Low Iron and Yeast Infections – Can Iron Deficiency Cause Yeast Infections in Women?

The question of whether or not there is a connection between low iron and yeast infection, particularly in women, is rather complex. But here, in simple language, you’ll find the answer as well as what actions to take.

Yeast infections are more common in individuals whose diets are usually low in iron. They are also very common in women during heavy menstruation when iron levels in the body diminish considerably. So there does seem to be a link between iron deficiency and yeast infections…

Yeast infections are caused by a yeast-like fungus called Candida albicans, which is normally kept under control by your body’s good bacteria. Only when it over-grows out of control does it turn into an infection.

So this good bacteria v bad bacteria ‘balance’ is important. But there are several things that can upset this balance. Two of them are a lowered immune system and friendly bacteria depletion…

1. Iron Deficiency and Your Immune System

One of the things that can affect your immune system is anemia which happens as a result of iron deficiency. So low iron, which leads to anemia, can compromise your immune system and so upset the delicate balance. This can then trigger an overgrowth of Candida leading to a yeast infection.

2. Bacteria and Iron Deficiency

Under healthy conditions, with optimum levels of iron, your beneficial bacteria work effectively. But so can the Candida, except that, the Candida needs ‘free’ iron to invade your body’s cells. And, in a healthy body, a protein called ‘Lactoferrin’ binds to the iron, so preventing the Candida from growing.

However, individuals with anemia have low levels of Lactoferrin. And because they have low iron their beneficial bacteria are less effective as well. So the balance is upset further still allowing the Candida to grow and spread.

So, if you suffer from low iron and you have a yeast infection then the two could be linked. For your general health in any case you need to get your iron back to optimum levels. And the best way is through diet…

Great sources of iron are; liver (especially), red meat, fish, poultry, eggs, whole grains, dark green leaf vegetables, peas, beans, potatoes, rice, and nuts. But ensure that the food you consume is sugar-free, because sugar is a staple diet of Candida.

You may also consider taking iron supplements but you must consult with your doctor before doing so. Another aid is vitamin C, which helps to absorb the iron. But again, talk to your doctor first to make sure that whatever you do is appropriate for your particular case, including your diet.

What Other Diseases "Masquerade" as Rheumatoid Arthritis? Part 2 – The Infectious Group

While rheumatoid arthritis (RA) is the most common form of inflammatory arthritis, the diagnosis is not always easy to make. The reason is that there are more than 100 different kinds of arthritis. Most of them involve inflammation. When a patient goes to a rheumatologist to get a diagnosis, there is a process of elimination in order to arrive at the proper diagnosis. This process of elimination is called “differential diagnosis.”

Differential diagnosis can be a difficult undertaking because so many forms of arthritis, particularly inflammatory forms of arthritis look alike. Generally it is helpful to divide the differential diagnosis of rheumatoid arthritis into two groups. The first group are the non-infectious diseases to consider and the second group are the infection-related conditions.

In part 1 of this article, I discussed the non-infectious causes of arthritis that need to be considered when assessing a patient with possible rheumatoid arthritis. In this article I will discuss those types of arthritis that are directly or indirectly due to infections.

Many infections can present with arthritis due to either direct inoculation of a joint (either from the outside or from a bloodstream infection) or due to autoimmune reactions. In many instances, infections lead to acute single joint arthritis; however, in some cases, chronic single or multiple joint arthritis can be present.

Missed infections can lead to significant complications; therefore, it is important to have a high index of suspicion for infection in any patient presenting with acute or chronic arthritis.

Here are some examples:

Gonococcal arthritis is an infection due to the organism that causes gonorrhea (N. gonorrhea). It usually affects a single joint (in 90% to 95% of cases). Symptoms include:

o Joint pain that migrates (jumps around) for 1 to 4 days;

o Pain in the hands/wrists due to inflammation of tendons;

o Sometimes a single joint can be inflamed;

o Fevers;

o Skin rash;

o Burning on urination;

o Lower abdominal pain.

The diagnosis of gonorrhea is made by taking the history and by culture or DNA polymerase chain reaction (PCR) analysis of areas of possible infection, including the throat, genitals, and anus. Since the organism that causes gonorrhea is difficult to grow, it can often be missed on culture. Gonococcal arthritis can usually be distinguished from rheumatoid arthritis (RA) by clinical presentation, blood tests, and cultures.

Lyme disease is a bacterial infection due to the spirochete Borrelia burgdorferi. It presents with a skin rash, swollen joints and flu-like symptoms, caused by the bite of an infected tick. Symptoms may include:

o A skin rash, often resembling a bulls-eye; the rash may be more widespread, though;

o Fever;

o Headache;

o Muscle pain;

o Stiff neck;

o Numbness and tingling

o Bell’s palsy

o Swelling of knees and other large joints.

