should be used as a guide to make wiser food choices to perform better all day long and feel better generally by keeping your blood glucose levels relatively constant.

Vegetables:

• Broccoli — 80g — 1

• Cabbage — 80g — 1

• Spinach — 80g — 1

• Asparagus — 80g — 1

• Carrot — 80g — 3

• Green peas — 80g — 3

• Broad beans — 80g — 9

• Parsnips — 80g — 12

• Sweet potato — 150g — 17

• Sweet corn — 150g — 17

• Baked potatoes — 150g — 26

Legumes:

• Soy beans — 150g — 1

• Lentils — 150g — 5

• Split peas — 150g — 6

• Baked beans — 150g — 7

• Red kidney beans — 150g — 7

• Garbanzos — 150g — 8

• Romano beans — 150g — 8

• Pinto beans — 150g — 10

• Navy beans — 150g — 12

Grains:

• Barley — 150g — 11

• Bulgur — 150g — 12

• Whole wheat kernels — 50g — 14

• Brown rice — 150g — 18

• Couscous — 150g — 23

• White rice — 150g — 23

Cereals:

• Muesli — 30g — 10

• Porridge — 250g — 12

• Kellogg’s All Bran — 30g — 12

• Swiss muesli — 30g — 13

• Oatmeal — 250g — 13

• Kellogg’s Special K — 30g — 14

• Puffed wheat — 30g — 16

• Instant oatmeal — 250g — 17

• Corn flakes — 30g — 19

• Coco pops — 30g — 20

baguette and tomatoes

Breads:

• Burgen fruit loaf — 30g — 6

• Pumpernickel Bread — 30g — 6

• Barley and sunflower bread — 30g — 6

• Rye bread — 30g — 7

• Rice bread — 30g — 8

• Whole wheat bread — 30g — 9

• White pita bread — 30g — 10

• Baguette — 30g — 10

• White bagel — 30g — 11

Snacks and Beverages:

• Tomato juice — 250ml — 2

• Apple juice — 250ml — 10

• Carrot juice — 250ml — 10

• Banana cake — 80g — 12

• Vanilla wafers — 25g — 14

• Corn tortilla — 60g — 14

• Pepsi — 250ml — 15

• Cranberry juice drink — 250ml — 16

• Sponge cake — 60g — 16

• Rice cakes — 25g — 17

• Snickers bar — 60g — 19

• Fanta — 250ml — 23 

*Foods with low GL values are almost always low in glycemic index too. Those with medium or high GL could be anything- from very low to very high GI.

*You can only see the glycemic load values of foods on the Glycemic Load Chart above, if you would like the glycemic index values as well, please refer to the Glycemic Index Chart, where you can make a comparison between glycemic index and glycemic load values of carbohydrate rich foods.

Carey Reams 1978 interview with ACRES USA on Hypoglycemia

ACRES USA: How widespread is hypoglycemia?

DR. REAMS: At least 20 million hypoglycemics is the estimate of Dr. Carlton Fredericks, president of the International Academy of Preventive Medicine. The problem is that the symptoms are almost identical with those of many varieties of mild, or even serious mental disturbances. Most doctors improperly diagnose hypoglycemia as a psychiatric disorder, a neurosis or worse. So they reach for a bottle of sedatives. Those few doctors who do suspect hypoglycemia use the glucose tolerance test. Unfortunately, this test is deeply flawed and cannot be relied upon.

ACRES USA: What is hypoglycemia?

DR. REAMS: Hypoglycemia is a particularly nasty disease in its effects on the sufferer. The dominant characteristics include tiredness and lack of energy, unusual nervousness and irritability, dizziness, and often the most excruciating headaches. It doesn’t sound like much, but when you have hypoglycemia, it’s almost impossible to perform well either on your job or in your marriage. On the one hand, you don’t have enough energy to do an adequate job or to cope with the strains of normal life. On the other hand, your nervousness and irritability makes you unpleasant to be with.  I’ve treated many hypoglycemics, even young men and women in their 20s, who were unable to hold down a job because of their disease. I’m convinced that hypoglycemia is one of the leading causes of divorce. If the disease makes you difficult to work with, it must make you almost impossible to live with.

ACRES USA: What are the other symptoms of hypoglycemia?

DR. REAMS: Well, insomnia is one. That of course adds to the victim’s lack of energy and nervousness. The inability to tolerate even mildly loud noises is another. If someone you know reacts particularly negatively—maybe starting to cry—to a dog’s barking or bottle dropping into a garbage can, that person may well suffer from hypoglycemia.  Hypoglycemics are also highly prone to allergies. Asthma attacks, too, can be precipitated by low blood sugar. One of the more exotic symptoms of low blood sugar is heart palpitations. You can feel your heart skip a beat and slow down. It feels as if your heart is trying to stop, Although these palpitations aren’t quite as intense as real angina pains, they’re understandably frightening, particularly since the hypoglycemia has made the person quite nervous to begin with. Dizziness and light-headedness are other symptoms of hypoglycemia: These can be particularly dangerous if you drive your car a lot. In a few cases, the dizziness is so extreme the person blacks out. Hypoglycemia frequently goes undiagnosed. The symptoms are all commonplace, like fatigue or headaches, so that most people don’t even know something is the matter with them. If they do go to a doctor, in many cases they won’t get relief beyond an aspirin because the doctors simply aren’t trained to spot it.

ACRES USA: What causes low blood sugar?

DR. REAMS: The true cause of hypoglycemia is a liver malfunction. In hypoglycemia, the liver malfunction affects you in several ways. To begin with, the liver is supposed to stabilize your blood sugar in several different ways: by storing sugar when there’s too much and releasing it when more is needed; by maintaining the right chemical balance for insulin—which is essential for proper maintenance of blood sugar levels; and by regulating the production of insulin by the pancreas. In hypoglycemia, the liver fails to properly convert excess sugar into reserve sugar, called glycogen. Because of this the liver doesn’t have enough reserve sugar to release when it’s needed. Moreover, the liver frequently allows the chemical balance of the blood to become too alkaline. This sharply increases the potency of the body’s insulin, which in turn then drives blood sugar levels down abnormally low. In other cases, the liver allows the blood to become too acidic. This decreases insulin’s potency, allowing the blood sugar to go too high. If you were healthy, your body would adjust the blood sugar back to normal. But when you’re hypoglycemic, your body overreacts and forces the blood sugar below normal. So in either case, an improper chemical balance in the blood-caused by a malfunctioning liver allows blood sugar levels to go below normal. In addition, when the liver malfunctions it fails to detoxify and remove various waste products from the body. These build up in the blood and also interfere with insulin’s ability to control blood sugar levels. Finally, when the liver malfunctions it allows the pancreas to produce too much insulin—which causes low blood sugar. This is the main reason for hypoglycemia.

ACRES USA: Why does hypoglycemia cause so many problems?

DR. REAMS: The liver malfunction causes low blood sugar. When your blood sugar is too low, your brain becomes starved for energy. This is because the brain burns only sugar, unlike other parts of the body which can burn either fats or sugars for energy. Natural consequences of a lack of fuel in the brain include the migraine headaches, dizziness, and the symptoms of mild mental disturbance. When the liver isn’t working properly, nutrients are not absorbed. So the patient is undernourished and it’s not surprising that he or she feels tired all the time. Likewise, when the .liver doesn’t work properly, it fails to produce enough hydrochloric acid for proper protein digestion. Urea, a waste product, builds up. This causes tension and insomnia. In turn, this leads to more fatigue, more headaches and more irritability—a vicious cycle. Finally, when the liver is weak, the body becomes hypersensitive to certain starches because it can’t metabolize them properly. It’s not necessarily all starches that cause problems, just some of them. Depending on the patient, it could be wheat, oats, potatoes or something else. Whatever the food, when the hypersensitive patient eats it, it breaks down too quickly into sugar. The blood sugar level, first soars too high, then plummets too low. This leads, as I pointed out earlier, to still more headaches and fatigue.

ACRES USA: What are the main reasons for this liver malfunction?

DR. REAMS: You could be deficient in chlorophyll, oxygen, or calcium—three nutritional elements essen­tial for the liver. When, for instance, the liver lacks calcium, it can’t produce enough hydrochloric acid to digest food properly. Another reason for a sluggish liver is that the person may be eating large amounts of certain foods which put stress on the liver. I’m referring to foods such as nuts & nut butters, meat, whole milk, and cheese. These foods require lots of hydrochloric acid for their digestion. The liver, which must produce the acid, wears down trying to meet the demand. Finally, the liver may malfunction because a person fails to drink enough pure water to keep the liver cleansed of wastes.

ACRES USA: Why is the glucose tolerance test not a reliable means of detecting low blood sugar?

DR. REAMS: First, the test itself is six hours long and is stressful. The stress and the patient’s natural nervousness about the test’s results can and often do affect blood sugar levels. Second, a person may not be sensitive to the glucose solution used in the test, but may be sensitive to other carbohydrates. In this case, the test will simply fail to detect the hypoglycemia. Third, the test only measures the levels of glucose in the blood. However, there are many other kinds of sugars besides glucose. If you don’t measure the total amounts of all kinds of sugars in the blood, you get an inaccurate reading. Fourth, the blood sugar can fluctuate so rapidly that even a series of readings won’t give you reliable data. Fifth, the patient’s blood sugar level may be normal most of the day, except for certain brief periods when it plunges too low. In such cases; the test will probably indicate a normal blood sugar—and miss the problem. Between these five factors, you can see that the glucose tolerance test will often give hypoglycemic readings when there are none; and vice versa, will often give “all okay” readings when hypoglycemia is actually present.

ACRES USA: Then how do you detect hypoglycemia?

DR. REAMS: We use the urine test. It measures the average blood sugar level by measuring urinary sugar levels. The sugar levels in the urine are relatively stable, so the urine test is superior to the glucose tolerance test in this respect. The urine test is non-stressful to the patient, so stress is eliminated as a factor. And the urine test measures all sugars, not just glucose. [Supplemental note: this test employs an ordinary brix refractometer.   According to the RBTI, a urine brix reading of 1.5 is perfect when all other equation numbers are perfect.]

ACRES USA: Can hypoglycemia be cured?

DR. REAMS: The program we recommend cures hypoglycemia in most cases. The secret is to correct the problem—liver malfunction—rather than to treat the symptom—low blood sugar. To correct the liver malfunction, we use the lemon water fast. The lemon water fast produces a rapid improvement in liver function. It also rejuvenates and detoxifies the body. As the body is detoxified and rebuilt, many hypoglycemics experience a “healing crisis” similar to what drug addicts go through in “withdrawal.” Nausea, vomiting and blackouts often occur. Vomiting is just one of the means by which the body rids itself of the poisons accumulated over the years. The blackouts occur, paradoxically, because the body is getting well so rapidly. What happens is that the liver begins to produce many previously lacking enzymes which are needed by the pancreas. When the pancreas suddenly receives this wealth of enzymes, it overreacts and for a short time produces too much insulin. This drives the blood sugar down too low and can cause a blackout. It’s unfortunate, but it is part of the natural healing process. Because the lemon water fast is so powerful, I want to warn all that no person should undertake this fast unless he or she first takes the urine test. Only then can one tell whether it is safe for them to do it without supervision.

