Gregory Kelly



Everyone new that ulcers were caused by stress, spicy food or by stomach acid. Well, everyone that is except a young Australian physician named Dr. Barry J. Marshall. He believed that bacteria called Helicobacter pylori (H. pylori) could cause peptic ulcers. Of course the medical establishment viewed this discovery as they do all new discoveries and they quickly dismissed it as "absurd".

After being ignored for years, Dr. Marshall, being so convinced that he was correct, decided to (and for those viewers at home we don't recommend that you do this) use himself as a guinea pig. Drinking the bacteria, he proved that exposure to the bacteria temporarily caused the inflammation and gastric irritation that we call an ulcer or gastritis. His ideas were eventually accepted and are now part of the dominant idea of ulcer causation (amazing how this happens).

Currently, H. pylori has been implicated in gastritis, peptic ulcer disease, gastric cancer, gastric lymphoma and recently, this organism has also been investigated in order to establish an association with heart disease.

Symptoms

Pain in the stomach area is the most predominant symptom, usually characterized as burning sensation made worse by eating for gastric ulcer and relieved by eating to return in 2-3 hours for duodenal ulcer. One third of patients with duodenal ulcers wake at night with pain and the pain tends to be episodic; lasting several days to weeks and then subsiding for weeks or months. Nausea, indigestion, gas and bloating are also common symptoms of infection. Less common symptoms include repeated vomiting and weight loss.

H. pylori might be an independent risk factor for gastric carcinoma (cancer of the stomach), auto immune disease and heart disease. Most gastric adenocarcinomas are associated with H. pylori and its presence confers an approximately six-fold increase in risk. Biopsy has demonstrated that 90% of Mucosa Associated Lymphoid Tissue (MALT) lymphomas are associated with H. pylori. Odds ratio for abnormal ECG is 3.82 for men infected with H. pylori after adjustment for a range of socioeconomic and risk factors associated with coronary heart disease.

Etiology/Epidemiology

H. pylori infection is thought to be spread by fecal/oral route. Having more than one person in a bedroom of a family house during childhood, shared beds, and no hot water in the house all increase the prevalence of H. pylori infection as an adult.

In general, the following comments can be made to summarize H. pylori prevalence in Western countries:

1. H. pylori infect about 20% of persons younger than 40, and 50% of those older than 50 years.

2. It is uncommonly found in young children.

3. Low socioeconomic status predicts infection.

4. About 92% of people with duodenal ulcer and about 70% of people with gastric ulcers are positive for H. pylori.

In developing countries most adults are infected and in parts of Africa there is 100% infection.

It is important to remember that although H. pylori is now considered to be a major cause of ulcer disease, not all individuals who have the disease show evidence of infection. Everyone who is exposed to the bacterium does not get the disease, nor do all those exposed to the organism develop long-term health problems. In fact, it is interesting to note that in parts of Africa, the prevalence of H. pylori has been shown to approach 100% and yet peptic ulcer is uncommon.

A Closer Look at H. pylori

H. pylori are a gram-negative microorganism that secretes many substances, including, ammonia, mucolytic enzymes (Adhesins, Catalase, and Urease), and acid secretion inhibitory proteins. Adhesin allows the organism to adhere (or act like Velcro and stick to gastric cells (note: this is important in its preference for O blood types)). Catalase might protect the organism from the immune system.

H. pylori increase the secretion of gastrin, which stimulates intestinal tissues to grow faster, and so could result in increased cancer risk. Urease is an enzyme responsible for hydrolyzing urea to ammonia and CO2. The CO2 may be protective by buffering pH locally. The ammonia is also protective by forming an alkaline environment around the organism. This combination of ammonia, CO2, and its acid secreting inhibitory proteins allows the bacteria to set up localized pockets where it can neutralize even the acidity of blood type O stomachs.

Blood Type Connections

Secretor/Non-secretor connections

The genetics of the secretor/non-secretor system interact to alter an individuals risk for ulcers. In several studies, non-secretors of ABO substances have been found to have a significantly higher rate of duodenal and peptic ulcers.

Because of the increased prevalence of ulcers among non-secretors, it should come as no surprise that researchers have suggested that secretor status might influence bacterial colonization density or the ability of H. pylori to attach to gastroduodenal cells.

Because non-secretors are limited in their ability to secrete blood group antigens (this is complicated stuff but trust me this is true) into the mucous secretions of their digestive tract, it has been proposed that they be at a competitive disadvantage from preventing H. pylori attachment. In other words, a non-secretor's lack of antigens in mucosal fluids might indirectly contribute to colonization by H. pylori.

