Looking for health-related research studies on Siberian pine nut oil? What can Sacramento's eastern European population teach us about pine nut oil as an old Siberian folk remedy for pylori bacteria in the stomach, for acid reflux, and even for peptic ulcers?
Sacramento's newest natural treatment for pylori and acid reflux in those over age 65 with a diminishing amount of hydrochloric acid and other digestive juices in the stomach is Siberian pine nut oil. With Sacramento's large Slavic immigrant population, an ancient folkloric remedy for pylori bacteria or acid reflux in older adults is to drink one or two teaspoons daily of Siberian pine nut oil. But does it work? And where can you find some of the clinical studies? The starting place is to find research on pine nut oil and whether it was studied in relation to acid reflux.
You might explore or research pine nut oil. Will it help your pylori or acid reflux? Can it help heal your pylori, peptic ulcers, and/or acid reflux conditions? The reason this article is about trying out pine nut oil is because it healed our family's acid reflux and pylori problems in a few days taking two teaspoons of it twice or three times daily. The idea of taking a small amount of pine nut oil is popular in Siberia among the indigenous peoples.
Here's how pine nut oil works on acid reflux issues, pylori bacteria, and peptic ulcers:
Helicobacter pylori is a spiral shaped bacterium that lives in the stomach and duodenum. It has a unique way of adapting in the harsh environment of the stomach. Since its discovery back in 1982, it has been studied rather extensively and believed by many in the allopathic medical community to play an important role in the development of peptic ulcers.
Consequently, there has been a fundamental shift in mainstream ulcer and gastritis care from the widespread use of antacids (which temporarily alleviated some symptoms, but did nothing to address the root cause of the problem) to the "treatment" of the ulcers/gastritis with potent antibiotics intended to kill H. pylori. The results of this approach have been mixed.
Although such antibiotics as metronidazole, tetracycline, clarithromycin and amoxicillin have now replaced antacid medications as the preferred mainstream method of dealing with peptic ulcers and gastritis, many unanswered questions about the role of H. pylori in the development of ulcers still remain.
For example, it is a well-known fact that the number of people who have the H. pylori bacteria present in their gastrointestinal systems far exceeds the number of people who actually develop peptic ulcers. In fact, nowadays as many as 50 percent of Americans (and 90-95 percent of people in some other countries) have H. pylori in their systems, but only a small minority of them ever develop ulcers. On the other hand, many ulcer sufferers (especially those with stomach ulcers) are not affected by H. pylori.
Moreover, an increasing number of doctors and medical researchers, led by Dr. Martin Blaser, President of the Infectious Diseases Society of America and founder of the Foundation for Bacteriology, think that Helicobacter pylori may be protective against gastroesophageal reflux disease (GERD), Barrett's esophagus, and adenocarcinoma of the esophagus and stomach cardia - a particularly deadly form of cancer that is becoming more and more widespread.
According to Dr. Martin, H. pylori and humans have co-evolved for many thousands of years, and, until very recently, all humans were colonized by these bacteria. This means that H. pylori must be a long-established part of our normal bacterial flora, or "indigenous biota".
In February 2005, Dr. Martin Blaser has published a landmark article about H. pylori, entitled "An Endangered Species in the Stomach: Scientific American," in Scientific American magazine, Feb. 2005. In this article, he has convincingly demonstrated that the decline of H. pylori in developed countries over the past 100 years has paralleled an upsurge in potentially fatal diseases of the esophagus. Here are some of Dr. Martin's conclusions presented in the article:
"The possibility that this bacterium may actually protect people against diseases of the esophagus has significant implications. For instance, current antibiotic treatments that eradicate H. pylori from the stomach may have to be reconsidered to ensure that the benefits are not outweighed by any potential harm.