The diagnosis of Lyme disease is typically made by blood tests. Standardization of Lyme tests has improved greatly in the last few years. If chronic single joint arthritis develops, joint fluid analysis or joint tissue biopsy may be necessary for diagnosis. Lyme arthritis can usually be distinguished from RA by clinical presentation and blood testing.

Acute rheumatic fever (ARF) is an inflammatory disease that may develop after an infection with Streptococcus, the bacteria that causes strep throat and scarlet fever. The disease can affect the heart, joints, skin, and brain. Symptoms include:

o Fever;

o Arthritis (mainly affecting the knees, elbows, ankles, and wrists);

o Skin rash and skin nodules;

o A peculiar movement disorder, called Sydenham’s chorea;

o Epistaxis (nosebleeds);

o Heart problems;

o Abdominal pain;

ARF is diagnosed by history, physical exam, and blood testing for antibodies against streptococcus. ARF and RA can have similar clinical features including arthritis and nodules. But, ARF can usually be distinguished from RA. For instance, rash and migratory arthritis (arthritis that moves from joint to joint) are unusual in RA. Blood tests are also useful for making the distinction.

Bacterial endocarditis (BE) happesn when bacteria from the skin, mouth or intestines enter the bloodstream and infect the heart valves and heart lining. Symptoms include fever, chills, and other flu-like symptoms as well as unexplained weight loss and weakness. Diagnosis is made by blood cultures and ultrasound imaging of heart valves. Rheumatoid factor can be elevated in endocarditis, so it is not useful for distinguishing BE from RA.

Arthritis may be a symptom of many viral illnesses. The duration is usually short. Clinical features in adults include:

Joint symptoms occur in up to 60%. Joint pains are more common than true joint inflammation. The joint pains usually don’t last long. They are symmetric, and affect small joints of the hands, wrists, knees, and ankle joints. Morning stiffness and swelling can be present. A rash may be present

The most common cause of viral arthritis is probably Parvovirus B19.

Diagnosis of viral arthritis is usually made by blood testing.

RF testing is not helpful in distinguishing between hepatitis C infection and RA because RF levels can be elevated in patients with hepatitis C. However, in these situations, testing for anti-cyclic citrullinated peptide (anti-CCP) can be useful since these antibodies are not significantly elevated in hepatitis C infections.

Alcoholism in the Irish Culture


Experience with alcoholics has put this writer in touch with various clients of Irish decent, all of whom have shared similarities in their descriptions of alcohol in their Irish culture. They describe that alcohol is drunk in excess at weddings, at funerals, on holidays, and on sad days. Alcohol is most appropriate on Saturdays and Sundays; and Mondays, Tuesdays, Wednesdays, Thursdays, and Fridays. Sober clients who are otherwise not so careful with “people, places, and things” still avoid the Irish Day Parade like the plague. What is the relationship between Ireland and Alcohol in context of history, social aspects, and medical considerations?

Historical Context:

As will be explained, the retail price of alcoholic drinks has consistently been considered an important regulator of alcohol consumption and by implication, a method of controlling the amount of excessive drinking. Regulating alcohol patterns has been a debated issue in Ireland as far back as 1791 when it was actually debated in the Irish parliament. Apparently the problems of alcoholism were rampant in Ireland already back then. At that time, the “Gin Act” in England was used as a proof that a parliament could regulate production and sales to help sober a country. This issue has never been resolved and while at the beginning of last century poverty was blamed for excessive drinking, nowadays affluence is frequently mentioned as a cause. These days, the popular mindset is described in the expression, “Alcoholism comes in people and not in bottles.” Irish parliament is still very much uninvolved in alcoholic litigation for various cultural, religious, and political reasons. These will all be touched upon again in farther discussion on the causes and trends of Irish drinking habits (Blaney, 1974).

How much do the Irish drink?

It is significant to mention that in spite of the numbers supporting the notion of higher alcohol consumption with Irish drinkers, a significant proportion of the Irish population do not drink any alcohol at all. In numerous studies, almost three times as many Irish citizens reported that they had not consumed any alcohol at all during the past 12 months than as in any Scandinavian countries and almost twice the abstinence rate as those reported in Germany, UK, France, and Italy (Ramstedt & Hope, 2003).