In a simplified sense, when specific antigens are free floating in the mucus, it probably acts to bind up some of the H. pylori before it can contact and attach to your tissues. In essence, being a secretor provides you with an ability to put some biological decoys or metabolic false targets (in the Navy we called these false targets "chaff" and they are part of the counter measures against incoming missiles or torpedoes) out into your secretions.

Non-secretor's, as a general rule, also show a significantly higher proportion of the H. pylori-seronegative subjects and a lower IgG (H. pylori immunoglobulin G (IgG) antibody) immune response to H. pylori antigens as compared with the individuals of the secretor phenotype.

This might indicate that non-secretor's are unable to mount an aggressive immune response against this organism in comparison with their secretor brethren. Evidence does suggest that both bacterial colonization and the resultant ensuing inflammatory response are influenced, at least in part, by the ability to secrete blood group antigens. This relationship is strongest among blood type O non-secretors.

Key Point: If you are a non-secretor (especially an O non-secretor), your immune response against H. pylori appears to be lower and H. pylori appear to attach with higher aggressiveness and cause more inflammation.

Blood Type O

Like lots of other bacteria in the gut, H. pylori have a favorite blood type: Type O. I have mentioned in past columns that bacterial infection must also be thought of in terms of adhesion/anti-adhesion. Basically, in order for an infectious organism to gain a foothold it must attach to something. In simple terms think of microorganisms as if they were a piece of Velcro. Velcro will not stick to just anything (it will slide off of a smooth wood surface). In fact, Velcro is quite specific; it will only stick to special plastic with tiny projections. The microbial world of adhesion/anti-adhesion is very similar to this Velcro action. And, H. pylori is much more like molecular Velcro for the O antigen, while the A and B antigen do not give it much to stick to.



Key point: in general terms, the ability of H. pylori to attach or gain a foothold is enhanced by cells that have blood group O antigens. No wonder O's get more ulcers.



Standard Medical Strategy

The therapy recommendation for eradication of H. pylori is triple regimens comprising colloidal bismuth subcitrate (2 tablets (512mg) four times dailt with meal), either amoxicillan (2 grams/day in divided doses) or tetracycline (500 mg three times daily), and metranidazole (250 mg three times daily with meals). A minimum of two weeks seems needed for elimination of the bacteria in order to better prevent relapse within a 12-month period. Lasting remission is estimated at 84%.

Accessory Strategies

Friendly probiotic bacteria should be a key (if not the key) component of your accessory strategy. Many strains of these probiotic bacteria act as natural antagonists to H. pylori. In addition, these probiotic bacteria should always be used to enhance the effectiveness of antibiotics. Remember, probiotic bacteria are also needed to prevent antibiotic-induced disruption of the friendly bacteria in your GI.

You can also use both foods and specific lectin blocking sugars to help facilitate anti-adherence as a strategy. Since the bacteria has a preference for the O antigen, fucose, is probably the most important of these anti-adhesion sugars. The primary food sources of this sugar are bladderwrack and kelp. Both of these foods make your cells much more slippery when it comes to the molecular Velcro H. pylori uses to adhere. Another option are the Deflect products.

Bismuth is a mineral with both anti-Helicobacter pylori and ulcer healing properties. The best real world example of a bismuth product is ‘Pepto-Bismol’. Bismuth is actually very effective against this organism and is relatively safe in the doses needed to eradicate H. pylori. This is the reason for the inclusion of bismuth in standard medical treatment of H. pylori. Since bismuth (like most minerals) can be toxic if consumed in large quantities, it is recommended that you consult a physician prior to starting supplementation with bismuth compounds.

An alkaloid called berberine which is found in herbs such as Golden Seal (Hydrastis canadensis) and coptis (Coptis chinensis) has been found to inhibit the growth of H. pylori.

DGL, a form of licorice with the component that can increase blood pressure removed, has a reputation for enhancing the integrity of the mucus lining of the digestive tract. This form of licorice also appears to be antagonistic to H. pylori.

References

General

Bernersen B, Johnson R, Bostad L, Straume B, Sommer AI, Berhol P. Is Helicobacter pylori the cause of dyspepsia? British Medical Journal. 1992; 304: 1276-8.

Bland J. Applying New Essentials in Nutritional Medicine-Helicobacter pylori and upper Gastrointestinal Disease. 1994. HealthCom; Seattle WA.

Desai HG, Gill HH, Shankaran K, Mehta PR, Prabhu SR. Dental plaque: a permanent reservoir of H. pylori? Scand J Gastroenter 1991; 26: 1205-1208.

Gibson GR, Cummings JH, Kelly SM, Dunn MRC. Isolation of H. pylori from patients in the UK - implications for treatment. Gastroenterology 1994; 106, 4 (2 suppl): 81.

