Heart Attack

IH - I a few months back my grandfather(70 years old) had a heart attack and was rushed off to hospital. When he was there they told him you 'HAVE' to have a stent or you will DIE! He still refused for quite some time, but nontheless the doctors persisted and used all the fear tactics possible to finally convince him to go ahead with getting the stent.

Anyway after all of that he was put on these drugs;
Plavix (Clopidogerel)
Lipitor (atorvastatin)
Nexium (esomeprazole)
Betaloc (metoprolol)
Avopro (irbesartan)
Aspirin

Now on top of this he's been told the usual no salt(even celtic) and no vitamin K(insanity I know). His diet is well above average and doesn't smoke, except unfortunately every night he gets wasted on wine. Also he needs to get more exercise which he is gradually doing more of.

IH would you be able to tell me specifically how those drugs are detrimental to his health and why he shouldn't be taking them? Mainly so i can convince him to get off of them. In order of most important would you be able to give me a list of everything he should be taking for his heart and health?

PS I don't know how you find the time or motivation to answer everyone's questions, but god bless you IH!

Silverlin - Absolutely everything his doctor has recommended is 100% wrong.

Staring wit the stent, this increases coronary incident risk by over 400%.

My guess with the Plavix is that he is on a medicated stent, which is worse than the old ones.

The threat about dieing is pretty sick, but it's pretty standard. If they actually read the studies they'd find
what they are doing is much more harm than good.

What they don't tell patients is that when an artery is occluded the body automatically via angiogenesis
builds collateral vessels.

The "plumbing theory of heart disease," while it does sound deceptively simple is not the REAL cause of a heart attack.
Unfortunately not one in a thousand cardiologist knows this. The evidence to the contrary comes out of Germany from the 1960's.

The underlying cause of a heart attack (myocardial infarction) is a destructive process from the accumulation of acid in the left ventricular tissue--completely unrelated to blockages in the coronary arteries.

This was latter confirmed here:

Am J Cardiol. 1988 Apr 1;61(10):677-84.
Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model.
Rentrop KP, Thornton JC, Feit F, Van Buskirk M.

St. Vincent's, Mount Sinai Medical Center, New York, New York.

Two indexes of collateral blood flow, the ratio of distal coronary occlusion pressure/aortic pressure (DCOP/Pao) and angiographic collateral class were determined during elective angioplasty in 36 patients with normal left ventricular function. The association between collateral indexes and 8 anatomic and clinical variables was assessed. A reduction in luminal diameter by greater than or equal to 70% predicted angiographically demonstrable collaterals with 100% specificity and 85% sensitivity. Lesion severity (stenosis) correlated with both collateral class and DCOP/Pao: DCOP/Pao = 2.8809 - 0.0729 X stenosis + 0.00049 X stenosis. The data suggest a quantitative relation between lesion severity and collateral development beyond a threshold value of 70% stenosis. Left ventricular ejection fraction during ischemia caused by balloon occlusion (EFo) was found to be primarily determined by lesion location; however, collateral flow modified EFo significantly. For mid-left anterior descending and right coronary artery: EFo = 59 + 26 X (DCOP/Pao); for proximal left anterior descending artery: EFo = 24 + 89 X (DCOP/Pao). A model predicting the hemodynamic and clinical consequences of abrupt coronary closure based on lesion location and severity was developed. In the second study phase, this model was tested retrospectively in a different group of 23 patients who experienced coronary occlusion as a complication of angioplasty. The data of both study phases suggest that left ventricular function and clinical outcome after abrupt coronary closure are determined by an interaction between location of the coronary artery obstruction and the amount of collateral flow. Lesion severity and the extent of functional impairment resulting from abrupt coronary closure are inversely related.

In other reports it was stated that there is clear refutation of the most common explanation used to date to dismiss autopsy findings which detect NO coronary thrombi, ie. that thrombi existed at infarction but have since lysed embolized or washed away.

It was found in the American Journal of Cardiology, the summarization goes like this:

"They found that in an advanced state of the narrowing of the coronary ateries the supply of blood to the heart muscles is fuly assured via collaterals that enlarge naturally in response to the blockage. Interestingly they observed that the more the conoraries narrow, the less danger there is of heart infarction.

If you're interested I can explain this in much further depth, because usually this sounds so over the top, it's hard to buy--until additional details are given.

Central to the condition of tissue acidosis, the Nexium is a killer. Probably the leading cause of Pneumonia.

Assuming he has a medicated stent, he would have to remain on the Plavix for at least a year. Sadly, this drug is less effective than aspirin. But getting off of Plavix after a medicated stend presents its own problems.

He should drop the statin immediately, the Nexium also. If he has problems with indigestion, it's more than likely he needs more stomach acid not less. Two Betaine HCL tablets following a meal is a good place to start.