To fully understand H. pylori's effects on health, researchers must investigate the complex web of interactions between this remarkable microbe and its hosts. Ultimately, the study of H. pylori may help us understand other bacteria that colonize the human body, as well as the evolutionary processes that allow humans and bacteria to develop such intimate relations with one another."1
Consequently, the jury is still out with regard to the exact role of Helicobacter pylori in health and disease. While there is a possibility that this bacterium plays a certain role in peptic ulcer development, there is also extensive data supporting the opposite point of view: namely, that H. pylori may, under certain adverse circumstances, become a contributing factor to the disease, but not its underlying cause.
And, taking into account the mounting evidence of a protective role played by Helicobacter pylori in relation to esophageal diseases, the currently popular medical practice of wholesale eradication of H. pylori by antibiotics may create more serious problems than the ones it is supposed to solve.
Without doubt, this issue requires a lot of additional research before any final conclusions can be drawn. However, it is definitely premature to recommend strong antibiotics as the "default" allopathic cure for peptic ulcers and gastritis, if only because bacteria tend to develop resistance toward antibiotics, leading to the appearance of new, antibiotic-resistant strains.
The strongly negative side effects of antibiotics, namely the extermination of the numerous beneficial strains of bacteria, leading to further damage to the gastrointestinal system, should not be overlooked, either. When a so-called "triple therapy" (two antibiotics plus an acid suppressor) is used, patients are required to take up to 20(!) pills a day. Side effects of "triple therapy" include nausea, vomiting, diarrhea, dark stools, metallic taste in the mouth, dizziness, headache, and yeast infections in women.
Another serious and potentially life-threatening condition that sometimes develops after the use of antibiotics is called pseudomembranous colitis. On average, it develops in 0.5 to 4 percent of those treated with antibiotics to eliminate peptic ulcers or gastritis.
It is easy to understand the enthusiasm with which the pharmaceutical industry is now promoting the use of antibiotics as a "cure-all" for peptic ulcers. After all, peptic ulcers in the United States alone are a $10 billion business, and the big drug manufacturers are not willing to give it up. However, an objective look at all the known facts surrounding the problem of peptic ulcers and their treatment points in an entirely different direction.
In analyzing the many factors thought to contribute to the formation of peptic ulcers and gastritis, a rather striking "coincidence" comes to mind. The rock-solid fact is that all known risk factors for erosive/ulcerative gastric and duodenal disorders – such as smoking, excess alcohol consumption, physical and emotional stress, and unhealthy eating habits – deplete the natural antioxidant defenses of our body and cause a free radical overload.
As a result, the gentle, fragile mucosal lining of the stomach and the duodenum becomes one of the first tissues to suffer from the damaging chain reactions induced by free radicals. Many scientists who have come across this "coincidence" in their ulcer and gastritis research think that this is exactly the area where the real answers and solutions to the problem are to be found.
Free radicals, also known as "reactive oxygen species" (ROS), are atoms or atomic groups that contain unpaired electrons. Since electrons have a very strong tendency to exist in a paired rather than an unpaired state, free radicals indiscriminately pick up electrons from other atoms, converting those other atoms into secondary free radicals, and thus setting up a chain reaction that can cause substantial biological damage. To protect itself from the damaging action of free radicals, our bodies use substances called antioxidants, which are also often referred to as free radical scavengers.
Oxidative stress is defined as the state in which the level of toxic reactive oxygen intermediates (ROI) overcomes the endogenous antioxidant defences of the host (Bulger EM, Helton WS; 1998). This state results in an excess of free radicals, which can react with cellular lipids, proteins, and nucleic acids, leading to local injury and eventual organ dysfunction.
Which clinical studies prove that peptic ulcers and gastritis are caused by a free radical overload?
There were many studies done worldwide to confirm that peptic ulcers and gastritis are caused and mediated by free radicals, and to justify using natural antioxidants to treat them. All of these studies pointed to the correctness of this assumption, but one of them merits particular attention.
The study in question, entitled The Role of Free Radicals in Peptic Ulcers and Gastritis,2 took place in Turkey in 2003, and covered 42 people. In a total group of 42, there were 15 cases of peptic ulcers, 14 cases of gastritis, and 13 controls. All 29 patients with peptic ulcers and gastritis were H. pylori-positive.