ACRES USA: What happens after the fast is completed?

DR. REAMS: Each person is different. However, the general guidelines we follow include a fairly low-fat, low protein diet high in natural carbohydrates. The diet includes grains, vegetables and fruits. Clean meats are allowed several times a week according to the kind of job the person holds. People in physically demanding occupations may require more meat than others. The diet is generous in what it allows. However, we do restrict certain foods to try to eliminate those carbohydrates to which the patient is hypersensitive. We usually remove the Irish white potato from the diet since many, many patients are hypersensitive to it. Another natural organic food which, seems to be harmful to many hypoglycemics is—surprisingly—honey. So often we eliminate honey from the diet, too. Many people who have no problem with one kind of starchy food cannot tolerate similar though somewhat different foods. For example, many people do just fine, with sweet potatoes but are hypersensitive to white potatoes. Others can tolerate maple syrup, yet are hypersensitive to honey. An integral part of the daily diet is fresh raw green salads. This is to supply chlorophyll which the liver needs to produce enzymes. Vegetables rich in chlorophyll include such things as lettuce, escarole, endive, romaine, comfrey, spinach, celery tops, onion tops, green beans and so forth. Chlorophyll in the form of “green drinks” is also important. Take the same type vegetables you used in your salad and juice them with a vegetable juicer or a blender.

ACRES USA: What else do you do to help the hypoglycemics?

DR. REAMS: One of the most important is the distilled water cleansing program. Although most people don’t realize it, they have a lot of sugar—including white sugar; sugar from honey; and sugar from fruit—packed into their muscles and fatty tissues. It’s packed in there because their sugar metabolism wasn’t functioning properly. Their body neither burned those sugars for energy nor excreted them. Until these stored sugars are flushed out of the system, the body may release them into the blood at any time, disrupting the blood sugar level. The distilled water cleansing program is designed to rid the body of these sugars—thus clearing the way for a stable blood sugar level. Next, we recommend that the patients take Min-Col, which is one of the finest mineral supplements available. You can never be sure that the vegetables and meats you eat contain essential minerals. Therefore, we suggest Min-Col capsules, which contain minerals in the same form as in fruits and vegetables. Then we tell patients to eat their fruits and starchy foods before two in the afternoon. Your body needs energy earlier in the day, not towards evening and bedtime. If starchy foods and fruits are eaten after 2 pm, the energy that’s released is not completely used, and the sugar builds up in the bloodstream. Finally, we insist that everyone get plenty of fresh air and do deep breathing exercises daily. This is to assure that your body gets plenty of oxygen.

“The high protein diet only provides temporary relief, but is not a cure.”

[ACRES OR HEALTHVIEW]: What do you think of the popular high-protein diet?

REAMS: I know some people feel better on the high protein diet. However, the high protein diet only provides temporary relief but is not a cure.

The short-term relief occurs because the diet eliminates many carbohydrates to which the patient was hypersensitive. However, by itself, the high protein diet does nothing to correct the malfunctioning of the liver and pancreas.

Moreover, over the long-term, the diet can actually worsen the problem. This is because large quantities of hydrochloric acid are needed to digest all the protein. The liver begins to wear down trying to meet the demand. As we’ve seen, it is this liver malfunction that originally causes hypoglycemia.

Finally, on the high protein diet, urea builds up due to poor protein digestion. This leads, as we saw last time, to explosive tension and heart attacks. Ironically, some hypoglycemic die from heart attacks brought on by the high protein diet, the commonly accepted cure.

[ACRES OR HEALTHVIEW]: How well does your program work, Dr. Reams?

REAMS: So far I have worked with several thousand patients and the great majority of them are now totally free of hypoglycemia.

Many of them see improvement only several days after starting the program. The first sign of health generally appears when the tongue once again assumes a healthy pink color. After that, the pale, worn-out look disappears and the color returns to the face. Wrinkles seem to vanish, almost as if the patients had a face lift.

Within a few weeks, the patients are amazed at how well they feel. The fatigue, tension and irritability are gone. Their zest for life comes back. The patients become easy to get along with and a joy to be around. With their newfound energy, they go back to the jobs and do, as a rule, far better than ever before.

One patient said, “It feels as if I were just born again.” Another recent one thanked me and said simply, “What blessed relief.” I have received hundreds of other notes and comments like these.

[ACRES OR HEALTHVIEW]: One last question, before we go on to diabetes. How permanent is this improvement? I mean, once the patients leave you, does the improvement stick?

REAMS: Generally yes. Once the hypoglycemics are well, the improvements are permanent, provided they stick to the program. Once the liver and pancreas are functioning properly, the patients can go from meal to meal – five hours apart – without a single snack. They can eat a wide variety of foods – including many carbohydrates – without fear of low blood sugar. Incidentally, the craving for sweets disappears for good. How long does this improvement last? Some of my patients who were treated ten years ago still keep in touch regularly. They’re doing fine.

“{Diabetes} often leads to blindness, loss of limbs and even to fatal heart disease.”

[ACRES OR HEALTHVIEW]: Turning now to the opposite condition, high blood sugar or diabetes, what are the symptoms?

REAMS: Many of the symptoms are similar to those of hypoglycemia. The victims are tired and lack energy. They’re unusually nervous and, like the hypoglycemic, quite unstable. Diabetics suffer from headaches, dizziness and lightheadedness. Like hypoglycemic, diabetics have notoriously “sweet tooths.”

However, diabetes is far more severe than hypoglycemia.

It often leads to blindness, loss of limbs and even to fatal heart disease. As you mentioned earlier, diabetes is the third worst killer in America, claiming over 300,000 lives a year.

Eye problems begin with blurred vision and pressure behind the eyes. Frequently, the eyeballs become dilated. If the condition is not corrected, all vision can be lost permanently. Indeed, diabetes is the leading cause of blindness in adults.

One little diabetic boy, just 14 months old, was well along the way to losing his vision. His eyes were puffy and swollen and looked as if they were going to pop out of his head. If his condition had not been corrected, this child would have been blind by the time he was ten.

Loss of limbs can and does result from seemingly minor skin rashes, cuts or sores. As the diabetes worsens, these take longer and longer to heal – sometimes months for a minor nick or scratch. Eventually, they don’t heal at all. Instead, gangrene sets in and amputation is the only way to save the person’s life.

Sexual problems are another unfortunate result of diabetes. Several studies show that 25% to 50% of male diabetics are impotent – percentages which are far higher than among healthy males.

Female diabetics fare even worse. Their genitals become itchy and infected with fungi. Quite often, they complain about foul smelling discharges from their urogenital tract.

Circulation problems are frequent among diabetics. As you’d expect, poor circulation leads to heart problems. Indeed, it’s well-established that diabetics are quite prone to heart attacks.

[ACRES OR HEALTHVIEW]: And don’t most diabetics have excessive thirst?

REAMS: Oh, yes, thank you. Diabetics often drink enormous quantities of liquids. As a result, they must urinate frequently. Certainly not serious, but quite an inconvenience on the job, while traveling, or when you are trying to sleep.

[ACRES OR HEALTHVIEW]: How does diabetes cause so many problems?

REAMS: It’s much the same mechanism as hypoglycemia – liver malfunction. The liver fails to stabilize blood sugar; fails to maintain the proper pH of the blood; and fails to process and absorb nutrients properly.

In diabetes, the liver frequently allows the blood to become too acidic. This reduces the potency of the body’s insulin. The consequence is that, overall, there is too much sugar in the blood.

[BEGIN JESSE PART OF INTERVIEW HERE]

However, the blood sugar level may fluctuate widely, plummeting down for short periods of time to abnormally low levels and then coming back up again. This occurs because the liver and pancreas are weak, and as a result, they continually overreact – first to high blood sugar levels and then to low blood sugar levels. These extreme blood sugar fluctuations disrupt the brain’s activity. It loses its ability to regulate the use of salts and sugars.

As a result, mineral salts accumulate in the blood vessels. This causes hardening of the arteries.  Simultaneously, various sugars accumulate in the tissues. This causes excessive thirst. It’s just your body’s natural cleansing mechanism telling you to flush out these excessive sugars.

ACRES: And why do cuts fail to heal? [This question & answer not in Dr. Jesse’s transcript]

REAMS: Liver malfunction prevents the proper absorption and use of vitamin A, which leads to a vitamin A deficiency. As you probably know, vitamin A is essential for proper healing. The lack of it is a major cause of the frequent rashes diabetics suffer and the reason why their cuts and sores fail to heal.  The lack of vitamin A is also the primary reason for the vision problems diabetics suffer. It is well known that vitamin A is essential for your eyes.

The reason why diabetes causes the sexual problems I described earlier isn’t completely known. However, there is research indicating that the diabetic’s liver malfunction causes a hormonal imbalance which could cause the problem.

ACRES: If both diabetics and hypoglycemics suffer from a liver malfunction, then what is the difference between the two diseases? [This question & answer not in Dr. Jesse’s transcript]

REAMS: Actually, hypoglycemia – low blood sugar – is just the forerunner of diabetes. If hypoglycemia goes undetected and untreated, it frequently degenerates into fully developed diabetes,

In diabetes, the liver malfunction is more severe than in hypoglycemia. Because of this severe liver malfunction, diabetics suffer from both high and low blood sugar, since their blood sugar may fluctuate widely up and down. For example, we had one diabetic patient whose blood sugar level fluctuated between 300 and 50 in just a few hours.  Diabetes, therefore, is characterized not only by the finding of high blood sugar, but also by the severity and frequency of blood sugar fluctuations.

There is one other factor that makes diabetes so much more severe than hypoglycemia. Ironically, it’s the treatment recommended by the medical orthodoxy – injected insulin.

Insulin can cause tremendous damage, In fact, its continual use may bring about an early death.

ACRES: Would you please explain why you say something like that? [This question & answer not in Dr. Jesse’s transcript]

REAMS: Yes, there are many reasons why insulin is so dangerous.

The insulin the doctors give doesn’t act the same as the insulin naturally produced by your own pancreas.  This induced insulin forms a crystalline salt which oxidizes and hardens the walls of the blood vessels. The result is hardening of the arteries.

One of our neighbors had a twelve year old girl who had been on insulin since she was two years old. The insulin had created severe hardening of the arteries in her brain. A blood vessel burst in her brain, causing cerebral hemorrhage which killed her.

Whenever young children receive insulin injections over a period of years, great damage is done. Insulin should never be used on children except as a last resort.  Diabetic children respond to diet. I’ve helped thousands and not a single one required insulin.

Another problem is that the doctor’s insulin usage never perfectly matches the requirements of the patient. Some days you consume more starches and sweets than other days. Some days, you over-exercise and consume more energy than at other times. It’s almost impossible to measure the insulin dosage to keep up with the body’s precise needs.