Krajden S, Fuksa M, Anderson J, et al. Examination of Human Stomach Biopsies, saliva, and dental plaque for Campylobacter pylori. J Clin Micribiol. 1991; 27: 1397-98.

Marshal BJ. Helicobacter Pylori. Unpublished, University of Virginia health Sciences Center. 1995.

Mendall MA, Goggin PM, Mollineux N, et al. Childhood living conditions and H. pylori seropositivity in adult life. Lancet. 1992; 339: 896-7.

Mendell MA, Goggin PM, Molineux N, et al. Relation of Helicobacter pylori infection and coronary heart disease. British Heart Journal. 1994; 71:437-39.

Miragliotta G, Fumarola D, Mosca A, Francavilla A, Monno RA. Campylobacter pylori associated gastritis and procoagulant activity production. American Society for Microbiology annual meeting 1989; abstr B222.

Parsonnet J, Blaser MJ, Perez GI, Hargrett BN, Tauxe RV. Symptoms and Risk Factors of H. pylori infection in a cohort of epidemiologists. Gastroenterology. 1992; 102: 41-6.

Parsonnet J, Friedman GD, Vandersteen DP, et al. H. pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991; 325: 1127-31.

Patel P, Mendall MA, Carrington D, Strachan DP, Leatham E, Molineax N, Levy J, Blakeston C, Seymour MA, Camm AJ, Northfield TC. Association of Helicobacter pylori and Chlamydia pneumoniae infections with coronary heart disease and cardiovascular risk factors. British Medical Journal. 1995; 311: 711-14.

Soll AH. Medical Treatment of Peptic Ulcer Disease. JAMA. 1996; 275: 622-29.

Secretor/Non-secretor

Odeigah PG. Influence of blood group and secretor genes on susceptibility to duodenal ulcer. East Afr Med J 1990 Jul;67(7):487-500

Suadicani P, Hein HO, Gyntelberg F. Genetic and life-style determinants of peptic ulcer. A study of 3387 men aged 54 to 74 years: The Copenhagen Male Study. Scand J Gastroenterol 1999 Jan;34(1):12-7

Dickey W, Collins JS, Watson RG, et al. Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. Gut 1993 Mar;34(3):351-3

Sumii K, Inbe A, Uemura N, et al. Multiplicative effect of hyperpepsinogenemia I and non-secretor status on the risk of duodenal ulcer in siblings. Gastroenterol Jpn 1990 Apr;25(2):157-61

Dickey W, Collins JS, Watson RG, et al. Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. Gut 1993 Mar;34(3):351-3

Oberhuber G, Kranz A, Dejaco C, et al. Blood groups Lewis(b) and ABH expression in gastric mucosa: lack of inter-relation with Helicobacter pylori colonisation and occurrence of gastric MALT lymphoma. Gut 1997 Jul;41(1):37-42

Su B, Hellstrom PM, Rubio C, et al. Type I Helicobacter pylori shows Lewis(b)-independent adherence to gastric cells requiring de novo protein synthesis in both host and bacteria. J Infect Dis 1998 Nov;178(5):1379-90

Alkout AM, Blackwell CC, Weir DM, et al. Isolation of a cell surface component of Helicobacter pylori that binds H type 2, Lewis(a), and Lewis(b) antigens. Gastroenterology 1997 Apr;112(4):1179-87

Klaamas K, Kurtenkov O, Ellamaa M, Wadstrom T. The Helicobacter pylori seroprevalence in blood donors related to Lewis (a,b) histo-blood group phenotype. Eur J Gastroenterol Hepatol 1997 Apr;9(4):367-70

Heneghan MA, Moran AP, Feeley KM, et al. Effect of host Lewis and ABO blood group antigen expression on Helicobacter pylori colonisation density and the consequent inflammatory response. FEMS Immunol Med Microbiol 1998 Apr;20(4):257-66

Mentis A, Blackwell CC, Weir DM, et al. ABO blood group, secretor status and detection of Helicobacter pylori among patients with gastric or duodenal ulcers. Epidemiol Infect 1991 Apr;106(2):221-9

by Gregory Kelly

Since the publication of Eat Right 4 Your Type nearly two years ago, we have found out a great deal about elderberry fruit. In fact, Peter and I have come to increasingly rely upon a great-tasting mix of elderberry, blueberry, and cherry in our clinical practice. While the versatility of elderberry and these other berries is incredible, this article is going to limit itself primarily to a focus on elderberry's most well known use---as a remedy in the common "flu".