The conclusion of this study, according to the abstract noted, "Depletion of gastric mucosal glutathione in cases with H.pylori positive peptic ulcer and gastritis may be caused by accumulation of free radicals that can initiate membrane damage by lipid peroxidation."
The study pursued two goals: 1) to verify that peptic ulcers and gastritis are closely related with the activity of free radicals; and 2) to see if there are signs of antioxidant depletion in the affected tissues. This was done by measuring the levels of gastric mucosal concentrations of malondialdehyde (MDA), which is the end product of lipid peroxidation caused by free radicals, as well as the levels of mucosal glutathione (GSH) – a powerful antioxidant peptide.
Levels of MDA reflect cell membrane damage inflicted by free radicals, whereas depletion of gastric mucosal GSH, which forms part of our bodies’ natural antioxidant protection system, results in the accumulation of free radicals that can initiate membrane damage by lipid peroxidation. The study has shown that gastric mucosal MDA levels were significantly (up to four times) higher, and gastric mucosal concentrations of GSH were significantly (up to five times) lower in peptic ulcer and gastritis patients compared to controls.
These results strongly suggest that the depletion of gastric mucosal glutathione in peptic ulcers and gastritis is caused by accumulation of free radicals that can initiate membrane damage by lipid peroxidation. The findings of the study also confirm that oxygen-derived free radicals play a major pathological role in peptic ulcers and gastritis.
The study mentions a number of other researchers who came to the same conclusions. For example, in 2000 a group of Indian scientists has shown that infection with H.pylori is associated with generation of free radicals, which leads to oxidative stress in the gastric mucosa.3
Another group of scientists, which has studied the role of glutathione in the anti-ulcer effect of black tea, showed that GSH plays a major role in cytoprotection against ulceration.4 Finally, a number of studies have investigated the influence of free radical scavengers (antioxidants) on the healing of gastric and duodenal ulcers resistant to therapy and found that antioxidative therapy stimulates the healing of therapy-resistant ulcers.5
All of these studies clearly confirm that peptic ulcers and gastritis are primarily caused by oxidative stress and free radical damage. Therefore, effective treatment and prevention of gastritis and peptic ulcers must be based on using the best available natural antioxidant complexes in order to enhance our body's depleted antioxidant shields. One such healing antioxidant complex, abundant in very potent and effective free radical scavengers, is contained in extra virgin pine nut oil (EVPO).
Extra virgin Siberian pine nut oil, (which help our family's acid reflux daily symptoms) is a time-tested natural remedy with a proven track record of alleviating ulcer- and gastritis-related pain and healing even the most therapy-resistant cases of peptic ulcers and gastritis
After the fact that gastritis and peptic ulcers are caused by free radicals has been proven by clinical studies, there has been a massive search in the naturopathic community for the best and most balanced natural sources of anti-ulcer antioxidants.
This search has produced some very encouraging and exciting results. Somewhat unexpectedly, the researchers have come across extra virgin pine nut oil – a golden-colored, tasty oil pressed from the seeds of Siberian pine (Pinus Sibirica).
It turned out that this little-known oil has been used in Russia and China for many centuries not just for food, but for successfully healing peptic ulcers and gastritis. Moreover, the oil proved to be such a powerful gastritis and ulcer ulcer treatment that, after extensive clinical studies, it has been officially approved as a gastritis and ulcer medication in Russia, China and Eastern Europe.
To better understand why pine nut oil is the best and the most effective natural remedy for healing gastritis peptic ulcers, it is necessary to go a little deeper into the mechanisms by which our body protects itself from the harmful effects of free radicals.
Our body has developed several endogenous antioxidant systems to deal with the production of free radicals. These systems may be divided into enzymatic and non-enzymatic groups.