So, often the diabetic’s insulin dosage will be too high. As a consequence, the patient’s blood sugar level is forced down too low – with all the problems that that creates. And particularly, when the insulin dosage is too low, another set of problems is created.

Still another problem is that the system slowly releases insulin into the muscle tissues. When the body turns the insulin loose, you get insulin shock as the blood sugar is driven too low.

Finally, in many cases, the body tissues become saturated with insulin. In these cases, the body can’t effectively use any more injected insulin. When a patient reaches this point, it’s possible for the muscle tissues to release a fatal dose of insulin into the bloodstream.

Before any patient takes insulin, he or she should be aware of all the problems it causes. The dangers of injected insulin shows the fallacy of trying to control blood sugar by external means – instead of helping the body to regulate it naturally. We find that improving the body chemistry almost always brings results.

ACRES: So, what do you do to help the diabetics? [This question & answer not in Dr. Jesse’s transcript]

REAMS: Since diabetes – like hypoglycemia – is caused by a liver malfunction – we use the same basic program to handle it.  We use the lemon water fast to improve the liver function; we use the distilled water cleansing program to flush toxins from the tissues.

From a 1977 Reams Lecture: You can write volumes and volumes about a malfunctioning pancreas but it is always due to a mineral deficiency.

Low or High blood sugar is not caused by what you eat. It is a malfunction of the pancreas which is a malfunction of the liver.  All malfunction of the liver is a mineral deficiency.

Then we use the same dietary program to correct deficiencies in minerals and chlorophyll and to rebuild the patient’s body. As with hypoglycemia, we insist on fresh air and exercise.

However, one difference between the care of hypoglycemics and diabetics is that diabetics have to reduce and eventually eliminate their own insulin dosage. This is something we cannot and will not do for any patient. However, patients do not find this a hard task. Once their liver function improves, their insulin requirements drop sharply, often in a matter of days.

For example there was one 40 year old diabetic man who had been on 120 units of insulin per day. By the fourth day, he was down to 30 units of insulin. By the sixth day, he felt a surge of energy which he had not felt in years. By the tenth day, he was off insulin completely, and returned home. He remains on the diet and has been checking with us regularly.  So far, he has been off insulin for over two years.

There was the diabetic man who was 100 pounds over-weight, and who couldn’t walk a hundred feet without having to sit down and rest. He had been on insulin for 20 years, 120 units a day. We gave him a diet and he regulated his insulin shots himself.

Several months later, his excess weight was gone and he was walking several miles a day. He felt 20 years younger and was just ecstatic about being off insulin. So far, this man has been off insulin for almost a year. It he continues on the program, he’ll never have to go back on insulin.

We also cared for a 32 year old diabetic mother; the wife of a doctor and herself a registered nurse. Her blood sugar was out of control in spite of the fact that she took insulin. Indeed, whenever she took insulin, it would drive her blood sugar down so fast and so low that she began to shake. She had lost so much weight that she was a pitiful sight to look at.

Today she is back at home and has been off insulin for more than three months. Although I still don’t consider her completely well, I think she has made enormous progress. She now looks simply marvelous and bubbles with enthusiasm.

Finally, I recall the little 3 year old boy – a full fledged diabetic who was brought here by his mother. He sat around all day and never felt like playing. In five days his blood sugar was down to normal, and three days later he was ready to go home.

So you see, our program has worked for thousands of diabetics, as well as hypoglycemics. This is because we correct the main cause of blood sugar problems – liver malfunction.

ChooseLife Notes : Bold sections added by ChooseLife.

In Choose Life Or Death, Carey Reams describes his recommendation for the Pancreas to function and meet it’s daily requirements of insulin production, this was 3oz of green juice. This would have been many years ago, plus Reams was a world class agronomist, this leads me to presume that nowadays it may require a multiple of this value, 6oz’s or more. Reams would have been feeding patients high brix green smoothies, having tested the quality of many fruits and vegetables nowadays here in the UK, it may take an even higher amount.

Carey Reams lost a large portion of his Pancreas due to shrapnel during service in WWII, he lived some 40+ years (to 82) with around 50% functioning Pancreas.

Calcium – Chlorophyll – Oxygen

Host- and Microbe-Dependent Dietary Lipid Metabolism in the Control of Allergy, Inflammation, and Immunity

Published : April 10th 2019

Athors : Azusa Saika, Takahiro Nagatake and Jun Kunisawa

Abstract

The intestine is the largest immune organ in the body, provides the first line of defense against pathogens, and prevents excessive immune reactions to harmless or beneficial non-self-materials, such as food and intestinal bacteria. Allergic and inflammatory diseases in the intestine occur as a result of dysregulation of immunological homeostasis mediated by intestinal immunity.

Several lines of evidence suggest that gut environmental factors, including nutrition and intestinal bacteria, play important roles in controlling host immune responses and maintaining homeostasis. Among nutritional factors, ω3 and ω6 essential polyunsaturated fatty acids (PUFAs) profoundly influence the host immune system.

Recent advances in lipidomics technology have led to the identification of lipid mediators derived from ω3- and ω6-PUFAs. In particular, lipid metabolites from ω3-PUFAs (e.g., eicosapentaenoic acid and docosahexaenoic acid) have recently been shown to exert anti-allergic and anti-inflammatory responses; these metabolites include resolvins, protectins, and maresins. Furthermore, a new class of anti-allergic and anti-inflammatory lipid metabolites of 17,18-epoxyeicosatetraenoic acid has recently been identified in the control of allergic and inflammatory diseases in the gut and skin.

Although these lipid metabolites were found to be endogenously generated in the host, accumulating evidence indicates that intestinal bacteria also participate in lipid metabolism and thus generate bioactive unique lipid mediators. In this review, we discuss the production machinery of lipid metabolites in the host and intestinal bacteria and the roles of these metabolites in the regulation of host immunity.

Keywords: lipid metabolites, dietary oil, intestinal immunity, inflammation, allergy, intestinal bacteria

Introduction

Lipid composition in organisms differs among species, in accordance with the expression levels of metabolic enzymes and dietary habits. Marine phytoplankton and seaweeds produce a large amount of the ω3-polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (1). Although fish do not generate EPA and DHA per se, they accumulate EPA and DHA by eating phytoplankton (1). In plants, linseed and perilla contain large amounts of α-linolenic acid, a precursor of EPA and DHA. In contrast, soybean oil and sesame oil contain copious quantities of the ω6-PUFA linoleic acid. The difference in the fatty acid composition of plants depends on the expression levels and activities of metabolic enzymes such as Δ12-desaturase and Δ15-desaturase, which are involved in the generation of linoleic acid and α-linolenic acid, respectively (23). Because mammals do not have either Δ12 or Δ15-desaturase, ω3- and ω6-PUFAs are categorized as essential fatty acids that must be obtained from the diet (3). Therefore, the balance of ω3 and ω6 lipids in the body largely depends on the quality of the dietary lipid consumed.

The beneficial effect of dietary ω3-PUFAs on human health was first reported in an epidemiological study in 1978 in which Greenland Eskimos, who consume high ω3-PUFA diets that include fish, were found to have a lower mortality from coronary heart disease than Danes and Americans, who eat much less ω3-PUFAs (4). Since then, accumulating evidence indicates that EPA and DHA have beneficial effects on the inhibition of various types of inflammatory and allergic diseases, including cardiovascular disease, Alzheimer’s disease, rheumatoid arthritis, inflammatory bowel disease, atopic dermatitis, asthma, and food allergy (513). Recent developments in analytical technology, including liquid chromatography (LC) and mass spectrometry (MS), have enabled us to identify EPA- and DHA-derived pro-resolving lipid mediators (SPMs), including resolvins (Rvs), protectins (PDs), maresins (MaRs), and 17,18-epoxyeicosatetraenoic acid (17,18-EpETE) for inhibition of inflammatory and allergic diseases (714).

Dietary lipids are metabolized not only by mammalian enzymes but also by bacterial enzymes. Microorganisms can generate unique lipid metabolites such as conjugated linoleic acids, hydroxy fatty acids, and oxo fatty acids. These bacteria-produced lipid metabolites show biological activity in the context of host health and diseases (1516). Here, we review our current understanding of ω3- and ω6-PUFA-derived lipid mediators in the control of inflammatory and allergic diseases.Go to:

ω6 Fatty Acid Metabolites Have Opposing Roles in Pro-and Anti-Inflammation

Dietary lipids are metabolized in the body to lipid mediators, which regulate host immune systems. Arachidonic acid (AA) is a metabolite of linoleic acid, and functions as a direct precursor of bioactive lipid mediators, which are known as eicosanoids. In addition to its biosynthesis in the body from linoleic acid, AA can be obtained from dietary sources, such as meat and eggs. AA is metabolized by cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP), and then converted into lipid mediators, including prostaglandins (PGs), leukotrienes (LTs), thromboxanes (TXs), and lipoxins (LXs) (Figure 1) (17). These AA-derived lipid meditators have both pro- and anti-inflammatory effects in the intestine.

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Lipid mediators derived from AA, EPA, and DHA. Various kinds of lipid mediators are produced from ω6- and ω3-PUFAs. AA, EPA, and DHA are converted to bioactive lipid mediators by the enzymatic activities of COX, LOX, and CYP. Lipid mediators exert their biological effects through binding to G-protein-coupled receptors. AA-derived lipid mediators have pro- and anti-inflammatory activities, whereas EPA- and DHA-derived lipid mediators exert anti-inflammatory or pro-resolution activities or both.

AA is converted into LTB4 by LOX activity. The LTB4-BLT1 axis plays a key role in the development of inflammatory diseases including inflammatory bowel disease by stimulating the recruitment of inflammatory cells and the production of pro-inflammatory cytokines (1820). LTB4 also activates another receptor BLT2 which is a high affinity receptor for 12-hydroxy-heptadecatrienoic acid (12-HHT). In contrast to pro-inflammatory role of BLT1, BLT2-deficient mice show transepidermal water loss, suggesting its anti-inflammatory role in the skin (21). Indeed, BLT2-mediated pathway induced the expression of claudin-4 for enhancement of epithelial barrier (21).

AA is converted into PGs by COX activity, which generate PGD2 and PGE2 as the representative lipid mediators. The PGD2-chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) pathway induces dextran sodium sulfate (DSS)- and trinitrobenzene sulfonic acid (TNBS)-induced colitis (2223). Eosinophil infiltration into colon is inhibited by CRTH2 antagonist treatment in TNBS-induced colitis (23). In contrast to pro-inflammatory properties, the PGD2-DP axis reduces granulocyte infiltration into the colonic mucosa in the mouse model of TNBS-induced colitis and colitis-associated colorectal cancer (2425) These opposing roles of CRTH2 and DP in chemotaxis are explained by different usage of G proteins. CRTH2 is coupled with Gαi while DP is coupled with Gαs, which induces decreased and increased in cAMP levels, respectively (26). Consistent with these findings when PGD2 acted on neutrophils CRTH2 pathway, it induced neutrophil migration to the intestinal lamina propria in the DSS-induced colitis model (22).