Many medical experts consider the influenza virus (cause of the "flu") to be the most dangerous virus in the world. Several times in past history, this virus has been responsible for killing huge numbers of people within a 1 to 2 year period. As an example, the "Spanish flu" (type A(H1N1)) of 1918-19 killed about 500,000 people in the U.S. and at least 20 million people worldwide. In 1957-58, the "Asian flu" (type A(H2N2)) resulted in 70,000 deaths in the U.S., and in 1968-69, the "Hong-Kong flu" (type (A(H3N2)) killed 34,000 in the U.S.

What is the Flu?

Let's pause here and take a moment to get a clearer picture of what the "flu" really is. Terminology and language can be fickle and non-specific masters, and so the common day-to-day use of the term "flu" has evolved to often encompass anything from a "common cold" to a true "flu". The "stomach flu" is another misleading term, often used to describe a gastrointestinal illness (the "stomach flu" is usually not even caused by a virus but by other microorganisms). So, the first critical point to understand is that a "flu" is not a common cold or a stomach infection.

When researchers, or doctors speak of the "flu", they are being very specific and mean an infection by the influenza virus. Epidemic influenza is divided into type A and type B. The most common presentation of influenza includes a fever (usually 100-103 degrees F in adults), respiratory symptoms (such as cough, sore throat, runny or stuffy nose), headache, muscle aches, and often extreme fatigue. So, the second key point is that public health officials and doctors mean influenza virus when they use the term "flu".

The year-in, year-out "flu" can be deadly (in an average year, influenza is associated with about 20,000 deaths), especially for the elderly, immuno-compromised, or those who have an existing condition, such as asthma, diabetes or heart disease. Even for those of us who are in generally good health, the "flu" can still really "take the wind out of our sails", causing us to feel miserable for several days to a week or two.

Currently there are three main variants of the "flu" circulating (two types "A" and one type "B"). The type A variants are the "Hong Kong" type A(H3N2) virus and its relatives (responsible for about 400,000 deaths in the United States since 1968 (90% of which are among the elderly), and distant relatives of the "Spanish Flu", type A(H1N1). The "H" and "N" refer to viral proteins called haemagglutinin (H) and the neuraminidase (N) (more on this in a bit).

Some medical and public health experts believe it is only a matter of time (in fact they think we are overdue) before a new pandemic (worldwide epidemic) of the "flu" occurs, killing many, many people.

Why has the flu been able to kill such large numbers of people so quickly in the past?

I am going to oversimplify here, but follow along.

The "flu" virus is able to mutate or change over time, allowing it to reinfect you year after year. Usually this is a slow and very gradual process (both type A and B influenza virus can change in this manner). As an example, if you were exposed to last year's "flu" virus, your immune system would have created a very specific memory of how to effectively deal with the virus. A new exposure to the same virus would not now be a problem. Since the virus changes a slight amount each year, last years immune memory will partially, but not completely protect you from this year's influenza infection. Think of it in terms of not seeing a friend for a long while...they will obviously look a bit different, so it might take a moment for you to recognize them and remember their name. However, once this moment passes and you remember the name, you now have a clear idea of how to greet them However, every once in a while, the type A "flu" virus (the type B does not change in this manner) will have a dramatic and abrupt change to either its haemagglutinin (H) and/or neuraminidase (N) proteins. This results in a new strain of the virus, which is not recognized as something your immune system dealt with in the past. It would be as if a new person moved into your town; you have no information in your memory to identify them as your friend and no idea of the name. In the years that the "flu" virus became a worldwide epidemic and killed into the millions of people, the "flu" virus changed in this manner.

Blood type and the "flu"?

Quite a few different researchers have investigated blood type and influenza. The volume of research alone is almost enough to suggest strong blood type connections, but let's look at the research just to be sure.

After exposure to the influenza virus, an immune process termed "seroconversion" should occur. This means that your immune system should be producing antibodies against the influenza virus. Researchers have found that after circulation of influenza A (type (H1N1) and (H3N2)) and influenza B viruses, the immune response (as measured in a rise in antihaemagglutinin antibodies against the virus) differ along blood type lines.

The following generalized immune observations apply:

Blood type A: Overall has a great ability to generate a quick and substantial antibody response against influenza type A(H1N1) and especially A(H3N2). Their antibody response against influenza B is not quite as dramatic.

Blood type AB: Relatively poor ability to generate high antibody levels against any of the influenza viruses.

Blood type B: Reasonable, but not great ability to generate an antibody response against influenza A(H1N1). Slowest (it can take them 3-5 months) and weakest ability to generate antibodies against influenza A(H3N2) of any blood type. Against influenza B virus, blood type B has a significant advantage and responds differently from either blood group A or O. The blood type B immune response happens much earlier and persists longer.

Blood type O: Relatively descent ability to generate antibody response against influenza A(H1N1) and A(H3N2) viruses. Antibody response against influenza B is not as dramatic as blood type B.