The enzymatic antioxidants include superoxide dismutase (SOD), catalase, and glutathione peroxidase. SOD catalyzes the breaking down of a free radical called superoxide, which plays a major role in lipid peroxidation, into oxygen and hydrogen peroxide, which is further decomposed into water and oxygen by catalase. Glutathione peroxidase is also used by the body to consume free peroxide in the cells.
It is very important to note that, for maximum efficiency, these antioxidant enzymes require trace metal cofactors. SOD, for example, consists of proteins co-factored with copper, zinc, manganese, or iron. Iron is also required as a co-factor for catalase.
The most well-researched non-enzymatic antioxidants include lipid-soluble vitamin E, vitamin A and carotenoids (including beta-carotene), as well as water-soluble vitamin C and glutathione (GSH). Glutathione, which is synthesized intracellularly from amino acids cysteine, glycine, and glutamate, is capable of scavenging free radicals either directly or enzymatically via glutathione peroxidase. In addition, GSH is crucial to the maintenance of enzymes and other cellular components in a reduced state.
Extra virgin Siberian pine nut oil is a uniquely potent natural source of powerful antioxidants, as well as antioxidant cofactors and “building blocks”. First, it contains up to 56 mg/100 g of natural alpha-tocopherol (vitamin E) – the most effective non-enzymatic antioxidant for terminating the chain reactions of lipid peroxidation in cell membranes.
Pine nut oil is significantly richer in vitamin E than any other common vegetable oil (for example, extra virgin olive oil contains five times less vitamin E than extra virgin pine nut oil). It is also very important that pine nut oil contains a natural, maximum-potency form of vitamin E (d-alpha-tocopherol), whereas a vast majority of vitamin E capsules sold as dietary supplements contain synthetic forms of tocopherol (primarily dl-alpha-tocopherol acetate), which are at best only half as potent as natural vitamin E.
The next important group of antioxidant compounds present in Siberian pine nut oil are carotenoids. Carotenoids are organic pigments occurring in plants and some types of algae and fungus. So far, more than 600 of them were identified. Their molecular structure makes them very efficient free radical scavengers, resulting in a powerful antioxidant effect. Some carotenoids (for example, beta-carotene) fall into the category of pro-vitamin A. From them, our body makes retinol (vitamin A), which is a potent antioxidant itself.
Pine nut oil is a rich source of carotenoids, supplying about 30 mg/100 g of these antioxidant and pro-vitamin compounds. The fact that these carotenoids are dissolved in oil greatly increases their bio-availability to our bodies in two ways. First, the carotenoids are already released from the plant matrix (under certain circumstances, this release may be difficult, making carotenoids in some foods less usable compared to others), and, second, fat is a necessary cofactor for carotenoid uptake.
The abundance of vitamin E and carotenoids alone would make extra virgin pine nut oil an excellent natural antioxidant supplement, but there is much more to its antioxidant activity. As noted above, another major antioxidant, glutathione, is a tripeptide synthesized by our cells from three amino acids: cysteine, glycine, and glutamate. Pine nut oil, rich in essential and non-essential amino acids, supplies all three of these glutathione building blocks. Therefore, it is also an important glutathione booster, capable of enhancing the free radical scavenging performance of this major antioxidant both directly and via glutathione peroxidase.
Finally, extra virgin Siberian pine nut oil is exceptionally rich in trace metal co-factors for enzymatic antioxidants superoxide dismutase (SOD) and catalase. It contains 20 mg/100 g of zinc, 16 mg/100 g of manganese, and 4 mg/100 g of copper – all of them required for maximum efficiency of SOD. It also supplies about 19 mg/100 g of iron, an essential co-factor for both SOD and catalase. Consequently, pine nut oil not only provides our body with a potent boost of “external”, non-enzymatic antioxidants (vitamin E and carotenoids), but also reinforces and optimizes its own enzymatic potential for scavenging free radicals expressed through superoxide dismutase, catalase, and glutathione peroxidase.