Betaloc is a beta blocker and this should be dropped, but if he's been on it for more than a week, then he'll need a doctor to help get him off of it. If it's been less than a week, try to get him to drop it. This drug will pervert the heart valves and reduce the force of the hearts contractions. It's a killer and usually a common cause of arrhythmia.

Avopro is more benign, but it isn't needed of course. Getting his Potassium, Magnesium balance would be much better.
Magnesium Orotate is outstanding for this, plus it relaxes vessels.

Get him back on the salt (preferably Himalayan or Celtic). The only people with trouble with salt have a low production of renin, but that happens from sodium chloride. Studies show that salt restriction increases death, not the other way around. If the heart or kidneys are damaged due to hyponatremia (low blood sodium levels), there's real risk of heat stroke, regular stroke and heart attack.

Asprin is another problem. Unfortunately many doctors do not screen for Aspirin resistance.

I got the following from (I forget), but it summarizes it here:

It is very important to identify patients having aspirin resistance as studies have shown that patients taking aspirin who had a high level of thromboxane in their urine had a 3.5 times higher risk of cardiovascular death than patients who had the lowest level. By detecting high levels of 11-dehydro thromboxane B2 in urine, patients can be segregated as responders and nonresponders. In the nonresponders an alternative antiplatelet therapy can be initiated, which can more effectively block thromboxane production. This technology can assess the patient's relative risk for heart attack by measuring the patient's aspirin resistance.

Regardless, Omega-3 fatty acid, preferably from Krill oil are vastly superior to aspirin. Also cardiovascular mortality is greatly lessened by sufficient intake of Omega-3 fatty acids.

Aside from that Vitamin D is extremely important on cardiac mortality. If he's indoors a lot, put him on 10,000 IU per day. If he's spends occasional time outside, then 5,000 IU per day.

The best form of exercise for heart is a rebounder. This is like a trampoline, but it has a stabilizer bar attached to it.
Just the process of the gravity and the "anti-gravity" effects during the rebound account for a significant increase in collateral vessel development.

Get him on the Vitamin K2. This stops blood sugar fluctuation and many men around the age of 70 develop problems with blood sugar. This is a primary heart risk factor.

Next: Ubiquinol (the active form of Co-Q10) He'll need 100 mg, but the more the better, especially after statin (lipitor use), because it stops co-Q10 production in the liver), it's exactly what his heart needs for fuel. Without Co-Q10 the heart is dead.

He will also need what is considered to be the "Anti-paralysis" vitamin, which is Adenine or B4. It doesn't exist in 99% of vitamin formulations. It's hard to acquire from food because it must be in raw form. Worse, most B-complex create a deficiency in adenine. The best sources are Brewer's yeast, Wheat Germ or possibly Spirulina. One of these three is highly recommended. If he prefers a supplement, Standard Process offers Cataplex B.

For improvement in blood flow. Sustained-release L-arginine, use 6 grams per day.

1,000 mg of Carnitine, a 1,000 mg of Taurine.

Polyphenols, such as Cocoa Flavanoids and Pomegranate. Both of these increase Nitric oxide and protect against free radicals. Mixed Tocopherols and Tocotrienols with Lipoic acid to accentuate the effects.

50 milligrams of DHEA in the a.m.

Consider testosterone therapy (absolutely amazing for heart disease).

If he needs convincing, it's not easy. But if he refuses. I'll talk to him if you want, I have a lot of practice
unfortunately.

Tell you one thing, when they get done (the skeptical ones) they are totally overwhelmed. Heart disease is
pretty easy compared to hair loss--no joke!

Forgot a few things.

D-Ribose 5 grams twice per day. This is the closest thing to regenerating heart tissue).
Ecklonia Cava -- It beats Nattokinase on fibrin reduction. 2 to 3 times per day.
Dosage on Krill Oil six 500 milligram caps per day.
Dosage or Magnesium Orotate 4 to 6 per day.

IH - WOW! Seriously ignorance is way underestimated!! Thank you soooo much for this info! You literally are a life saver!!!

Just so i can start him off and make things more practical for him immediately what would be the top ten things for him to take in order(with dosage)?

Thanks soo much IH, hopefully im able to convince him with this info so he is confident in standing up to the doctors when he has to go back for a check up. Also thanks for the generous offer to personal talk to him if I don't succeed in convincing him. They have literally told him on his last check up that if he goes off the drugs he will surely DIE!

CausticSymmetry wrote:Heart disease is pretty easy compared to hair loss--no joke!

Now from knowing all this info i wish i had heart disease rather then hairloss! Lol

Silverlin - I forgot just one other thing. If he has any angina, there is marvelous herb called Terminalia arjuna.
It's superior to nitroglycerin and it continues to work with continued use, whereas Nitro does not.