Some researchers have hypothesized that one explanation for the typical emergence of the new epidemic strains of influenza in Asia is connected to blood type (and the relatively high proportion of type B blood found in Asia). It seems that blood type B has a genetic predisposition to latent (chronic) persistence of influenza A virus (especially A(H3N2) "Hong Kong" variants). Often, the influenza virus antigen can still be found in healthy type B individuals as much as 5 months after a "flu". This means that although they might not have symptoms, they are providing a safe harbor for the virus.

With these differences in immune responses, we would expect to see differences in susceptibility to and severity of influenza infection between the different blood types...and indeed we do. What we find is that the susceptibility to influenza changes based upon your blood type and the properties of the circulating strains of influenza virus.

Looking at influenza A as a whole, the following blood type generalities exist. People with blood type B (and A are going to be much more susceptible to infection during times when new antigenic variants and serotype's of influenza virus appear. This is actually particularly bad news for B's and AB's, since this is the type of influenza A virus change that results in widespread flu pandemics. Blood type O individuals tend to be susceptible to influenza infection at the period of the circulation of virulent strains (so in years when the flu is making people feel really sick, type O will be hit the hardest). Type A's are the lucky ones when it comes to influenza A; they have a generalized susceptibility to the less virulent strains of influenza A.

Overall, influenza is probably most problematic year to year for Type AB's. In general, they are more sensitive to infection by both influenza A and B than the other blood types. They are affected by these viruses earlier and more severely than those with the other blood groups (and they need to be extra cautious regarding an abrupt change in the influenza A virus as well) . Blood type B is going to be most severely affected when the influenza A(H3N2) (this in the "Hong Kong" variety and its relatives) is in circulation, has relatively little difficulty with influenza B, and has to be very concerned about an abrupt change in the influenza A strains. Type O gets less influenza A(H1N1) and more A(H3N2). Type A blood indirectly offers relative protection against both strains of influenza A.

Will the flu shot protect me?

Does the flu shot protect the blood types differently? Well, what the research shows is that all blood types will have similar seroconversion frequencies to both the live attenuated and killed subunit vaccines after the administration of TWO doses. But after only ONE dose of the live vaccine, blood type A is much more likely than the other blood types to seroconvert. The lesson to be learned here is that blood types B, AB and O really should probably get two doses of the live vaccine for best results (most type A's can probably get away with just one dose). With the killed subunit vaccine, type O produces the greatest anti-haemagglutinin antibody response. Again two doses generally places the blood types on equal ground.

In addition to the blood type information, remember the following. This year's "flu" shot is made from the most common "flu" viruses in circulation last year. So, in most years, when the virus changes only a tiny bit from last year, the "flu" shot will offer some protection.

Note: There are many people nevertheless who benefit significantly from the "flu" shot including elderly, chronically ill, and immuno-compromised individuals. For more information on who should receive this vaccination it is advised that you contact a physician or the department of public health.

Essentially, the effectiveness of the flu shot is always going to be dependent on how closely the vaccine matches the strain of flu virus in current circulation. So, if the virus changes dramatically from last year (as it did in the pandemic years), the "flu" shot will be of little to no use, because, in essence, it is not providing you with any one who knows this new person in town. So a key point then with regards to the "flu" shot is that it offers protection in most years, but probably not from a pandemic "flu".

Antivirals and the "flu"

Amantadine and rimantadine are chemically related drugs that interfere with the replication cycle of influenza type A viruses (they are not effective against influenza type . They both offer a descent degree of protection against infection if taken daily during "flu" season; however, cost, compliance, and side-effects limit this type of use for most people.

Amantadine and rimantadine are also useful in treatment of the "flu"; able to reduce the severity and shorten the duration of influenza A if given within the first 48 hours. One huge drawback with these antiviral's is that they result in Amantadine- and rimantadine-resistant influenza A viruses when they are used for treatment (a very poor long-term strategy resulting essentially in a possible ineffectiveness of these drugs when you might need them the most for a severe or life-threatening "flu").

Zanamivir and Neuraminidase Inhibitors.

Zanamivir was the first in a new class of drugs known as selective viral neuraminidase inhibitors. And, if in fact the old saying that "imitation is the most sincere form of flattery" holds true, this type of drug must hold tremendous promise. Pharmaceutical and biotechnology companies (including one of the industry giants---Hoffman La Roche) have quickly jumped on the neuraminidase band-wagon and are now either planning a launch or are in the process of developing their own neuraminidase inhibitors.

The reason Zanamivir is such a promising development is that in humans it not only prevents influenza infection, but also reduces the duration and intensity of the typical symptoms if given within the first 30 hours during an influenza infection. Let's take a moment here to discuss haemagglutinins and neuraminidase in the context of influenza (remember these are the H and N in the A(H1N1) and A(H3N2) strains).