As we can see, extra virgin pine nut oil is an outstanding concentrate of powerful free radical scavengers fully capable of preventing or reversing even the strongest oxidative stress leading to gastritis and peptic ulcers. There is also some evidence suggesting that pine nut oil may be capable of working against gastroduodenal ulcerative disorders in more than one way, its potent antioxidant activity being just one of the factors contributing to its effectiveness as a natural ulcer and gastritis remedy.
For example, a number of researchers suggest that the oil contains some unique fatty acids with strong anti-inflammatory and protective effects on the gastric and duodenal mucosa. This is quite possible, but, no matter which specific properties of pine nut oil apart from its antioxidant activity account for its anti-ulcer action, one thing is for sure: extra virgin pine nut oil is an effective, time-tested and proven natural ulcer and gastritis healer.
Check out the testimonials regarding peptic ulcers and gastritis healed with extra virgin pine nut oil at the site. This information has been given with written permission from Alex Maksimov, Siberian Tiger Naturals, Inc.
PO Box 479, Springfield, VT 05156. Check out the website for further information and a list of medical studies.
More information about extra virgin pine nut oil is available on these pages
1. What is Extra virgin pine nut oil (EVPO)? Is it safe to use?
2. How does pine nut oil work to heal peptic ulcers and alleviate gastritis-related inflammation?
3. What causes peptic ulcers and gastritis?
4. Were there any clinical studies performed to ascertain the effectiveness of extra virgin pine nut oil as a gastrointestinal remedy?
5. What about H. Pylori? Isn't it enough to kill this "bug" to get rid of peptic ulcers?
6. Does extra virgin pine nut oil relieve ulcer- and gastritis-related abdominal pain?
7. Are there any side effects associated with the use of pine nut oil?
8. My doctor has prescribed antibiotics and antacids for my ulcer. Can I combine extra virgin pine nut oil with these medications?
9. How would the use of pine nut oil react with a person who has had the gallbladder removed?
10. Do have any suggestions for taking your pine nut oil besides just straight?
11. What are free radicals and antioxidants? How do their affect our health?
12. How does our body protect itself from free radicals? What can we do to help it protect itself?
13. What makes extra virgin pine nut oil such a powerful concentrate of antioxidants?
14. How much extra virgin pine nut oil should I take to alleviate pain and heal peptic ulcers?
15. What is cholecystokinin (CCK)? How does it enhance metabolism and assist digestion?
16. What is pinolenic acid (PNA)?
17. What is the recommended daily dosage of pine nut oil required for optimizing digestion?
18. I do not need to lose any weight. I will be using the oil as a gastrointestinal remedy. Will it suppress my appetite?
Medical Studies Articles
1. Kissileff HR, Pi-Sunyer FX, Thornton J, and Smith GP. Cholecystokinin decreases food intake in man. American Journal of Clinical Nutrition, 34: 154-160, 1981.
2. Harry R. Kissileff, Julie C. Carretta, Allan Geliebter, and F. Xavier Pi-Sunyer. Cholecystokinin and stomach distension combine to reduce food intake in humans. American Journal of Physiology, 285: R992-R998, 2003.
3. Stephen C. Woods. Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake. American Journal of Physiology, 286: G7-G13, 2004.
3. Moran TH and Schwartz GJ. Neurobiology of Cholecystokinin. Critical Review of Neurobiology, 9: 1-28, 1994.
4. Muurahainenn N, Kissileff HR, Derogatis AJ, and Pi-Sunyer FX. Effects of cholecystokinin-octapeptide (CCK-8) on food intake and gastric emptying in man. Physiology & Behavior, 44: 644-649, 1988.
5. Smith GP and Gibbs J. The development and proof of the cholecystokinin hypothesis of satiety. In: Multiple Cholecystokinin Receptors in the CNS, edited by Dourish CT, Cooper SJ, Iversen SD, and Iversen LL. Oxford: Oxford University Press, 1992, p. 166-182.