Also here's a study on medicated stents.

http://atvb.ahajournals.org/cgi/content/full/27/2/261

Top ten things to take:

Ubiquinol (Active form of Co-Q10) 100 to 300 mgs (towards the higher amount if his ejection fraction is below 40).
D-Ribose 5 grams twice per day. (rejuvenates heart tissue)
Krill Oil (six, 500 milligrams capsules per day). This replaces a whole lot of drugs
Magnesium Orotate 4 to 6, 500 milligram tablets per day.
Ecklonia Cava (Fibroboost) 2 to 3 of these per day. Beats any drug and doesn't kill anyone.
Vitamin D (5,000 IU to 10,000 IU) per day.
Source of Adenine (could be either Wheat germ, Brewer's yeast or Spirulina)
Terminalia arjuna 500 milligrams three times daily.
6,000 milligrams of sustained release Arginine (also known as AAKG).
1,000 milligrams Carnitine

If arrhythmia exists get him on Iodine.
Also check thyroid function. Low thyroid accounts for 70% of heart disease patients.
Betaine HCL is also critically important, since he was told to take Nexium (a Proton pump inhibitor poison).

Because I've been down this road so many times before. Standing up to doctors is not usually a good idea. They don't want to be told they are wrong, especially by a patient. Plenty of them get information from well meaning patients and they rarely if at all read it. After all, they were taught by "the best" and if they don't know it, "it can't be true."

Also, the pressure to get the routine screenings and operations is pretty intense. They stand to lose revenue and that isn't going to go down too well. They use common scare tactics, "ticking time bomb," and you will die if you don't do this.
There's nothing like fear (False Expectation Appearing to be Real).

These doctors are well meaning and usually and honesty believe what they recommend is right, but they will probably not take it well if the patient is questioning treatments. The #1 question integrative physicians get from their heart patients is, "What do I tell my primary care doctor or cardiologist?"

If his doctor is open minded and willing to work with him, that's great (not likely). Assuming he won't, he may want to find an integrative physician.

http://www.acamnet.org/site/c.ltJWJ4MPIwE/b.2242497/k.2C78/Integrative_Medicine_Physicians/apps/kb/cs/contactsearch.asp

IH - Thanks yet again for the wealth of information and immense help you've given.

Well its looks like he will be on plavix and the beta blocker for a fair while longer and hopefully I can get him to drop the rest of the other drugs in the mean time.

Do you know of any negative interaction from the supps you've suggested that could interfer with the plavix or beta blocker? Just wondering because the doctors were telling him to avoid things like vitamin K and some other things because of the supposed negative reaction it would have with one or more of the drugs.

Also the reason he was put on Nexium was because after his surgery while he was still in hospital he was constantly throwing up for two hours straight. The doctors said he had some blood in his throw-up and so put him on Nexium. My grandfather said he's found blood in his stools on 4 occasions months ago, but it hasn't reoccurred.

I just can't thank you enough for your help IH, Thanks

Silverlin - There are no interactions between Vitamin K2 and the Beta Blocker or Plavix. Perhaps the doctor is citing caution since the blood thinner Coumadin is generally contraindicated with K1 or K2 use. However, newer studies reveal the opposite to be the case even in Coumadin use.

K2 keeps the calcium out of the arteries and improves bone remodeling.

Try to get him off of Nexium as soon as you can (no more symptoms). Not only does this double risk of pneumonia,
blocking stomach acid severely weakens the immune system and impairs mineral and protein absorption.

Hopefully he can get off the beta blocker if his symptoms improve and his doctor is willing. Integrative cardiologists
will seek to rid patients off of a beta blocker as soon as it is appropriate.

IH - Thanks for making everything clear. Not sure how long it will take, but once he is on this regimen and off the drugs ill report back to let you know how things end up.

As always, thanks to infinity IH

IH, you mentioned "...He should drop the statin immediately, the Nexium also. If he has problems with indigestion, it's more than likely he needs more stomach acid not less. Two Betaine HCL tablets following a meal is a good place to start..."

I thought the proton pumps are used for inhibiting stomach acid - can you clarify why more acid is needed via Betaine HCL?

My mom had stomach ulcer and she was put on a 4-6 week proton pump protocol, my understanding was that she was having too much acidity and needed to reduce some acid there - hence the proton pump inhibitor. I am a little confused here.

Take HCL tablet just BEFORE meals not after, otherwise you risk dumping acid into an already acidified stomach (increasing risk for too much acid).

Lund - The marketing of anti-acids and Protonics is a brilliant marketing scheme, because its convinced virtually everyone, including most doctors that stomach acid is the problem.