PGE2 stimulates four distinct types of receptors EP1 to EP4. The PGE2-EP2 axis in neutrophils and tumor-associated fibroblasts promotes colon tumorigenesis by inducing expression of inflammation- and growth-related genes, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and Wnt5A (27). In contrast to EP2-mediated carcinogenic effects, EP3-mediated signals show anti-carcinogenic effects, which are consistent with different types of G protein pathways; EP2 activates Gαs, while EP3 activates Gαi (27).

Therefore, it is suggested that the opposing roles in pro- and anti-inflammation of ω6-PUFAs derived lipid mediators are determined by target cell types and receptor types.

In addition to these factors, cellular source of PGD2 affects in its activity in pro- and anti-inflammation in croton oil-induced skin inflammation model (28). In the initial phase of the dermatitis when few inflammatory cells exist in the skin, endothelial cells show highest COX-2 activity and produce PGD2, which leads to DP activation on endothelial cells, and inhibits vascular leakage. On the other hand, in the late phase of the dermatitis, many types of hematopoietic inflammatory cells produce PGD2, which stimulate CRTH2 on inflammatory cells for infiltration to the inflamed skin, and exacerbates skin inflammation (2829). These findings suggest that stage of inflammatory process is a determinant of the effects of AA-derived metabolites through distinct site of the mediator production.

Dietary ω3-PUFAs Inhibit the Development of Allergic Disease

We and others have shown the anti-inflammatory and anti-allergic effects of dietary ω3-PUFAs (47812133034).

Fish oil is a representative ω3-PUFA-rich dietary oil which contains plenty amount of EPA and DHA. Dietary fish oil ameliorated asthma by decreasing eosinophil infiltration, mucus production, and peribronchiolar fibrosis, which was associated with inhibition of cytokine production by downregulation of nuclear factor (NF)-κB and GATA-3 (30). These anti-allergic effects may be caused by decreased amount of ω6-PUFA-derived lipid mediators such as PGD2, LTB4, and LTE4 which exacerbate airway inflammation and increasing ω3-PUFA-derived lipid mediators, for example, RvD1 is reported to decrease allergic airway responses (63536). Further, fish oil-fed mice reduced acute allergic skin response in food allergy model sensitized by peanut and whey by reducing mucosal mast cell protease-1 and antigen specific IgE in serum (31).

Linseed oil contains large amount of α-linolenic acid, which is converted into EPA and DHA in the body. One study reported that linseed oil-fed mice alleviated pollen-induced allergic conjunctivitis by decreasing the production of ω6-PUFA-derived pro-inflammatory lipid mediators, and reducing eosinophil infiltration into the conjunctiva (13). We also found that linseed oil-fed mice reduced allergic diarrhea in ovalbumin (OVA)-induced food allergy model (7). In this model, allergic diarrhea occurs as a consequence of a dominant Th2-type environment and the presence of allergen-specific serum IgE, which induces mast cell degranulation in the gut. We found that in linseed oil-fed mice, the Th1–Th2 balance, allergen-specific IgE level, and mast cell numbers in the gut did not change compared with those in soybean oil-fed mice in the OVA-induced food allergy model. However, we found that mast cell degranulation was profoundly inhibited in linseed oil-fed mice (7).

We also assessed fatty acid composition in intestinal tissues and found that the amounts of α-linolenic acid and its metabolites of EPA and DHA were increased in linseed oil-fed mice when compared with those in soybean oil-fed mice (7). In contrast, linoleic acid and AA levels were higher in soybean oil-fed mice than linseed oil-fed mice (7). Imaging MS analysis revealed that increased amounts of α-linolenic acid, EPA and DHA were found in the lamina propria compartment where large numbers of immune cells such as T cells, plasma cells, and dendritic cells are present (7). These findings collectively demonstrated that the composition of essential fatty acids in dietary oils directly reflect the lipid composition in the gut, which, in turn, may influence the host immune system.

ω3 Fatty Acid Metabolites Have Roles in Anti-Inflammation and Pro-Resolution

EPA and DHA are representative ω3-PUFAs, which compete with AA in the AA cascade. Therefore, it has long been considered that the beneficial effects of dietary ω3-PUFAs against inflammatory diseases stem from decreased amounts of AA-derived eicosanoids. In addition, recent technology developments in LC and MS have led to the identification of trace and novel lipid mediators, including Rvs, PDs, and MaRs, which are produced from EPA and DHA in the body (37). These metabolites have anti-inflammatory or pro-resolution properties (or both) and are known as SPMs (Figure 1) (37). Although the receptors for SPMs have not been fully elucidated, some SPMs have been shown to interact with specific receptors. For example, Rvs derived from EPA and DHA use distinct types of receptors. RvE1 interacts with BLT1 and ChemR23, while RvD1 interacts with G-protein-coupled receptor (GPR) 32 and ALX (3839).

Examples of how SPMs affect intestinal inflammation include their involvement in the RvE1–ChemR23 axis, which actively inhibits colonic inflammation in the DSS-induced colitis model by suppressing the TNF-α-induced nuclear translocation of NF-κB and the expression of inflammatory cytokines, including TNF-α and IL-12p40, from macrophages (40). Furthermore, RvE1 and PD1 enhance the resolution of inflammation by stimulating macrophage phagocytosis of apoptotic cells in zymosan-induced peritonitis (4142). MaR1 is reported to attenuate both DSS- and TNBS-induced colitis by inhibiting NF-κB activation and inflammatory cytokine production (43). Thus, multiple types of SPMs exert their anti-inflammatory properties by using different mechanisms for the regulation of colitis.

17,18-Epoxyeicosatetraenoic Acid is a New Class of Anti-Allergy Lipid Mediator

As mentioned above, dietary linseed oil inhibited the development of food allergy with increased amounts of α-linolenic acid, EPA and DHA in the intestine (7), which prompted us to investigate mediator profiles by using LC-MS/MS analysis. We found that 17,18-EpETE was the metabolite whose levels increased the most in the gut of linseed oil-fed mice (7). When 17,18-EpETE was intraperitoneally injected into soybean oil-fed mice, development of allergic diarrhea and degranulation of mast cells were inhibited, which was similar to observation in linseed oil-fed mice (Figure 2) (7). Consistent with its action at the late stage of the allergic response, 17,18-EpETE was effective as a prophylactic and a therapeutic treatment for food allergy (7).

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Figure 2

17,18-EpETE is a new class of anti-allergy and anti-inflammatory lipid mediator. 17,18-EpETE is produced by CYP from EPA. 17,18-EpETE suppresses contact hypersensitivity by reducing neutrophil infiltration into the skin by inhibiting Rac activation and migration through GPR40 signaling. 17,18-EpETE also indirectly inhibits the development of food allergy by inhibiting mast cell degranulation. Given that mast cells do not express GPR40, the detailed mechanisms responsible for this inhibition of mast cell degranulation remain unclear.

17,18-EpETE Ameliorates Contact Hypersensitivity Through GPR40-Mediated Inhibition of Neutrophil Migration

To evaluate the biological role of 17,18-EpETE in the regulation of other types of allergic inflammatory disease, we examined the effect of 17,18-EpETE on the regulation of contact hypersensitivity (CHS) in the hapten-induced CHS model. We found that 17,18-EpETE showed both prophylactic and therapeutic anti-inflammatory effects on CHS in mice and cynomolgus macaques (44). 17,18-EpETE did not affect T cell or dendritic cell functions, including inducible skin-associated lymphoid tissue formation, but it did selectively inhibit neutrophil infiltration into the skin (44). Indeed, 17,18-EpETE reduced neutrophil mobility by inhibiting Rac-activation and pseudopod formation in a GPR40-dependent fashion (44).

Consistent with this selective influence on neutrophils, GPR40 was highly expressed by neutrophils, but not T cells or other leukocytes in the skin. It is worth noting that mast cells do not express GPR40; so, given that mast cell degranulation was inhibited by 17,18-EpETE treatment in the food allergy model (744), this finding suggests that 17,18-EpETE inhibits mast cell degranulation indirectly (Figure 2). Of note, the activation of GPR40 in intestinal epithelial cells has been reported to improve intestinal barrier function by enhancing occludin expression (45). Therefore, it is likely that the improvement in intestinal barrier function induced by 17,18-EpETE via GPR40 in epithelial cells led to decreased allergen penetration, which, in turn, resulted in decreased mast cell degranulation and inhibited food allergy development.

Structure-Activity Relationships Among the GPR40-Dependent Anti-Allergic and Anti-Inflammation Effects of 17,18-EpETE

17,18-EpETE is further metabolized by soluble epoxide hydrolase to 17,18-dihydroxy-eicosatetraenoic acid (17,18-diHETE). However, 17,18-diHETE has little effect on the development of food allergy, and 14,15-epoxyeicosatetraenoic acid (14,15-EpETE), which has an epoxy structure at the ω6 position, also lacks the ability to inhibit food allergy (7). In addition, 17,18-diHETE has little effect on the development of CHS (44). Although 17,18-EpETE activates GPR40, 17,18-diHETE does not activate GPR40, which is consistent with its lack of anti-allergic and anti-inflammatory properties (744). These findings therefore suggest that the 17,18-epoxy ring structure at the ω3 position in EPA is important for GPR40-mediated anti-allergic and anti-inflammatory activity.

17,18-EpETE is synthesized from EPA through the enzymatic activity of CYP and has two isomers, 17(S),18(R)-EpETE and 17(R),18(S)-EpETE. Among the CYP subfamilies in mice, five CYP isoforms (Cyp1a2, 2c50, 4a12a, 4a12b, and 4f18) are known to convert EPA into 17,18-EpETE (46). Cyp1a2 displays high stereoselectivity for producing 17(R),18(S)-EpETE, whereas Cyp4f18 displays stereoselectivity for producing 17(S),18(R)-EpETE (46). In contrast, Cyp2c50, Cyp4a12a, and Cyp4a12b display less stereoselectivity and produce a mixture of 17(S),18(R)-EpETE and 17(R),18(S)-EpETE (46). 17(R),18(S)-EpETE, but not 17(S),18(R)-EpETE, is a potent vasodilator (47). Indeed, 17(R),18(S)-EpETE activates calcium-activated potassium channels, which lead to relaxation of rat cerebral artery vascular smooth muscle cells (47). Whether stereoselectivity of 17,18-EpETE contributes to the anti-allergy and anti-inflammatory effects of 17,18-EpETE have not been evaluated in food allergy and CHS, because we used racemic compounds in our studies (744). The CYP isoform and polymorphisms determine the metabolic properties of CYP and stereoselectivity. Therefore, the anti-allergic and anti-inflammatory health benefits derived from ω3-PUFA intake may be influenced by the expression levels of the various types of CYP in the body.