The influenza virus forms haemagglutinins (essentially protein spikes) which release an enzyme called neuraminidase in order to spread to new cells and propagate the infection. From a biochemistry perspective, neuraminidase is an enzyme that cleaves terminal sialic acid residues from glycoconjugates (Does the term glycoconjugate remind you of anything? It should, because the antigens on your cells like your ABO marker are gycoconjugates). By cleaving off the sialic acid sugar, the virus can escape from infected cells, spread to new cells, and make the mucus you produce in response to an infection less effective (yes, the runny nose and mucus you produce in response to a cold or flu are actually part of your body's defense strategy).

It was assumed that an ability to inhibit neuraminidase would be a useful medical intervention for treating (and maybe preventing) the "flu". So far in the trials on Zanamivir, this assumption appears to be true. The biggest disadvantage with Zanamivir is that it is not well absorbed orally, so must be given by inhalation. Its use might also be limited by its cost. So far, researchers claim that resistance of the virus to the drug has been only rarely observed (but remains a possible area of concern).

Elderberry and the "Flu"

So where does elderberry fit in this portrait of the "flu". I have mentioned it was used historically, but does it work? In experiments, elderberry actually does inhibit replication of all strains of human influenza (both A and viruses tested.

In an actual placebo-controlled, double blind study (the scientific gold-standard so to speak) an extract of elderberry fruit has been shown to be effective for treating influenza B. What this research showed was that people using the elderberry extract got better much quicker (more than 70% were better after 2 days and over 90% of people completely resolved the infection within 3 days). In contrast, the people given a placebo often needed as much as 6 days to feel well.

Why does elderberry work? Well, the researchers found two reasons really. People taking the elderberry were able to produce higher anti-haemagglutination titers to influenza B (meaning their immune system essentially performed better and they now have a higher level of recognition should this "flu" return). And, elderberry inhibits neuraminidase (yes, that is the same neuraminidase that scientists are spending millions of dollars designing drugs against). (Editor's note: Zanamivir to an extent duplicates this neuraminidase blocking ability of elderberry, but does not appear to have elderberry's beneficial impact on the immune system).

An important question that has not been answered yet is...will elderberry work as well against influenza A strains? I don't have a definitive answer for you on this yet, but based upon its method of action, its in vitro ability, and my clinical observations, the answer is probably yes. Our patients taking the elderberry, blueberry, cherry and apple concentrate mixture, seemed to pass easily through this past "flu" season. The one word of caution I leave you with is that when it comes to daily use of elderberry, more is not always better. Large doses will lead to nausea. If you are trying to avoid a "flu" a small amount daily might help. I recommend elderberry especially for type B's and AB's because of their general susceptibility to the virus. For treatment we use 2 tablespoons 3-4 times daily for adults and less for children depending upon their body weight.

So, the final key point is...next "flu" season remember your friendly elderberry.

You can order our PROBERRY CAPS (elderberry/larch/bioflavanoid product HERE!



You can order our PROBERRY 3 elderberry syrup product (great with kids!) HERE!





REFERENCES

Naikhin AN, Katorgina LG, Tsaritsyna IM, et al. Indicators of collective immunity to influenza depending on the blood group and sex of the population. Vopr Virusol 1989 Jul-Aug;34(4):419-23 [Article in Russian]

Aho K, Pyhala R, Visakorpi R. ABO associated genetic determinant in H1N1 influenza. Tissue Antigens 1980 Oct;16(4):310-3

Lebiush M, Rannon L, Kark JD. The relationship between epidemic influenza (A(H1N1) and ABO blood group. J Hyg (Lond) 1981 Aug;87(1):139-46

Sominina AA, Tsubalova LM, Karpova LS, et al. Genetic predisposition to latent influenza A virus in children with blood type B(III) as a possible cause of new epidemiologic strains in the countries of South-Eastern Asia. Vestn Ross Akad Med Nauk 1994;(9):21-4 [Article in Russian]

Fedorova GI, Slepushkin AN, Popova NS, et al. Correlations of the antigenic specificity of human blood with the levels of antihemagglutinins to influenza viruses. Vopr Virusol 1983 Jan-Feb;28(1):54-7 [Article in Russian]

Mackenzie JS, Fimmel PJ. The effect of ABO blood groups on the incidence of epidemic influenza and on the response to live attenuated and detergent split influenza virus vaccines. J Hyg (Lond) 1978 Feb;80(1):21-30

Mackenzie JS, Wetherall JD, Fimmel PJ, et al. Host factors and susceptibility to influenza A infection: the effect of ABO blood groups and HL-A antigens. Dev Biol Stand 1977 Jun 1-3;39:355-62