While Ireland has the highest level of abstinence amid the aforementioned countries, it also boasts twice as high levels of alcohol consumption compared to those same countries. This means that those who do drink in Ireland drink much higher quantities per person as other regions (Ramstedt & Hope, 2003). The most recent statistics of the World Health Organization (2011) reports that Irish drinkers consume an average of 14.41 liters of alcohol per year, the highest among all countries mentioned thus far. This amount is measured in the amount of pure ethyl alcohol. In comparison, the average drinker in the United States only consumes 9.44 liters. That is approximately 5 liters of alcohol less per person than drinkers in Ireland. Amongst the Irish that do drink, the heaviest drinking occurs with Irish second generation (Mullen, Williams, & Hunt, 1996). Ramstedt & Hope (2003) state that the higher overall level of drinking in Ireland is directly associated with higher alcohol-related mortality related to deaths from liver cirrhosis, accidents, and homicide.

Amazingly, daily drinking in the same countries mentioned is lowest in Ireland in spite of the high alcohol consumption per year. Only 1.6% of Irish men drink every day. Comparatively, 42% of men drink every day in Italy, 21% in France, and 12% in Germany. These percentage differentiations are similar among women as well (Ramstedt & Hope, 2003). This would seem to suggest that while the Irish may not drink every day, when they do drink it is in vastly greater quantities per drink.

Why do Irish Drink? Causes and Trends:

Blaney (1974) describes various explanations as to why there is such a link between the Irish and Alcohol. Irish weather and climate is commonly believed to be an important cause of Irish overindulgence. The basic idea is that the damp climate and inclement weather cause people to seek modes of stimulation such as alcohol. This theory was especially prevalent in the mid nineteenth-century.

Lack of quality food has also been blamed. Theorists seek to show how the Irish have a general tendency for substitute drinking for eating in response to certain situations. Additionally, a lack of alternative drinking establishments has long been blamed in Ireland for excessive consumption of alcohol. It is believed that the development of the Cafe and Coffee-House Movement towards the end of the last century occurred in direct response to this association. The political rhetoric of the time included statements like “there are few places to go except the pub” and “there is nothing else for young people to do on Friday nights than to start drinking.”

Another cultural dynamic in Ireland is the pervasive availability of open alcohol eateries known as “public houses” or “pubs.” Ireland also has very loose legal constraints monitoring public alcohol sales in groceries. The corresponding modern view is that availability of alcohol in public houses and supermarkets leads to excessive drinking – especially in women. On these fronts, licensing laws regulating the availability of alcohol are rapidly re-evolving and researchers are closely following correlations between alcohol litigation and excessive drinking trends.

Obviously, these considerations of pinpointing availability of alcohol – or unavailability of other beverages – as the causes of excessive use of alcohol in Ireland is somewhat faulty. While these may explain the continuation or perpetuation of high rates of alcoholism in second generation Irish youth, it fails to explain how the evolution of an exclusive cultural relationship with alcohol was initiated to begin with. These factors are significant however, in understanding causes for new trends of alcoholism in modern Irish culture.

There is another popular theory that Irish people are physically and psychologically prone to alcoholism. No specific genetic theories have yet become available, but at least one researcher states that “the taste of alcohol in the mouth is more attractive to the Irish than to others.” Recent psychological studies point to an “Irish Psychological Constitution” that causes an actual predisposition to alcoholism (Blaney, 1974).

It will be explained further that Bales (1962) understood that the social patterns of Irish drinking actually predisposes the culture to higher rates of alcoholism. In this context, Irish political forces are attempting to counteract the Irish practice of drinking in large groups where each person gets a turn to buy the rest of the group a round of drinks. This is an old Irish social custom which is still being implicated today and seen as a large hurdle in the fight against alcoholism.


Butler & Jordan (2006) explain the religious influence of alcoholism in Ireland. Ireland is a Catholic based country. Catholicism considers Protestants as one of the largest threats to traditional Catholic culture. The idea of self-control, temperance, and abstinence is a very Protestant initiative and traditional Catholicism is quite skeptical of the entire notion. In fact, it will be explained later how the Irish Church was against the establishment of AA for this very reason.

Mullen, Williams, and Hunt (1996) explore the common stereotype of the Irish and heavy drinking within this religious context as well. Quoting O’Connor (1978) it is posited that the historical ideas about the medical treatment for alcoholism in both the Irish and the English cultures were similar as both were eventually affected heavily by the religiously orientated temperance movement. As was mentioned, this is in spite of resistance from the Irish Catholic Church (Butler & Jordan, 2006). Mullen, Williams, and Hunt (1996) quote other studies as well finding Irish and English drinking in American cities to be fairly similar. Differences were mainly in comparison with Italians and Jews and with English from a rural or southern Protestant background with strong Baptist and Methodist affiliations. This strongly suggests that religion plays a role as well in drinking patterns and would therefore be an important clinical factor. Indeed, based on data from two studies carried out Ireland, one quantitative, the other qualitative, significant differences according to religious affiliation is shown.