The excess acids that contribute to reflux occurs only when our own hydrochloric acid, the only inorganic substance the body makes is low. When it is lacking, the food becomes a pile of poorly digested acid waste residues called acids of fermentation.

Probably the best book written about this is, "Why Stomach Acid is Good for You." By Jonathan V. Wright.
http://www.amazon.com/Why-Stomach-Acid-Good-You/dp/0871319314/ref=pd_bbs_2?ie=UTF8&s=books&qid=1236034548&sr=8-2

The anti-acids only "cover up" the problem by suppressing all acids, both good and bad.
The only true resolution to this is to add more stomach acid (not reduce it). This is accomplished by taking Betaine Hydrochloride tablets (with Pepsin). By increasing the inorganic HCL, will decrease the fermenting organic acids.

Further, it will assimilate the minerals better, promote much better digestion and allow much better elimination.

Yet with too much residue of fermenting acids, the food stagnates in the system and is left for the bacteria to devour the mess. Refined carbohydrates are the major culprits, as they promote this acid condition.

Discomfort from stomach/acid indigestion is a result from fermenting waste acids. Also the esophageal sphincter
does not stay shut during times of low stomach acid. Ordinarily when food is ingested it is designed to shut immediately, but often stays open during low HCL production. There's a supplement that works pretty well for this problem called "Heart Burn Free" from Enzymatic Therapy. It increases the surface tension and "trains" the valve to stay shut. It takes 20 days with one pill taken every other day.

Another thing about hydrochloric acid, it's our major defense against pathogens, as we age our real stomach acids production begins to dwindle, with that goes our immunity with respect to bacteria. Hydrochloric acid cleans up acid waste products, so supplementation is a good idea, especially if indigestion is present.

B12 and the eight essential amino acids are dependent upon adequate stomach acid. Two good books on this are "Three Years of HCL Therapy" & "Why stomach acid is good for you."
not digest minerals, proteins. It is this type of acid that will help alkalize the system.

The system become acidic when processed foods are eaten, as this produces fermenting waste acids, which deplete production of real stomach acid (hydrochloric acid). There sometimes is a Helicobacter Pylori connection, as this literally soaks up good stomach acids.

Without enough hydrochloric acid, the immune system is compromised, this is why pneumonia runs so rampant (double the risk). Low stomach acid equals infection, low phagocytosis more bacteria, etc.

So, IH, are you saying that too much acidity in the stomach is the wrong diagnosis and that the issue is invariably always less acid?

Less stomach acid --> causes acids of fermentation (poorly digested food) --> causes GERD / gastritis / Acid reflux

So the protocol should be to increase stomach acid and not reduce it.

I do not have a lot of trust in traditional medicine either, but for them to get it 180 degree wrong gets a little interesting. Both proton pump and h2 blockers (pepcid ac, zantac ,etc) tend to inhibit acid in stomach (of course via different pathways). If the issue is less acidity to begin with, this would amount to a totally flawed protocol.

You may be right, I have come across this suggestion before at earthclinic but discarded it - time to read again.

Thanks for your clarification.

But you tell me one thing then, OK so my mom and dad have indigestion (perhaps low acid as you are suggesting), they take proton pump inhibitor or H2 blockers (Zantac), they eat food, they feel alright - no indigestion, no fould burps, no gas - life is good.

If their problem was less acid to begin with, taking these meds should cause them to have more problems - as these meds would even reduce the little acid they have to being with?

lund - It is quite a phenomenon to see commercials advertising products that stop the secretion of stomach acid for up to 12 hours. It seems almost a "regular" thing to expect medicine to have it 180 degrees wrong. Many take anti-acids for years with no apparent problem. Others just for a short time. The trouble is the accumulated effects over time. The problem is the while the symptom is covered, the real problem however large or small is not addressed.

One theory that doesn't get much attention as it did in the early 1900's is the amino acid Glycine. Glycine deficiency is believed to be a main cause of stomach acid deficiency. Whey protein which is abundant in Glycine is useful in preventing gastric ulcers.

Here is an article written by Jonathan Wright who also authored the link below it, "Why stomach acid is good for you."

http://www.vrp.com/articles.aspx?ProdID=art784&zTYPE=2

On this link, check out all the reviews of this book:

http://www.amazon.com/Why-Stomach-Acid-Good-You/dp/0871319314/ref=pd_bbs_2?ie=UTF8&s=books&qid=1236034548&sr=8-2

IH - Do you know if there is a direct or indirect relationship in getting wasted on wine everynight and heart disease? if so would you be able to explain it to me? I want to try and educate my grandfather on what damage he is doing to himself everytime he gets wasted in the hope that he'll either cut down or give it up.