Frolov VK, Sokhin AA, Sotnik AY, et al. Polymorphism of human blood groups and incidence of influenza A/Hong Kong (H3N2). Acta Virol 1975 Sep;19(5):406-12

Karpova LS, Popova TL, Oleinikova EV, et al. Significance of persons with different blood groups in the influenza type A epidemic process. Zh Mikrobiol Epidemiol Immunobiol 1982;(11):86-91 [Article in Russian]

Waghorn SL, Goa KL. Zanamivir. Drugs 1998;55:721-25

Zakay-Jones Z, Varsano N, Zlotnik M, et al. Inhibition of several strains of influenza virus in vitro and reduction of symptoms by an elderberry extract (Sambucus nigra L.) during an outbreak of influenza B Panama

By John K. Harris

First there have been some questions about the use of either apple or pear concentrate in Proberry 3, as apple juice is an “avoid” for the O nonsecretor. As of the first of the year, only pear concentrate is being used as the base.

Second, the apple pectin, a source of soluble fiber in each of the Protein Blends, is a “neutral” category for all ABO secretors and nonsecretors, and is clearly stated as such in TYPEbase® 3. Apple pectin has been of concern to some people.

Third, the Secretor Wallet Cards (one for each ABO blood type, listing all “beneficials” and “avoids”) are now available for ordering from NAP. Having done the research for them, I have just begun doing the research for the Nonsecretor Wallet Cards. Hopefully we will have these available for you in the next few months. Now, for the Protein Blends.

In the following paragraphs, I’ll give you an overview of the unique formula for each Protein Blend, then look at the value of using whole food protein sources, consider the amino acid profile – particularly the branched-chain amino acids, and then discuss the unique component called Fibersol-2. By the time you finish reading, I think you’ll see why Protein Blends, with their unique, synergistic ingredients, can provide a health-enhancing benefit for people of all ages.

To begin, you can see by looking at the information at The Blood Store, linked from www.dadamo.com, or directly at www.4yourtype.com, or in the latest ‘4 Your Type Journal linked at either site, that Protein Blends are uniquely formulated, ABO-targeted, high protein content powders – Rice Protein and Egg Whites for the O; Soybean Protein Powder, Pea Protein Powder, and Rice Protein Powder for the A; and Whey Protein Concentrate, Rice Protein Powder, and Egg Whites for the B/AB. They have no added sugar, no fillers, are neutral in taste, and contain only pure, non-genetically altered, natural whole food sources.

But what makes them even more unique is that they each have nutrient cofactors such as Larch Arabinogalactan (a prebiotic, source of soluble fiber, and an immune system modulator), Bromelain (a proteolytic digestive enzyme and an anti-inflamatory), Apple Fiber and Pectin (both sources of soluble fiber), Lipoic Acid (a potent antioxidant), and a unique ingredient called Fibersol-2, which provides an additional source of soluble fiber. Beet Juice Powder and Vitamin A Palmitate, Natural Vitamin E Acetate, and Biotin round out the formulas in the A, B/AB, and O Protein Blends respectively.

Next, all protein sources used are from whole foods with their complete matrix of nutrients. In the A Protein Blend this is particularly important, because soy is one of the protein sources. I’ve observed that most other protein powders that use soy as a base, use a soy protein isolate, a concentrated fraction of soy, which boosts the protein value, but which can have a negative effect on certain hormone balances. Also in the A Blend, the level of protein has been kept at 15 grams per serving, rather than the 20 grams in the O and B/AB. As for the whey protein concentrate in the B/AB Blend, it is not the same as an isolate. The entire nutrient matrix is included in the concentrate.

Moving on to the amino acids, here’s a primer. They are the basic building blocks of the body. They carry oxygen throughout the body and are involved in muscle activity, they form antibodies to defend against invading bacteria and viruses, build cells and repair tissue, build nucleoproteins (RNA and DNA), and are part of the hormonal and enzyme systems. When digestion breaks down protein, the result is 22 known amino acids. Eight of them are essential, which means they cannot be manufactured by the body. The rest are nonessential, which means they can be manufactured by the body with proper nutrition.

Each of our Protein Blends contains 18 of the 22 known amino acids and all eight of the essential amino acids, and the profile and level of each amino acid is phenomenal. The essential amino acids are isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine. The nonessential amino acids that our Protein Blends contain are alanine, arginine, aspartic acid, cystine, glutamic acic, glycine, histidine, proline, serine, and tyrosine. It is important to keep in mind that these amino acids are what naturally occur from the whole food protein sources that form the basis for the Blends. They are not manufactured synthetically in a laboratory.