CYP is also found in microorganisms. For example, it has been reported that bacterial CYP (e.g., BM-3 derived from Bacillus megateirum) metabolizes PUFAs and produces hydroxy and epoxy fatty acids (48). Bacillus, Streptomyces, Pseudomonas, and Mycobacterium also have CYP (4953). These findings suggest that many types of microorganisms are involved in lipid metabolism. In addition, other metabolic enzymes, such as COX and LOX, are thought to be expressed by some bacteria, including Pseudomonas aeruginosa, Shewanella woodyi, Mytococcus fulrus, and Burkholderia thailandensis (5455). Some microorganisms described above are present in environment, suggesting that in addition to mammalian expression of metabolic enzymes, various microorganisms may be a determinant of the efficacy of ω3-PUFA in the context of the regulation of inflammation.

Bacterial-Conjugated Linoleic Acid has a Role in Anti-Inflammation

Intestinal bacteria have been shown to express unique unsaturated fatty acid-metabolic enzymes and to produce bioactive lipid mediators that are not generated by mammalian cells (Figure 3). Ruminal bacteria including Butyrivibrio, Lactobacillus, and Megasphaera can produce conjugated linoleic acid (CLA), which is an isomer of linoleic acid that has conjugated double bounds (5658). It is known that CLA has some isomers such as cis-9-trans-11-octadecenoic acid (c9,t11-CLA), trans-10-cis-12-octadecenoic acid (t10,c12-CLA) and trans-9-trans-11-octadecenoic acid (t9,t11-CLA). These isomers have different activities for insulin sensitivity and atherosclerosis.

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Figure 3

Physiological functions of CLA and HYA. CLA and HYA are produced from linoleic acid by intestinal bacteria. c9,t11-CLA ameliorates insulin sensitivity and prevents atherosclerosist10,c12-CLA deteriorates insulin sensitivity and promotes atherosclerosis, and t9,t11-CLA prevents atherosclerosis. HYA enhances intestinal barrier function by increasing occludin expression and inhibiting intestinal inflammation in a GPR40-dependent manner. HYA inhibits atopic dermatitis by increasing claudin-1 expression and enhancing skin barrier function. HYA also inhibits gastric Helicobacter infections by blocking the bacterial futalosine pathways.

For example, c9,t11-CLA shows beneficial effects on insulin sensitivity by enhancing glucose uptake and adipokine production such as leptin and adiponectin, and on atherosclerosis by suppressing macrophage infiltration and activation, and reducing plaque development through an increase in expression of PPARγ, while t10,c12-CLA shows adverse effects through a decrease in expression of PPARγ (5963). In addition, t10,c12-CLA reduces expression of liver X receptor α (LXRα) which induces expression of ATP-binding cassette (ABC) transporter A1, ABCG1, and sterol regulatory element binding protein 1c which involved in reverse cholesterol transport (6465). Therefore, t10,c12-CLA shows pro-atherosclerosis effects (6668). On the other hand, t9,t11-CLA is effective for the treatment of atherosclerosis by activation of LXRα (69). These results indicate that each isomers exert different bioactivities through distinct transcriptional regulation and activation of PPARγ and LXRα for the control of insulin sensitivity and atherosclerosis.

Compared with chemical production, microbial fermentation offers better ways to produce isomer-specific CLAs. The CLA isomers are produced at different ratios, depending on the type of bacteria. Lactobacillusstrains (L. acidophilus, L. plantarum, L. casei, L. reuteri, L. rhamnosus, and L. pentosus), Bifidobacteriumstrains (B. dentium, B. breve, and B. lactis), and Propionibacterium freudenreichii can convert linoleic acid to c9,t11-CLA and t10,c12-CLA, and these bacteria produce higher levels of c9,t11-CLA than of t10,c12-CLA (15577072). Some Lactobacillus and Bifidobacterium strains also produce t9,t11-CLA with c9,t11-CLA and/or t10,c12-CLA (57). L. paracasei and B. bifidum produce c9,t11-CLA stereoselectively, whereas Megasphaera eldsenii produces t10,c12-CLA stereoselectively (7173). Given that these CLAs have different biological activities which depend on their 3D-structure, it is important to select appropriate bacteria as a probiotics or producer for obtaining required beneficial effects.

Bacterial Production of Unique Hydroxy and Oxo Fatty Acids and Their Multiple Biological Activities

L. plantarum, an intestinal bacteria, produces hydroxy fatty acids (i.e., 10-hydroxy-cis-12-octadecenoic acid [HYA], 10-hydroxy-trans-11-octadecenoic acid [HYC], 10-hydroxy-octadecanoic acid [HYB]) and oxo fatty acids (10-oxo-cis-12-octadecenoic acid [KetoA], 10-oxo-trans-11-octadecenoic acid [KetoC], 10-oxo-octadecanoic acid [KetoB]) as intermediate products of CLA production (16). Recently, these metabolic intermediates have been shown to contribute to the regulation of host health and diseases. HYA is the first metabolite produced from linoleic acid by L. plantarum, and it enhances intestinal barrier function and suppresses the development of DSS-induced colitis in mice in a GPR40-dependent manner (45). Furthermore, HYA prevents Helicobacter infections by blocking their futalosine pathways, which is an alternative menaquinone biosynthetic pathway and an essential metabolic pathway for the growth of Helicobacter. Moreover, HYA treatment suppresses the formation of lymphoid follicles in the gastric mucus layer after H. suis infection, and therefore HYA treatment protects mice against the formation of gastric mucosa-associated lymphoid tissue lymphoma induced by infection with Helicobacter (74). HYA also ameliorates the pathological scores of atopic dermatitis in NC/Nga mice by decreasing plasma IgE levels and reducing mast cell infiltration into the skin (7576). KetoA enhances adiponectin production and glucose uptake in a proliferator-activated receptor γ (PPARγ)-dependent manner, and is effective for the prevention and amelioration of metabolic abnormalities associated with obesity (77).

The production of these hydroxy and oxo fatty acids depends on the unique bacterial enzymes CLA-HY (unsaturated fatty acid hydratase), CLA-DH (hydroxy fatty acid dehydrogenase), CLA-DC (isomerase), and CLA-ER (enone reductase) in L. plantarum AKU1009a (1678). The hydroxy activity is found not only in Lactobacillus but also in a broad spectrum of bacteria. Oleate hydratase belongs to the FAD-dependent myosin cross-reactive antigen (MCRA) protein family, which is found in gram-positive and -negative bacteria; it catalyzes the conversion of linoleic acid to HYA. For example, Lactobacillus, Bifidobacterium, Streptococcus, and Stenotrophomonas bacteria are reported to have MCRA, and indeed they have the ability to produce HYA (7982).

Together, these findings indicate that intestinal bacteria metabolize dietary lipids and produce lipid metabolites that can regulate host immune systems. Therefore, to obtain beneficial lipid metabolites and regulate intestinal inflammation, we need to consider not only host enzymes but also enzymes produced by intestinal bacteria. In addition, we must consider how dietary lipid intake causes changes in the intestinal microbiota.

Conclusion

Recent technological developments in lipidomics research initiated a new era of lipid biology by helping researchers to identify novel lipid metabolites from ω3- and ω6-PUFAs, which actively regulate the host immune system and play important roles in the control of health and diseases. Given that the production of lipid metabolites is influenced by complex factors, including diet, intestinal bacteria, and enzyme expression, combined studies on nutrition, metabolomics, and the metagenomics of the microbiota, as well as informatics, may provide powerful insights to further our understanding of the lipid network in the host immune system.

Author Contributions

All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

We thank laboratory members for helpful discussion. The results described in the review were obtained, at least in part, from research supported by grants from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (MEXT) and the Japan Society for the Promotion of Science (JSPS; KAKENHI [JP15K19142 to TN; JP15H05790, JP18H02150, JP18H02674, JP17K09604, JP26670241, and JP26293111 to JK]); the Japan Agency for Medical Research and Development (AMED; [JP17ek0410032s0102, JP17ek0210078h0002, JP17ak0101068h0001, JP17gm1010006s0101, JP18ck0106243h0003, and 19ek0410062h0001 to JK]); the Ministry of Health and Welfare of Japan (to JK); the Science and Technology Research Promotion Program for Agriculture, Forestry, Fisheries, and Food Industry (to JK); grants-in-aid for Scientific Research on Innovative Areas from MEXT (JP23116506, JP16H01373, and JP25116706 to JK); Cross-ministerial Strategic Innovation Promotion Program (SIP); the Ono Medical Research Foundation; and the Canon Foundation (to JK).

Glossary

Abbreviations

12-HHT12-hydroxy-heptadecatrienoic acid
14,15-EpETE14,15-epoxyeicosatetraenoic acid
17,18-EpETE17,18-epoxyeicosatetraenoic acid
17,18-diHETE17,18-dihydroxy-eicosatetraenoic acid
AAarachidonic acid
CHScontact hypersensitivity
CLAconjugated linoleic acid
COXcyclooxygenase
CRTH2chemoattractant receptor-homologous molecule expressed on Th2 cells
CYPcytochrome P450
DCdendritic cell
DHAdocosahexaenoic acid
DSSdextran sodium sulfate
EPAeicosapentaenoic acid
GPRG-protein-coupled receptor
HYA10-hydroxy-cis-12-octadecenoic acid
HYB10-hydroxy-octadecanoic acid
HYC10-hydroxy-trans-11-octadecenoic acid
ILinterleukin
KetoA10-oxo-cis-12-octadecenoic acid
KetoB10-oxo-octadecanoic acid
KetoC10-oxo-trans-11-octadecenoic acid
LCliquid chromatography
LOXlipoxygenase
LTleukotriene
MaRmaresin
MCRAmyosin cross-reactive antigen
MSmass spectrometry
NFnuclear factor
OVAovalbumin
PDprotectin
PGprostaglandin
PPARperoxisome proliferator-activated receptor
PUFApolyunsaturated fatty acid
Rvresolvin
SPMspecialized pro-resolving lipid mediator
TNFtumor necrosis factor
TXthromboxane.

Full Article (including references) :
https://www.frontiersin.org/articles/10.3389/fnut.2019.00036/full

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468274/

Bold sections applied by ChooseLife.

Infection and pH

Meridian Institute News Vol. 7 No. 3 May, 2003

pH-Dependent Viruses

   For over five years researchers at Meridian Institute have been looking into the connection between pH (acid/alkaline) balance and viral infection – a link noted by Edgar Cayce in several of his psychic readings. With the recent epidemic of severe acute respiratory syndrome (SARS) and continued concerns about common conditions such as colds and flu, our interest in this field has expanded to explore basic science and clinical projects to test the Cayce hypothesis.  Here is an overview of what we have found so far and where we are headed.  Some simple preventive measures will also be discussed. 
Understanding Viruses
    Viruses are extremely small parasitic life forms, the smallest living things on Earth. In essence, a virus is a minuscule pocket of protein that contains genetic material.

    Although viruses can remain dormant outside a living body, they only become active when in contact with live tissue. Once a virus infects a cell by penetrating the cell membrane, it can either lay dormant (lysogenic infection) or begin reproducing itself (lytic infection – the more common pattern).  When a cell becomes full of virus, it bursts releasing the virus to infect other host cells.