If the universe is indeed linked in an interconnected collective consciousness then your in luck IH because Im sending you the best of wishes. Thanks yet again for the constant and consistent help you always provide

Siverlin - Thanks for the well wishes.

There's an interesting book where I think the author might have nailed the solution as far as alcohol goes. It doesn't involve any willpower abstinence, check it out:

http://www.amazon.com/Cure-Alcoholism-Willpower-Abstinence-Discomfort/dp/1933771550/ref=pd_sim_b_6

Alcohol when in excess (a little is actually protective against strokes and some cardiovascular diseases), causes severe free-radical damage. Both liver and intestinal environments are changed for the worse.

It's a lot like the destruction of refined sugars but more concentrated.

There is a doctor Bert Berkson who has done some very interesting research on Lipoic acid over the years. I used his protocol for patients with severe liver problems, such as biliary cirrhosis, liver poisoning and hepatitis C. This involves a "Triple therapy" involving Lipoic Acid, Milk Thistle, Selenium and Vitamin C.

I think Curcumin based on the research is highly protective of the liver also.

I was reading more on the digestion and came across this very informative post from someone's (not mine) personal research into this matter:

========================

This material is from my personal research into the significance of pH level. My particular area of interest is in the minerals required for absorption of nutrients, so names of minerals have been highlighted (bold) here, even though they were not highlighted in the source material. Where conflicting information on pH level was found; material from each source is provided.

~Mistral (formerly #72081)

4/19/07: WARNING: This material frequently mentions sulfation. Please be aware that G6PD deficiency is a common enzyme deficiency that causes severe anemia and other issues when taking medicines/supplements/foods containing significant amounts of sulphur.



MOUTH/PHARYNX/ESOPHAGUS

The digestive process begins as food enters the mouth. In the first stage of digestion, the salivary glands secrete ptyalin (an alpha-amalyse digestive enzyme) which works to break down long-chain carbohydrates into successively smaller starches and ultimately maltose.(1) Salivary amylase (ptyalin) is a calcium-dependent metalloenzyme. A chloride ion is also involved. Salivary amalyse is most effective in the presence of chlorine and/or bromine.(1) It is slightly less effective in the presence of iodine, and least effective in the presence of sulfate and phosphate.(1) Saliva is only slightly acidic with a pH of 6.35-6.85(9), and the optimal pH for this enzyme is 6.7.( The throat and the esophagus secrete mucus to help in swallowing.(9)

The digestive process continues as food passes through the throat to the esophagus. The normal pH level of the esophagus is 6 to 7.(2, 3) "In the mouth, pharynx, and esophagus, pH is typically about 6.8, a very weak acid."( An esophageal pH level 4.0 or below is considered a gastro-esophageal reflux event.(3)

STOMACH

As the chewed food moves down the esophagus to the stomach, the stomach begins to secrete the digestive hormone gastrin in anticipation of a meal. The stomach normally has a pH between 5.0 and 6.0 before food arrives.(11) The process of activating gastrin requires sulfation.(6) Salivary amylase continues the digestion process until it is inactivated when stomach acid causes pH to drop below 5.0.(11,1) There are three types of cells in the stomach lining. Mucous neck cells produce mucus to protect the stomach lining. Chief cells secrete gastric lipase and pepsinogen. Pepsinogen is converted to pepsin in strong acidity (4). Parietal cells produce intrisic factor and Hydrochloric Acid (HCl). (9) The stomach lining consists of sulfated mucin proteins which influence the absorbability of nutrients, the adhesion/lubrication of proteins and peptides, and influence their form and election charge. The negative charge on the sulfated mucin lining of the stomach cause the food peptides to elongate as the sulfate groups within them, also negatively charged, repel from the negative charge of the mucin lining. Digestive conditions such as H. Pylori infection, irritable bowel syndrome, gut permeability, and autism have been tied to sulfation dysfunction in the mucin lining of the digestive system. Lack of sulfation (leading to lack of a negative charge) may also be linked to Candida (normally repeled by negative charge), and alterations in the gut flora.(6)


The distention of the stomach and pressure on the vagus nerve cause the release of gastrin.(4) Gastrin stimulates the parietal cells of the stomach to secrete hydrogen ions (H+) and chloride (Cl-) resulting in Hydrochloric Acid (HCl).(9) Calcium has been shown to increase gastric acid secretion from the parietal cells.(22) Stomach acid secretion continues until the pH level of the stomach contents is at least 3.0. This takes about 45 minutes in young healthy adults, however the amount of time required increases with age.(11) "The pH of the stomach in a normal, healthy human is in the 1-3 range."(16) Gastrin also stimulates the chief cells to secrete pepsinogen (, an enzyme that initiates the digestion and breakdown of proteins."(16) High stomach acidity is required to activate pepsinogen.(16) The strong acidity of the stomach also causes the proteins in the chyme (food in the stomach) to partially unfold. The high acidity also kills many microbes, and stimulates the secretion of hormones that begin the flow of bile and pancreatic juices.(9)