The association of the Irish with Catholicism is strong if not overwhelming in many areas. Religious identity is stronger in Ireland than political identity and conflict in Ireland is more often religious than political. Theorists do in fact hypothesize a close link between Catholic culture and the Irish drinking. Studies show that in Irish-American communities, Irish Catholic drinking practices and problems were seen to relate to a somewhat tolerant normative religious structure which begins a cycle of abusive drinking and “reinstatements” like confession, forgiveness, and re-incorporation into group life that is easily transferable from religious to secular domains. Similar to Butler & Jordan (2006), Mullen, Williams, and Hunt (1996) also quote clear research literature showing that high levels of alcohol consumption are often assumed with Catholic subcultures being viewed as encouraging permissive drinking norms while the Protestant cultures are more ambivalent.

Irish and Jews:

Levin (1995) explains that while we have seen how the Irish have both high levels of consumption as well as significantly high levels of abstinence, Jews were found to exhibit neither high levels of consumption or abstinence. While Jews were found to drink almost exclusively at home with family or as part of religious ceremonies, the Irish rarely drink at home as the majority of drinking done in Ireland is in public houses, as has previously been mentioned. Lastly, the Irish mindset states that getting drunk is excusable and a socially acceptable form of relief and escape, while traditional Jewish values suggests that to get drunk in this manner is “unjewish.” Jewish drinking is sacred, formal, and ceremonial.

Bales (1962) studied and compared the ‘convivial’ or ‘utilitarian’ drinking of the Irish with the ‘ritual’ drinking of the Jews. He defines four categories or attitudes. They are abstinence, ritual, convivial, and utilitarian. Defining Irish as convivial and utilitarian means that there is no significance to one’s drinking outside of social solidarity and self gratification. The ritual consumption of Jewish drinkers however represents the use of alcohol as a symbolism of communion with God. The theory is that ritual drinking patterns can inhibit and even inoculate members against alcoholism, while utilitarian drinking may actually predispose the drinkers in that culture to eventual abuse and dependency. This theory seeks to explain how the differences in mindset evolved within these cultures.

Alcoholics Anonymous:

The Irish religious arena played a central role in the early foundation of AA in Ireland as well. Butler & Jordan (2006) explain the exact relationship in detail. Historically, AA was quickly accepted in strong Protestant-oriented traditions. Ireland is predominantly Roman-Catholic or Irish- Catholic. Catholicism however, took issue with AA on a few fronts. First and foremost was the fact that AA was conceived through tenants of a non denomination Christian group called the Oxford Group.

Additionally, Irish Catholic bishops favored a centralized teaching authority and found the AA approach heterodoxical. This was because of AA’s use of a Higher Power and “God as we understood him” in addition to individual group autonomy and the group conscience. These were seen as a rival to the structure and moral monopoly of the Catholic Church in Ireland.

Lastly, all religious elements in Ireland – even the more “progressive” Catholic Temperance League – were apposed to the disease concept of alcoholism. Traditional belief understands alcoholism as volitional in nature. People drink because they chose to. If they chose otherwise, they could become and remain abstinent if they so desired – particularly by using their Church membership to invoke God’s help.

On November 18, 1946 an AA member from Philadelphia, Connor F., established the first AA meeting in Dublin. This was the very first AA meeting held in all of Europe. Connor however, faced the following large hurdles. He first approached religious clergy who informed him there are no alcoholics in Ireland. He then approached medical hospitals who told him to take his [big] book and never come back.

Although Connor himself was protestant, ninety five percent of Ireland at the time was Catholic. No Catholic church was willing to host an AA meeting and no Catholic was willing to even enter a protestant church – even if only to attend an AA meeting. AA could not find any clergy or newspaper to give them positive publicity. The fact that AA originated in the USA was an additional hurdle. The Irish considered the US to be “the land of freak religions” and wanted no part in this new American movement.

The secretary of Dublin’s AA group was a man named Sackville who had been asked to retire from the English Army prematurely because of his pervasive alcoholism. In January 1972, Sackville and an English Catholic member of AA obtained a private audience with Pope Paul VI. The Pope described AA as “fine work, a real apostolate.” He gave AA his blessing and stated that he would keep AA in his prayers. With endorsement from the Pope, AA in Ireland no longer had any real fear of being censured by the local Catholic Church.


Bales, R. F. (1962). Attitudes Towards Drinking in the Irish Culture, 157-187. Found in Pittman, D. & Snyder, C. Society, Culture, and Drinking Patterns. Wiley.