    A wide variety of diseases are caused by viruses including the common cold, flu, warts, measles, hepatitis, herpes, smallpox, and AIDS.  SARS is just the latest in a long list of viral parasites.

    Unlike bacteria that can usually be effectively treated with antibiotics, viral infections are often unresponsive to modern medical treatment.  If the virus causing a disease has been discovered, a serum may be developed to provide inoculation against that specific virus.  The most common approach to virus protection is to avoid contamination by infected individuals. 
 Viral pH Dependency

    Laboratory experiments (in vitro) have confirmed that many viruses require a mildly acidic environment to attack host cells.  At Meridian Institute we are interested in determining exactly how this physiological fact manifests within the human body (in vivo). Understanding the role of pH balance in viral infections may provide preventive and therapeutic breakthroughs for dealing with epidemics including the recent outbreak of SARS.

    To appreciate the relevance of pH for viral infection, let’s first review some facts about acid/alkaline balance.  The acid/alkaline continuum ranges from 0-14 with 7 as neutral. The lower end of the scale (below 7) is acid and above 7 is alkaline.

    Acid/alkaline balance is extremely important to normal physiology. For example, the blood will maintain a slightly alkaline range of 7.35 to 7.45. Extended pH imbalances of any kind are not well tolerated by the body. The management of the pH factor is so important that the body’s primary regulatory systems (especially breathing, circulation, and eliminations) closely regulate acid-alkaline balance in every cell and system.

    Certain viruses (including the rhinoviruses and coronaviruses that are most often responsible for the common cold and influenza viruses that produce flu) infect host cells by fusion with cellular membranes at low pH.  Thus they are classified as “pH-dependent viruses.”

    Drugs that increase intracellular pH (alkalinity within the cell) have been shown to decrease infectivity of pH-dependent viruses.  Since such drugs can provoke negative side effects, the obvious question is whether more natural techniques can produce the same result. 
 Possible Relevance to SARS
    The World Health Organization has concluded that SARS is produced by a new virulent strain of coronavirus. Specific research on the possible pH dependency of the SARS virus has not yet been done.  It is well known that coronavirus infectivity is exquisitely sensitive to pH.  For example, the MHV-A59 strain of coronavirus is quite stable at pH 6.0 (acidic) but becomes rapidly and irreversibly inactivated by brief treatment at pH 8.0 (alkaline).  Human coronavirus strain 229E is maximally infective at pH 6.0.  Infection of cells by murine coronavirus A59 at pH 6.0 (acidic) rather than pH 7.0 (neutral) yields a tenfold increase in the infectivity of the virus.

    If the strain of coronavirus responsible for SARS shares the pH characteristics of these other coronaviruses that are pH-dependent, this could be a valuable clue to effective prevention and treatment strategies for this frightening epidemic. Perhaps keeping a balanced or slightly alkaline pH environment for the body’s tissues can provide viral protection or enhanced healing for SARS and common viral agents that cause respiratory infections. 
 Edgar Cayce’s Recommendations
    Edgar Cayce affirmed the importance of pH balance with regard to common viruses that cause colds and flu.  Cayce repeatedly insisted that such infectious agents do not thrive in an alkaline environment. When asked how to prevent colds, Cayce replied, “by keeping the body alkaline. Only in acids do colds attack the body.” (3248-1)

    Cayce recommended using litmus paper to test the pH of urine and saliva as an indication of the pH balance of the body.  We now have more precise means for monitoring pH in the form of pH paper and digital pH meters.

    As a practical preventive measure, Cayce’s suggestions for alkalizing the body emphasized eating an abundance of fresh fruits and vegetables, especially salads:   “…  if an alkalinity is maintained in the system – especially with lettuce, carrots and celery, these in the blood supply will maintain such a condition as to immunize a person.”  (480-19)  Consuming citrus fruit and juices was also a common alkalizing suggestion in the readings that addressed concerns about cold and flu infections. 
 Meridian Institute Research
    We reported a preliminary study on dietary effects of urine pH in January 1999 (Vol 3 No 1). The study was done to test Edgar Cayce’s recommendations for testing urine as a marker for systemic pH balance.  Our conclusion was that following Cayce dietary recommendations of eating primarily alkaline-producing foods (such as fruits and vegetables) does indeed tend to alkalize the urine.

    We have contacted leading researchers in the field of rhinovirus infection studies to make them aware of the possible role of acid/alkaline balance and seek feedback on how to do scientific studies to test the Cayce hypothesis in vivo – with human subjects.  If it turns out that SARS is produced by a pH-dependent coronavirus, we will certainly make sure that the clinical researchers who do in vivo studies of viral infections are made aware of this potentially important factor.

    Rhinovirus infection studies are done at several leading universities, usually to test the effectiveness of drugs that may help to prevent or relieve the symptoms of colds.  Small amounts of solution containing rhinovirus are dropped into the noses of subjects to intentionally infect them under controlled conditions.  Interestingly, about five to fifteen percent of subjects do not get colds even when the virus is carefully placed onto the nasal mucosa.  Could it be that the pH of the resistant subject’s nasal mucosa is alkaline (or neutral), preventing the rhinovirus from infecting the cells inside of the nose?

    There have been several published studies on nasal mucosal pH with varying results.  Some researchers have concluded that the pH of nasal secretions vary with sleep, rest, ingestion of food, emotional states, and menstrual cycles.  Other scientists, using different technology, have failed to confirm these results.  Clearly much work needs to be done in this area to establish consistent outcomes.

    We have tested equipment from two of the leading companies that sell devices that can measure nasal pH and have learned that there is significant variability in the instruments, apart from the complexities of measuring pH in different people and within the same person over time.

    The picture on page 1 shows a pH sensitive microelectrode that we are currently using to measure nasal mucosa pH.  The device was developed for insertion through the nose and down into the esophagus in acid reflux patients.  Since the system is already FDA approved for measuring pH in humans by insertion via the nasal cavity, it is ideally suited for our purposes.  This particular model seems to be more sensitive and accurate than one we tested from another leading supplier of this type of instrument.

    So far we have done a series of nasal mucosa pH measurements on two individuals.  One of the notable outcomes from our preliminary efforts in this area is that psychological stress can have profound effects on nasal mucosa pH, causing a major drop (acidification) in pH. We will be doing more work with nasal mucosal pH with additional subjects to determine the possible relevance of this measure with regard to upper respiratory viral infection.  We are also hoping to be able to do a collaborative study with established researchers who regularly conduct in vivo studies involving intentional infection with rhinovirus (the “common cold”) to explore the possible connection between life-style factors (such as diet) and the infectivity of pH-dependent viruses. 
 

CAYCE CONCEPTS 

MYSTERIOUS CANCER SERUM

    A couple of Edgar Cayce’s readings describe a hypothetical treatment technique that involves using part of the rabbit leg to create a serum for treating cancer. It is not clear that this particular technique was ever actually used. The generally accepted explanation of this concept is that it somehow involves utilizing the tendon of the rabbit.

    Tom Stonebraker, a veterinarian from Kentucky (Edgar Cayce’s home state), has provided a fascinating explanation of Cayce’s recommendation.  Dr. Stonebraker believes that an uncommon parasite is the key to understanding Cayce’s suggestion.  Here is an excerpt from a Cayce reading that discusses the development of a cancer serum based on this concept:

… a serum made from that as is called the “wolve” in the beef or the hare, at this season, and injections made … For this region of system this would be materially aided, or checked – or NICCOLITE, as this becomes.. 
(Q) How can this be made? 
(A) This should be drawn off – that is, the wolve, see? – PUNCTURED by an hypodermic, see? This drawn off and then a culture made into the flesh of the same animal from which it’s drawn, whether beef or hare. Then the culture applied to the HUMAN body, see? or blood drawn and a culture made FOR the human body and then applied to the body. There must necessarily be experimentations, with the proper heat, the proper precautions taken as to the character of cell as is destroyed in the culture made, and in the activity of the animal as well as human when being used; but for this character of the condition this would be MOST effective in at least fifty percent of such ills.  (2457-4, BREAST CANCER)

    Another reading (4444-2, SKIN CANCER) also describes this technique, mentioning a “parasite” that infects rabbits and the production of “niccolite” as a therapeutic agent.  Cayce stated that niccolite is “Oxygen, Nitrogen, and action on the force of putrified matter in the animal …”

    Here are Dr. Stonebraker’s insights:

    “I believe you can easily confirm “wolf or wolve” is a common name referring to an unusual parasite often found in the rabbit and bovine (beef) but also seen to a lesser degree in all warm blooded animals.  Specifically, wolf (wolve) refers to the larval (maggot) stage of the cuterebra fly.  The small cuterebra fly is unique in several ways.

    “1. It lays only one egg as opposed to large numbers.

    “2. It lays its egg on the skin of a live host animal as opposed to decaying matter.

    “3. The hatching larva has the ability to penetrate the unbroken skin.

    “4. Just under the skin the larva lives, grows, and matures while maintaining a small open air hole to the surface.

    “5. The larva stimulates a much stronger inflammatory reaction from the host compared to most parasites resulting in much local infiltration of tissues, subsequent swelling, and draining from the air hole on the surface.  All signs of the body’s defense mechanism go in high gear protecting by attacking not only the intruder, but the surrounding tissues which may be supporting the invader.

    “Despite this local war, the host leads an otherwise normal life until the larva is killed or expelled or leaves of it’s own volition (or is surgically removed) and the host seems no worse for wear, maybe even better from the challenge.

    “My take on this revolves around stimulating immune response to abnormal cells that try to take on a life of their own (cancer).  Edgar Cayce was once again way ahead of his time by proposing a vaccine-like approach to treating cancer utilizing an obscure parasite.”

    We thank Dr. Stonebraker for sharing his thoughts on this fascinating topic. Does anyone else have ideas about Cayce’s mysterious cancer serum? 

Source : https://www.meridianinstitute.com/newslet/Vol7-3/7-3.html

Infection and pH

This is the first in a series of essays, or articles, related to terrain (pH chiefly). Areas of chief interest in Bold.

Viral Infections are pH Sensitive

Published on September 1, 2014
Author: Dr Sirius

http://education.expasy.org/images/Filovirus_virion.jpg


Filamentous 790 nm long for Marburg virus and 970 nm long for Ebola virus. Diameter is about 80nm.

According to doctors at the Broad Institute of MIT and Harvard University Ebola is becoming harder to treat because rapid mutation could “render treatment and vaccines ineffective.” American scientists indicate that the initial patients diagnosed with the virus in Sierra Leone revealed more than 300 genetic modifications.

Traditional approaches to Ebola are being outclassed by the virus so we have to turn to more fundamental approaches that will stop the virus no matter what its gene sequence mutates to. Blasting Ebola with waves of alkalinity will work because many if not most viruses require a mildly acidic environment to infect the cell. They require mild acidity for maximum infectivity.