"Chemoreceptors in the stomach monitor the pH of the stomach chyme."(9) When the pH level of the stomach contents reaches 3, secretion of gastrin is inhibited.(4) The pH within the stomach rarely, if ever, drops below 3.0. Pure stomach acid has a pH of 1.8 when it first enters the stomach, but is quickly diluted in the presence of food.(11) Typically, hydrochloric acid lowers the pH level of the stomach contents to a level between 2 to 3.(7) As gastric pH lowers, "blood pH correspondingly increases, particularly in those segments of the circulatory system associated with supplying the gastrointestinal tract. This increase in blood pH is known as the 'alkaline tide', and is caused by bicarbonate ions that are secreted into extracellular fluid of the stomach, then into venous blood."(16)


A magnesium-dependent H+/K+ ATPase or "proton pump" is involved in the secretion of stomach acid.
[The following material has been shortened and paraphrased slightly.]
"The current model for explaining acid secretion is as follows:
o Hydrogen ions are generated within the parietal cell from dissociation of water. The hydroxyl ions formed in this process rapidly combine with carbon dioxide to form bicarbonate ions, a reaction cataylzed by the zinc-dependent enzyme carbonic anhydrase.
o Bicarbonate is transported out of the basolateral membrane in exchange for chloride.
o Chloride and potassium ions are necessary for secretion of acid and are transported through conductance channels.
o A Hydrogen ion is pumped out of the cell, into the lumen, in exchange for potassium through the action of the proton pump; potassium is thus effectively recycled.
o Accumulation of osmotically-active hydrogen ions results in outward diffusion of water. The resulting gastric juice is 155 mM HCl and 15 mM KCl with a small amount of NaCl."
(22)
The stomach acid itself does not digest protein. Rather, it activates the pepsinogen enzyme which then becomes pepsin.(10) Pepsin is only active within the pH range of 3.0 to 5.0.(11) Pepsin is one of several digestive enzymes involved in the breakdown of proteins. Its function is to break down proteins into peptides.(5, 7) Pepsin contains calcium, zinc, and iron.(10)

The chyme then leaves the stomach and enters the small intestine.


SMALL INTESTINES

DUODENUM

The chyme moves through the sphincter at the base of the stomach into the duodenum (the first part of the small intestine) in slow rhythmic contractions. Within two to four hours after eating a meal, the stomach has emptied its contents into the duodenum.(9) "The pH of the duodenum is 6 to 6.5. The majority of nutrients, vitamins, and drugs are absorbed in this 6 inch area of the gastrointestinal tract. In addition to water, mucus, and electrolytes, secretions from the liver and pancreas join secretions from the intestinal mucosa to facilitate digestion and absorption. The lining of the small intestines is composed of many villi, or finger like projections, which extend even more as projections called the brush border."(16) "Upon emptying into the small intestines, potential hydrogen (pH) changes dramatically from a strong acid to an alkaline content. The pancreas secretes bicarbonate to neutralize the acid from the stomach, and the mucus secreted in the tissue lining the intestines is alkaline which promotes digestive enzyme activity."( "The duodenal glands (Brunner's glands) are found only in the duodenum. They are tortuous and branching; their mucus-containing secretion has a pH of 5.8-7.6."(17) "The pH can reach 7 to 8 in this area."(16) "The mucosal tissue of the small intestines is alkaline, creating a pH of about 8.5, thus enabling absorption in a mild alkaline environment."(23) "Intestinal juice is slightly alkaline (pH 7.6). Together, pancreatic and intestinal juices provide a liquid medium that aids the absorption of substances from chyme as they come in contact with the microvilli."(9)

As partially digested food enters from the stomach, the mucous membrane of the duodenum manufactures the hormone secretin. Secretin decreases gastric secretions (9) and stimulates the pancreatic duct to release pancreatic juice.(17) Pancreatic juice contains pancreatin, "a mixture of the three digestive enzymes trypsin (which digests protein), lipase (which digests fat), and amylase (which digests starch)." The pH of the pancreatic juice is 7-8.(9) "Sodium bicarbonate makes pancreatic juice slightly alkaline (pH 7.1-8.2).(9) "Epithelial cells in pancreatic ducts are the source of the bicarbonate and water secreted by the pancreas. Bicarbonate is a base and critical to neutralizing the acid coming into the small intestine from the stomach. The mechanism underlying bicarbonate secretion is essentially the same as for acid secretion parietal cells and is dependent on the [zinc-dependent] enzyme carbonic anhydrase. In pancreatic duct cells, the bicarbonate is secreted into the lumen of the duct and hence into pancreatic juice."(13) "Carbonic anhydrases are enzymes that catalyze the hydration of carbon dioxide and the dehydration of bicarbonate:
CO2 + H2O <-----> HCO3- + H+
Pancreatic duct cells do essentially the opposite [meaning they reduce acidity using the enzyme carbonic anhydrase], with bicarbonate as their main secretory product."(13)