Here’s the amino acid breakdown for each Blend:

For the O Protein Blend (in milligrams): Alanine (1159), Arginine (1602), Aspartic Acid (1558), Cystine (759), Glutamic Acid (2507), Glycine (1052), Histidine (782), Isoleucine (996), Leucine (1511), Lysine (914), Methionine (784), Phenylalanine (1112), Proline (1110), Serine (1160), Threonine (924), Tryptophan (653), Tyrosine (1122), Valine (1055).

For the A Protein Blend (in milligrams): Alanine (717), Arginine (1165), Aspartic Acid (1448), Cystine (359), Glutamic Acid (2211), Glycine (693), Histidine (491), Isoleucine (700), Leucine (1163), Lysine (932), Methionine (357), Phenylalanine (839), Proline (709), Serine (818), Threonine (632), Tryptophan (326), Tyrosine (703), Valine (758).

For the B/AB Protein Blend (in milligrams): Alanine (1109), Arginine (1116), Aspartic Acid (1889), Cystine (607), Glutamic Acid (3066), Glycine (759), Histidine (602), Isoleucine (1098), Leucine (1810), Lysine (1356), Methionine (634), Phenylalanine (844), Proline (1208), Serine (1110), Threonine (1159), Tryptophan (482), Tyrosine (854), Valine (1111).

Now, let’s consider the branched-chain amino acids. Branched-chain amino acids comprise isoleucine, leucine, and valine – all part of the essential amino acid group. This group of amino acids helps to build and maintain muscle mass, and this group is needed during times of physical stress and intense exercise. As you can see from the profiles above, these amino acids are abundantly expressed in each Protein Blend.

As an aside, when I reflect on my first patient visit with Peter more than six years ago, I recall seeing a framed page of health recommendations he had in his office. One of these recommendations was for the use of branched-chain amino acids as a safe way to help build muscle mass. Considering all the sports supplements on the market today designed to help build muscle mass – many with pronounced side effects I’ve observed in a client/customer base in Maine, Protein Blends offer a safe way to help tone your muscles. And for body builders, adding in some of NAP’s Aromastat, might help even more.

Lastly, I think you should know more about the Fibersol-2 component in each of the Protein Blends. Fibersol-2 (also known as “digestive resistant maltodextrin”) is a soluble dietary fiber produced from cornstarch. It is NOT the same as the maltodextrin that is on the “avoid” list for the O secretor and nonsecretor, the A nonsecretor, the B secretor and nonsecretor, and the AB secretor and nonsecretor.

In basic terms, what makes Fibersol-2 different from maltodextrin is that the chemical bonds have been modified via a proprietary process that results in 90% soluble fiber rather than carbohydrate (regular maltodextrin).

In technical terms, Fibersol-2 is a “digestive resistant maltodextrin” produced by purposeful rearrangement of starch or hydrolyzed starch to convert a portion of the normal alpha-1,4 glucose linkages to random 1,2-,1,3-, and 1,4- alpha or beta linkages. The human digestive system effectively digests only alpha 1,4-linkages, therefore the other linkages render the molecule resistant to digestion.

About now, you’re probably wondering about the cornstarch source. Well, there are no corn lectins nor are there any corn residuals remaining from the original cornstarch source in Fibersol-2.

So why was it included in Protein Blends? In the U.S. nearly all people consume only half the recommended daily amount of fiber, which is approximately 25-35 grams. Protein Blend contains a modest amount of Fibersol-2 (as well as the other soluble fiber sources I’ve mentioned) to help fill this gap and to support overall intestinal health.

Additionally, Fibersol-2 has been shown to improve intestinal microflora, increase fecal volume and intestinal regularity, maintain a healthy gastrointestinal tract, prevent intestinal mucosal atrophy due to the long term administration of enteral nutrition (direct infusion into the intestines of nutrients in liquid form), increase Bifidobacterium in the large intestine, reduce the postprandial (after a meal) rise in glucose levels, lower serum cholesterol levels and triglyceride levels while not reducing HDL-cholesterol levels, and decrease fat in internal organs.

Furthermore, Fibersol-2 has low viscosity, is quickly and completely soluble, is completely transparent, has a clean taste, and maintains its stability in varying acidic conditions. For these reasons, Dr. D’Adamo has included it in each Protein Blend.

To recap, I’ve given you an overview of the formula for each Protein Blend, discussed the value of using whole food protein sources, presented you with their phenomenal amino acid profiles, highlighted the branched-chain amino acid component and its value in helping to build and maintain muscle mass, and defined the incredible benefits of Fibersol-2.

Dr. D’Adamo, in typical fashion, has once again formulated a unique, cutting edge natural product, that, because of demand, we are having a hard time keeping on the shelf at NAP. I think you’ll agree that Protein Blends are in a class by themselves.