Viruses are extremely small parasitic life forms, the smallest living things on Earth. In essence, a virus is a minuscule pocket of protein that contains genetic material. Although viruses can remain dormant outside a living body, they only become active when in contact with live tissue. Once a virus infects a cell by penetrating the cell membrane, it can either lay dormant (lysogenic infection) or begin reproducing itself (lytic infection – the more common pattern). When a cell becomes full of virus, it bursts, releasing the virus to infect other host cells.

Certain viruses (including the rhinoviruses and coronaviruses that are most often responsible for the common cold and influenza viruses that produce flu) infect host cells by fusion with cellular membranes at low pH. Thus they are classified as “pH-dependent viruses.”

Fusion of viral and cellular membranes is pH dependent. “The plasma membrane of eukaryotic cells serves as a barrier against invading parasites and viruses. To infect a cell, viruses must be capable of transporting their genome and accessory proteins into the host cell, bypassing or modifying the barrier properties imposed by the plasma membrane. Entry into the host cells always involves a step of membrane fusion for enveloped animal viruses. Other enveloped viruses such as orthomyxoviruses, alphaviruses or rhabdoviruses enter the cells by the endocytic pathway, and fusion depends on the acidification of the endosomal compartment. Fusion at the endosome level is triggered by conformational changes in viral glycoproteins induced by the low pH of this cellular compartment.”[1]

In membrane biology, fusion is the process by which two initially distinct lipid bilayers merge their hydrophobic cores, resulting in one interconnected structure. The conformational transition occurs in a narrow pH range, corresponding to the optimal pH of fusion, in which the protein acquires the ability to interact with detergent micelles and lipid vesicles. This interaction leads to the insertion of the fusion peptide into the membrane, where a pore is formed. It has been suggested that the hepatitis C virus (HCV) infects host cells through a pH-dependent internalization mechanism. This HCVpp-mediated fusion was dependent on low pH, with a threshold of 6.3 and an optimum at about 5.5.[

When pH drops to 6 or below, rapid fusion between the membranes of viruses and the liposomes occurs. This results in the transfer of viral nucleocapsids into the liposomes. Ebola virions are taken into endothelial cells via macropinocytosis. After their formation, macropinosomes move further into the cytoplasm to acquire new markers or fuse with other vesicles of the standard endolysosomal pathway. This eventually moves the Ebola virions to more acidic compartments such as early and late endosomes that assist in the pH dependent fusion of viral and cellular membranes.[3] During this process, the cell detaches from its neighbors and loses contact with its basement membrane thanks to a mechanism of glycan mediated steric occlusion by GP.[4] The newly created particles then leave via lipid rafts, leaving a destabilized vascular system responsible for the massive blood loss characteristic of Ebola patients.[5]

Induction of Poliovirus Entry by Exposure of the Cells to Low pH

In the case of a number of enveloped viruses and diphtheria toxin, the acidic vesicles can be bypassed if cells with surface-bound virus or toxin are exposed to low pH. Under these conditions entry apparently occurs directly from the cell surface. Scientific investigation indicates that low pH is indeed required for the entry of poliovirus. The ability of cells to alter poliovirus in the presence of monensin was strongly increased at low pH. The main finding of one study is that a strain of poliovirus type 1 requires low pH for injection of its genome into the cytosol.[6]

Coronavirus infectivity is exquisitely sensitive to pH.  For example, the MHV-A59 strain of coronavirus is quite stable at pH 6.0 (acidic) but becomes rapidly and irreversibly inactivated by brief treatment at pH 8.0 (alkaline). Human coronavirus strain 229E is maximally infective at pH 6.0. Infection of cells by murine coronavirus A59 at pH 6.0 (acidic) rather than pH 7.0 (neutral) yields a tenfold increase in the infectivity of the virus.

Acidic extracellular pH activates secreted lysosomal enzymes that have an optimal pH in the acidic range.[7] Hypoxia and extracellular acidity are, while being independent from each other, deeply associated with the cellular microenvironment  and the spread of cancer. Intracellular pH is generally between ~6.8 and 7.4 in the cytosol and ~4.5 and 6.0 in the cell’s acidic organelles. Unlike intracellular free Ca2+ concentrations, which can rapidly change by perhaps 100-fold, pH inside a cell varies by only fractions of a pH unit, and such changes may occur quite slowly.

Inhibition of vesicular stomatitis virus (VSV) replication in LB cells by interferon (IFN) is pH sensitive. Using sensitive intracellular pH (pHi) indicators, researchers found that IFN treatment significantly raised the pHi. The increase in pHi correlated with an enhancement of the antiviral activity of IFN by primary amines. These results indicated that the IFN-induced increase in pHi may be responsible for the accumulation of G in the TGN, thereby producing G-deficient virus particles with reduced infectivity.[8]

http://www.influenzareport.com/ir/images/image26.jpg

It is the low pH inside the endosomes (pH 5–6), maintained by proton pumps within the endosomal membrane, that triggers the fusion reaction between the viral envelope and the endosomal membrane. This is a key step in the viral infection mechanism. At low pH, a major conformational change in the HA spike is induced.

Once bound, influenza enters the host cell by endocytosis. The internalization of influenza virus is not a simple process and can be highly cell-type dependent. Viruses have been shown to enter cells by both clathrin-dependent and clathrin-independent endocytosis, as well as by macropinocytosis. Acidic environments of the endosome triggers conformational changes in HA that expose the fusion peptide, allowing for viral-endosomal fusion.[9] Exposure to low endosomal pH is also necessary for release of the individual viral ribonucleoproteins (vRNPs) from the Viruses matrix (M1) protein.

http://www.mcvitamins.com/images/pH-Acid.jpg

As it is with viral infections it is with cancer. The external pH of solid tumors is acidic as a consequence of increased metabolism of glucose and poor perfusion. Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells before tail vein injection in vivo.[10]

Drugs that increase intracellular pH (alkalinity within the cell) have been shown to decrease infectivity of pH-dependent viruses. However pharmaceutical  drugs that do this can provoke negative side effects. Sodium bicarbonate is the best way to increase pH in clinical emergency conditions and has been known as far back as the Spanish Flu pandemic of 1918 to save lives.

The proven value of Arm & Hammer Pure Bicarbonate of Soda as a therapeutic (healing) agent is further evinced by the following voluntary testimony of Edward R. Hays, M.D. , in his latter no the Church & Dwight Company:

In 1918 and 1919 while fighting the ‘Flu’ with the U.S. Public Health Service it was brought to my attention that rarely anyone who had been thoroughly alkalinized with Bicarbonate of Soda contracted the disease, and those who did contract it, if alkalinized early, would invariably have mild attacks. I have since that time treated all cases of “Cold,” Influenza and LaGripe by first giving generous doses of Bicarbonate of Soda, and in many, many instances within 36 hours the symptoms would have entirely abated.

Further, within my own household, before Woman’s Clubs and Parent-Teachers’ Associations, I have advocated the use of Bicarbonate of Soda as a preventive for “Colds,” with the result that now many reports are coming in stating that those who took “Soda” were not affected, while nearly everyone around them had the “Flu.”

“Besides doing good in respiratory affections, Bicarbonate of Soda is of inestimable value in the treatment of Alimentary Intoxication, Pyelitis (inflammation of the pelvis), Hyper-Acidity of urine, uric acid disturbance, rheumatism and burns. An occasional three-day course of Bicarbonate of Soda elimination increases the resisting power of the body to all Infectious Diseases.

Dr. Volney S. Cheney reported[11] that, “A number of cases of colds of varying severity were carefully studied in the laboratory. Observation was made as to the degree of acidity of the urine; the CO2, combining power of the blood as an indicator of the alkaline reserve; tests were also made to determine the calcium content of the blood, the sugar content; non-protein nitrogen and the basal metabolism. The urine invariably carried a higher degree of acidity than the normal-in some cases as high as 800 (normal 350); the CO2 combining power of the blood in all cases was low, the highest being 52 per cent; the sugar content of the blood was generally decreased (below 100 mg. per 100 c.c.); the metabolic rate was always on the minus side. (These cases were carefully selected because of their lack of any symptoms of disturbed thyroid activity.) There is a change in the blood chemistry and, consequently, there must be a change in the tissues supplied by the blood. There is a decrease in the bicarbonates or reserve bases contained in the blood plasma and the tissues. These findings seem to point the way to the conclusion that a cold is a disturbance of the alkaline balance or reserve, in other words, a mild acidosis, or perhaps better stated, a lessening of the “buffer” action of the blood plasma through a decrease in its bicarbonate content.”

Sodium bicarbonate is the important medicine because it gives more carbon dioxide to the body and especially the blood in the form of bicarbonates. Bicarbonate in the blood is easily turned into carbon dioxide (CO2) and the reverse is true in biochemical reactions that happen almost at the speed of light. The bottom line to what happens when one takes sodium bicarbonate orally is that it turns to CO2 in the stomach driving bicarbonates into the blood, which helps more blood and oxygen delivery to the cells.

After doing his experiments, Dr. Cheney reported: “I have been able to induce all the symptoms of a cold, in varying degree from a simple coryza to that of la grippe and the “flu,” by the induction of an artificial acidosis through the administration of ammonium and calcium chlorides. The degree of severity of the symptoms was in direct ratio to the degree of acidosis induced. In the more severe degree of acidosis, all the classical symptoms of the “flu” were present, even including a low degree of fever. The symptoms rapidly subsided upon the administration of sodium bicarbonate in large doses by mouth and by rectum.

Sodium Bicarbonate is one of the most flexible medicinals in terms of methods and modes of administration. It can be injected in emergency room situations, taken orally, nebulized, used transdermally as a lotion or paste, put in enemas and in larger quantities in therapeutic baths. Just dissolve it in water or when treating cancer it can also be mixed with Blackstrap Molasses, maple syrup, or a good honey as well as with lemon or mix with citric acid for use in baths or when making your own bath bombs.

There is no question that plasma bicarbonate concentrations are shown to increase after oral ingestion. The most important effect of bicarbonate ingestion is the change in acid-base balance in biological fluids. In Europe, spa-goers drink bicarbonate-rich water to heal ulcers, colitis and other gastric disorders. Ingesting bicarbonate by way of bathing stimulates circulation, possibly benefiting those with high blood pressure and moderate atherosclerosis. It would be highly negligent to exclude it from Ebola treatments.

Increases of Carbon Dioxide and Bicarbonates Lead to Increased Oxygen

The most important factor in creating proper pH is increasing oxygen because no wastes or toxins can leave the body without first combining. with oxygen. The more alkaline you are, the more oxygen your fluids can hold and keep. Oxygen also buffers/oxidizes metabolic waste acids helping to keep you more alkaline. “The Secret of Life is both to feed and nourish the cells and let them flush their waste and toxins”, according to Dr. Alexis Carrell, Nobel Prize recipient in 1912. Dr. Otto Warburg, also a Nobel Prize recipient, in 1931 & 1944, said, “If our internal environment was changed from an acidic oxygen deprived environment to an alkaline environment full of oxygen, viruses, bacteria and fungus cannot live.”