"The two major pancreatic proteases are trypsin and chymotrypsin, which are synthesized and packaged into secretory vesicles as the inactive proenzymes trypsinogen and chymotrypsinogen. Trypsinogen is activated by the enzyme enterokinase, which is embedded in the [small] intestinal mucosa."(13) Pancreatic proteases such as trypsin and chymotrypsin complete digestion of proteins to their amino acid building blocks throgh proteolysis. Pancreatic proteases require sulfation. Without sulfation, instead of amino acids, peptides are found in the gastrointestinal tract.(6) Chymotrypsin contains a di-sulphide bond.(20) "Trypsin and chymotrypsin... cannot digest proteins and peptides to single amino acids. Some of the other proteases from the pancreas, for instance carboxypeptidase, have that ability, but the final digestion of peptides into amino acids is largely the effect of peptidases on the surface of small intestinal epithelial cells."(13) Pancreatic carboxypeptidase A enzymes (CPA-1 and CPA-2) are zinc-dependent metalloenzymes.(15,18) Enterokinase is the protease in the intestinal brush border that is responsible for generation of active trypsin from trypsinogen; trypsin, in turn, activates other digestive enzymes. The mature enteropeptidase has heavy and light chains, connected by a disulphide bond.(21)

In response to fat in the chyme, enteroendocrine cells in the duodenum also release cholecystokinin (CCK). CCK inhibits stomach emptying (9), activates the release of digestive enzymes in the pancreas, and stimulates the emptying of bile in the gall bladder.( The process of activating cholecystokinin requires sulfation.(6)

"The principal triglyceride-digesting enzyme in adults is called pancreatic lipase."(9) Pancreatic lipase is a constituent of pancreatic juice.(13) Sufficient quantities of bile salts must be present in the lumen of the intestine for pancreatic lipase to efficiently digest dietary triglycerides and to absorb the resulting fatty acids and monoglycerides. "This means that normal digestion and absorption of dietary fat is critically dependent on secretions from both the pancreas and liver."(13)

"Amalayse is present in the small intestines and works with other enzymes to complete the breakdown of carbohydrate into a monosaccharide which is absorbed into the surrounding capillaries of the villi."( Pancreatic amalyse is a calcium-dependent metalloenzyme.(1)

"In addition to the proteases, lipase and amylase, the pancreas produces a host of other digestive enzymes, including ribonuclease, deoxyribonuclease, gelatinase and elastase."(13)

Bile from the gallbladder(7) also enters the duodenum through the pancreatic duct. Bile acts as an emulsifier, eroding the edges of the larger complex fat globules into smaller globules for further digestion. "The introduction of lipase, along with the concentration of bile salts, in contact with the brush border of the mucosal cells, creates the correct environment for final stage breakdown of fats. Final absorption of fat into the body occurs in the villi."( "Bile, a yellow, brownish, or olive-green liquid has a pH of 7.6-8.6 and consists mostly of water and bile acids, bile salts, cholesterol, a phospholipid called lecithin, bile pigments, and several ions. Bile salts, which are sodium salts and potassium salts of bile acids, play a role in the breakdown and absorption of lipids. Acidic chyme entering the duodenum stimulates other enteroendocrine cells to secrete the hormone secretin into the blood, and CCK causes contraction of the wall of the gallbladder, which squeezes stored bile out of the gallbladder." (9) Bile from the gallbladder has an average 6.0 pH (5.6-8.0). Hepatic bile (where it originates) averages 7.5 pH (6.2-8.5)(16) Pancreatin-bile salts contain calcium, zinc, and iron.(10)

"Altogether, chyme remains in the small intestine for 3-5 hours. The completion of the digestion of carbohydrates, proteins, and lipids is a collective effort of pancreatic juice, bile, and intestinal juice in the small intestine."(9) 90% of the water in the chyme is absorbed in the small intestine.(9)


JEJENUM/ILEUM

"Further along the small intestine, beyond the duodenum, lies the jejunum and ileum. As we get further away from the stomach, the pH rises to about 7.5 in this region."(16) Most nutrient absorption takes place in the jejenum (with the exception of iron which is absorbed in the duodenum, and Vitamin B12 which is absorbed in the ileum). Digestive fats are absorbed into lymphatic (lacteal) capillaries, eventually ending up in the circulatory system. Other nutrients are absorbed into non-lacteal capillaries.(24) "Nutrients in the blood are transported to the liver via the hepatic portal circuit, or loop, where final carbohydrate digestion is accomplished in the liver. The liver accomplishes carbohydrate digestion in response to the hormones insulin and glucagon. As blood glucose levels increase following digestion of a meal, the pancreas secretes insulin causing the liver to transform glusose to glycogen, which is stored in the liver, adipose tissue, and in muscle cells, preventing hyperglycemia. A few hours following a meal, blood glucose will drop due to muscle activity, and the pancreas will now secrete glycogon which causes glycogen to be converted into glucose to prevent hypoglycemia."(


LARGE INTESTINES

"The first remnants of a meal reach the beginning of the large intestine in about four hours."(9) The pH of the large intestine ranges from 5.5 to 7.(16) "There is almost no digestion in the large intestine. The task of the colon is to absorb most of the remaining fluid and electrolytes from the chyme."(17) The large intestine continues the process of absorbing water from the feces. "The large intestine also absorbs ions, including sodium and chloride, and some vitamins."(9) In the large intestines, the chyme has a pH of 7.0-7.5.(17) The chyme remains in the large intestine 3 to 10 hours.(9)

1. is there a possible use case where the patient has ulcer in stomach and also low in stomach acid? Taking in extra HCL while may help the digestion, would it not exacerbate the ulcer as well?

2. I get that low acid is the cause and one needs to add it if low - however; I am still not sure as to how the PPIs able to help (even at the surface) the issue of gastritis. If gastritis was happening due to less acid, even lesser acid due to PPI should cause even more problems, is not it?

I am just trying to understand - thanks

Lund - With ulcers the problem is with acid, but in the wrong place. Essentially the lower esophageal sphincter opens at the wrong time, even if there's a small amount of acid in the stomach.

Provided the lower esophageal sphincter remains closed, heartburn and reflux won't exist.

That said, only fixing the valve problem will resolve heartburn and GERD, but using anti-acids will only provide temporarily relief.

The lower esophageal sphincter normally opens to allow food in, but will stay open for burping or vomiting. Using Nexium for vomiting would be a good reason since it should be short-term.

However if the sphincter is working, it would never matter how much acid there is in the stomach, it won't back up into the esophagus.

If there is an ulcer, or if there are particular foods that cause a problem, taking Zinc-L-Carnosine (PepZinGI) would help.

If there is some heartburn, maybe due to certain foods, etc., DGL with Glycine is excellent:

http://www.iherb.com/ProductDetails.aspx?pid=530

IH - My OTHER grandfather at 84 has found out he has some calcification on his heart valve. I understand vitamin k2, vitamin D, Ubiquinol, magnesium in particular will help to reverse the calification, but i was wondering if you have a more specific regimen and in what dosage to tackle the calcification directly. Basically if my (other)grandfather sees results with reversing the calcification he will be sold on the fact the doctors don't know what there talking about.

This product might be over kill in the long long term, but do you think its over kill for the short term in my grandfathers case?
http://www.iherb.com/Life-Extension-Super-K-with-Advanced-K2-Complex-90-Softgels/14619?at=0

Thanks again for your time CS

Silverlin - It would not be overkill, actually more vitamin K2 is better the older you are, and it's especially good for prostate issues too. One critical nutrient for calcification is Omega-3 fatty acids. This is important to diffuse calcium.

On a different note, but still an example is that cervical dysplasia often occurs during the summer months when there is abundant vitamin D, which helps build up the calcium when there is a deficiency of Omega-3 fatty acids required to diffuse the calcium accumulation. Omega-3 fatty acids prevent this accumulation.

The only other element that could be added is something like Ecklonia cava, since it acts in a similar fashion to doxycycline by antagonizing bacteria. Normally I would suggest EDTA chelation to address metals, which is always found with calcium accumulation but for reasons unknown, those over the age of 60 do not seem to benefit from metal chelation for this purpose. It could be that they simply have too much metal stored in the bone and during remodeling or bone turnover there is a recirculation of metal back into the tissues.

Bacteria, calcification and metal all relate to calcium deposition. I suspect that vitamin K does a lot more than keep calcium in check via Gla matrix proteins. Ecklonia cava would also add to the anti-fibrinolytic effect to keep the blood thinner to prevent the sludging blood effect which is what causes friction to the endothelium.

Thanks CS ... from an interested observer of the post. Really informative.

hawthorn ..

Yes. A doctor but my dad on hawthorne for congestive heart failure. That and ribose, co-q10, magnesium and on and on.

CS:
An integrative doctor on the radio here in NY mentioned this form of magnesium. I realize he's selling it on his site.

http://www.drhoffman.com/page.cfm/519

Any thoughts?