The position of the oxygen disassociation curve (ODC) is influenced directly by pH, core body temperature and carbon dioxide pressure. According to Warburg, it is the increased amounts of carcinogens, toxicity and pollution that cause cells to be unable to uptake oxygen efficiently. This is connected with over-acidity, which itself is created principally under low oxygen conditions.

According to Annelie Pompe, a prominent mountaineer and world-champion free diver, alkaline tissues can hold up to 20 times more oxygen than acidic ones. When our body cells and tissues are acidic (below pH of 6.5-7.0), they lose their ability to exchange oxygen, and cancer cells love that.

Special Note: This is not the only way to skin the cat (virus). Directly supporting the immune system through a number of natural means and replenishing Vitamin C faster than Ebola strips it from the body creating lightening Scurvy and massive hemorrhage is another. Hitting the body hard with Glutathione and selenium is yet another potent and intelligent avenue of treatment that is not being pursued by the western medical establishment that prefers to complain that there is no treatment.

Original Article:

ChooseLife Notes : Dr Sirius supports the Sodium Bicarb path towards lower acidity (or higher pH). Moreless used to support this method also, but moved on to Calcium and Magnesium as focal points due to the potential dangers to the heart, so I am merely highlighting the data, rather than promoting any background theory, supplements, or diet. My brother in law is a consultant Anaesthetist, when he was formerly a Cardiac Dr I asked him what was the first move, by and large, in A&E “Sodium Bicarbonate drip to stabilise the pH”.

Advances in Nutritional Research on Regulatory T-Cells

Abstract

Many clinical and animal studies have shown that certain dietary components exert anti-inflammatory properties that aid in the amelioration of chronic inflammatory diseases. Among the various proposed channels through which dietary components affect immune responses, regulatory T-cells (Tregs) are emerging as key targets for the dietary prevention of chronic inflammatory diseases. In this review, immunoregulation by Tregs is briefly described, followed by a summary of recent advances and possible applications of techniques for the study of Tregs. In addition, this review provides an overview of the current knowledge on Treg regulation by certain dietary components, including vitamins, omega-3 polyunsaturated fatty acids, and polyphenols. The caveats of previous studies are also discussed in order to highlight the distinctions between dietary studies and immunological approaches. Consequently, this review may help to clarify the means by which nutritional components influence Tregs.

Keywords: nutrition, immunology, regulatory T-cells, Tregs, anti-inflammatory

4. Dietary Regulation of Tregs

4.1. Vitamins

Following dietary consumption and absorption in the intestines, water-insoluble vitamin A (all-trans-retinol) is carried by cellular retinol binding protein (CRBP) in an aqueous environment to be transported into the cytoplasm. Subsequently, retinol is oxidized to retinal by retinol dehydrogenase, and then retinal is further oxidized to retinoic acid by retinal dehydrogenase [25]. With respect to the role of vitamin A in the development of Tregs, Bai et al. [26] demonstrated that the population of Tregs derived from biopsies of ulcerative colitis patients increases following ex vivo culture in the presence of retinoic acid, a potent metabolite of vitamin A. In the same study, using a chemical (2,4,6-trinitrobenzene sulfonic acid, TNBS)-induced murine colitis model, it was further elucidated that dietary vitamin A ameliorated colitis, which is accompanied by an increased population of Tregs. Wu et al. [27] further reported that intraperitoneal administration of all-trans retinoic acid aided in the attenuation of airway inflammation by inducing Treg development in a model of experimental allergic asthma. Moreover, a dietary study demonstrated that retinal intervention in mice upregulated Tregs, which further assisted in the treatment of autoimmune inflammatory disorders, including rheumatoid arthritis [28]. Overall, these animal studies indicate that vitamin A and its metabolites affect populations of Tregs, thereby suppressing chronic inflammatory diseases. However, it remains unclear whether vitamin A affects Tregs directly, indirectly, or both. Indeed, Chang et al. demonstrated that dendritic cells also promote the generation of Tregs in response to retinoic acid, at least in vitro [29], exemplifying that in vivo models are more complicated for elucidating the mechanism of action of dietary components.

With respect to water-soluble vitamins, Kunisawa et al. [30] showed that Tregs express high levels of vitamin B9 (folic acid) receptor on their cell surfaces. Furthermore, vitamin B9 was demonstrated to be a survival factor for Tregs; in a vitamin B9-deficient culture, naïve CD4+ T-cells successfully differentiated into Foxp3+ Tregs but failed to survive. Moreover, it was found that mice fed a vitamin B9-deficient diet exhibited a decreased number of Tregs in the small intestine, where vitamin B9 is absorbed.

4.2. Dietary Fatty Acids

A significant quantity of data has indicated that dietary omega-3 polyunsaturated fatty acids (PUFA) may prevent or ameliorate chronic inflammatory diseases, including inflammatory bowel diseases [31,32,33,34]. These studies have identified multiple anti-inflammatory mechanisms of omega-3 PUFA: cytokine production, antagonism to omega-6 PUFA metabolism, binding to nuclear receptors as ligands, the alteration of signaling protein acylation, and the modulation of signaling platform lipid rafts in various immune cell models. With respect to CD4+ T-cell mediated inflammatory responses, several studies using dietary intervention with either purified omega-3 PUFA or fish oil (which is rich in omega-3 PUFA) demonstrated that CD4+ T-cell functions, as assessed by cytokine production and proliferation, were suppressed in both humans [35,36,37] and experimental animals [38,39].

As for the effect of omega-3 PUFA on Tregs, it was shown that the omega-3 PUFA abundant in fermented fish oil enhanced the development of Foxp3+ Tregs in vivo [40]. Moreover, intraperitoneal injection of eicosapentaenoic acid (EPA), an omega-3 PUFA, resulted in prolongation of graft survival in a murine transplant model, accompanied by an increased population of Tregs [41]. However, those studies do not conclusively demonstrate a direct function of omega-3 PUFA on the differentiation and/or function of Tregs, given the caveat that in vivo administration of omega-3 PUFA can affect diverse types of accessory cells. Indeed, it was found that dendritic cells cultured in docosahexaenoic acid (DHA, an omega-3 PUFA)-rich conditions facilitated the development of Tregs, at least in vitro [42], indicating an indirect modulation of Treg development by omega-3 PUFA. However, despite the increase in the development of Tregs, the favorable effect of omega-3 PUFA on Tregs is still controversial because it has also been observed that DHA inhibited the suppressive effect of Tregs on effector T-cell proliferations in a dose-dependent manner in vitro [43].

4.3. Dietary Polyphenols

Dietary polyphenols are well known for their antioxidant properties, which can further suppress inflammatory responses by reducing nitric oxide. In addition to their archetypal antioxidant capacities, immunoregulatory effects of select polyphenols on Tregs have been characterized as follows. Wang et al. [44] reported that ex vivo development of CD4+ Foxp3+ Tregs was induced in the presence of the flavonoid naringenin in part via activation of the aryl hydrocarbon receptor, a transcription factor. As well, increased Treg differentiation suppressed the proliferation of effector T-cells. In addition, dietary naringenin was found to suppress cholesterol-induced systemic inflammation, metabolic dysregulation, atherosclerosis, and allergen-induced airway inflammation [45,46], although it was not clear whether those inhibitory effects were Treg-dependent. In a mouse model of T-cell mediated inflammatory disease of the central nervous system, dietary intake of epigallocatechin gallate (EGCG), a catechin derivative, exerted a favorable effect, in part by increasing the Treg population in the spinal cord [47]. Furthermore, fermented grape marc (FGM) was found to promote Treg differentiation of human CD4+ T-cells [48].Go to:

5. Conclusions

Due to the relatively short history of studies on Tregs, investigations of the direct effects of a variety of dietary components on Treg conversion are limited at present (summarized in Table 1 and previously reviewed elsewhere [49]). It seems that a majority of the anti-inflammatory functional studies have been conducted in vivo by observing physiological outcomes, such as symptoms of chronic inflammation and accumulation of certain immune cell types. Even though in vivo studies are indispensable for nutritional studies, simpler model systems must be developed to dissect the detailed mechanisms by which dietary components regulate physiological systems. Therefore, further studies using more sophisticated and appropriate in vivo model systems are needed to draw solid conclusions. In this regard, as introduced in this review, the protocol for Treg differentiation from naïve CD4+ T cells could be effectively utilized to determine the direct effects of a variety of promising dietary Treg modulators present in foods.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847731/

Published: October 28th 2013

Total Harmony Of Mankind – Donald-Gene Kraus

“He furthered his education under Biochemist/Physicist Dr. Carey Reams; Herbalist Dr. John R. Christopher; and Iridologist Dr. Bernard Jenson from 1974-1978.”

The Concept Of Sticky Foods

Question: You talked about yeasty foods, the breads, the cheeses and the milk forming mucous; I do not quite understand that concept. It does not form mucous in itself… does not the peristaltic action get it out of the system?

No, we are talking about a mucous that is formed from foods that feed yeast when food stays too long in the body. When foods or liquids are sticky (starches, grains and meats), they do not have enough lubrication, so they do not get through the system quick enough; and if you do not have enough oxygen in your reserve bank account, these unfriendly critters come in, eat it, and form the bad mucous bacteria.

Question: Yeast is just a sticky substance, eventually your body gets rid of it does not it; or you eliminate it?

No, not if you do not have enough oxygen or lubrication (mucus membranes that produce lubricant). Will become a hard mass attaching itself to the intestinal tract.

Excerpts from : Total Harmony.pdf

More from this Author : Not Eating The Right Fats

Extracellular Brain pH and Outcome following Severe Traumatic Brain Injury.

Gupta AK, et al.

Abstract

The ability to measure brain tissue chemistry has led to valuable information regarding pathophysiological changes in patients with traumatic brain injury (TBI). Over the last few years, the focus has been on monitoring changes in brain tissue oxygen to determine thresholds of ischemia that affect outcome. However, the variability of this measurement suggests that it may not be a robust method. We have therefore investigated the relationship of brain tissue pH (pH(b)) and outcome in patients with TBI. We retrospectively analyzed prospectively collected data of 38 patients admitted to the Neurosciences Critical Care Unit with TBI between 1998 and 2003, and who had a multiparameter tissue gas sensor inserted into the brain. All patients were managed using an evidence-based protocol targeting CPP > 70 mm Hg. Physiological variables were averaged over 4 min and analyzed using a generalized least squares random effects model to determine the temporal profile of pH(b) and its association with outcome. Median (IQR) minimum pH(b) was 7.00 (6.89, 7.08), median (IQR) maximum pH(b) was 7.25 (7.18, 7.33), and median (IQR) patient averaged pH(b) was 7.13 (7.07, 7.17). pH(b) was significantly lower in those who did not survive their hospital stay compared to those that survived. In addition, those with unfavorable neurological outcome had lower pH(b) values than those with favorable neurological outcome. pH(b) differentiated between survivors and non-survivors. Measurement of pH(b) may be a useful indicator of outcome in patients with TBI.

PMID 15253796 [Indexed for MEDLINE]

Source = https://www.ncbi.nlm.nih.gov/m/pubmed/15253796/