Blaney, R. (1974). Alcoholism in Ireland: Medical and Social Aspects. Journal of the Statistical and Social Inquiry Society of Ireland 23(1). Retrieved March 2, 2011

Butler, S. and Jordon, T. (2006) Alcoholics Anonymous in Ireland: AA’s first European Experience. Addiction, 102(6), 879 – 886 Retrieved March 2, 2011

Levin, J. D. (1995). Introduction to Alcoholism Counseling: a Bio-Psycho-Social Approach. Taylor & Francis.

Mullen K., Williams R., and Hunt K. (1996) Irish descent, Religion, Alcohol, and Tobacco Use. Addiction, 1996, 91(2), 243-254. Retrieved March 2, 2011

O’Connor, J. (1978). The Young Drinkers. London, Tavistock.

Ramstedt M. & Hope A. (2003). The Irish Drinking Culture – Drinking and Drinking-Related Harm, a European Comparison. Retrieved March 2, 2011

World Health Organization (2011). Global Status Report on Alcohol and Health. WHO Press. Switzerland. Retrieved March 2, 2011

Tickling – Good Clean Fun – Or Abuse?

Probably everyone in America has been tickled and/or has tickled someone else in his or her lifetime. And we may have a range of emotions attached to the experience, from very good to very bad.

Why do we do it? Do people like it or hate it? Like many things in life, tickling can be used for either benefit or harm.

So we know that people always laugh when tickled, and that laughter is good for us. Studies have shown that laughing increases blood flow and immune response; lowers blood pressure, risk of heart disease, depression, anger, anxiety, and stress; and induces relaxation and sleep.

Yet laughing is simply not funny when it happens in the context of abusive tickling. But wait a minute–can tickling really be called abuse? Some children beg to be tickled, and since children don’t request things they hate, they must enjoy it! Certainly they like the attention, the physical contact, and the pleasurable sensations associated with laughter.

But there’s a dark side to tickling. The problem stems from the fact that laughter is generally a sign of pleasure, so it is assumed that the person being tickled is having an outrageously good time of it. But the laughter resulting from being tickled is a reflex, and the person being tickled cannot stop. While some people may be ignorant of the fact that their victim doesn’t like it, others know and don’t care. Consider these comments I found on a question-and-answer site (I’ve changed some wording to protect the identity of the posters):

“The tickler has hijacked your body and you are powerless.”

“Excessive, forceful tickling for a prolonged period is a malicious act with intent to torture.”

“I honestly believed that [this adult] was very jealous of me and was trying to kill me.”

Some stated that they were tickled until they cried, vomited, choked, and/or wet their pants. It’s also noteworthy that in my research for this article, the first few results that came up for “tickle abuse” were for, shall we say, adult-oriented websites!

Tickling actually has been used as a form of torture in history. Both the Han Dynasty in China and ancient Rome used this practice, one of the benefits being that it left no mark on the victim! There are anecdotal reports of people being driven insane by being tickled, and of laughing unto death by heart attack, aneurysm, or some other pre-existing weakened condition. It cannot be stated unequivocally whether or not it’s possible to be tickled to death.

If tickling is so awful, why do we laugh? The answer includes these factors:

1. nerve stimulation (an innate reflex)

2. trust (we laugh only when the tickler is someone we know)

3. surprise (we can’t tickle ourselves)

Beyond these, it seems science doesn’t know for sure why we laugh when tickled. So what kind of sense are we to make of the tickling phenomenon?

Here’s what I see:

In modern America, tickling is usually done in the context of a friendly or loving relationship–parent/child, boyfriend/girlfriend, etc. So it would seem that it is usually intended as a bonding experience, and the resulting laughter confirms that it’s a pleasurable experience. It is also often done by a perpetrator who is bigger and stronger, or sometimes in pairs or groups of ticklers who “gang up” on the victim, which changes the picture somewhat.

Once the victim is laughing so hard as to be unable to catch his or her breath, the victim cannot signal “stop.”

Here’s how to avoid being a “tickle abuser”:

1. Observe if the person being tickled is still smiling at the end of the tickling session–or if he is angry, sullen, embarrassed, and/or in pain.

2. Ask the person before or after–not during–a tickling session if she really enjoys it. Don’t take “yes” at face value. Read the body language, facial expression, and tone of voice. She may be saying yes just to please you, or as a result of social pressure. (“Don’t be such a spoilsport.”) Pre-arrange a “stop” signal.

3. Ask yourself if you’re willing to submit to a role reversal. Now, this isn’t fair if the person you’re tickling is much smaller–a child or a girlfriend, say–so you’ll need to be willing to submit to a “team” of ticklers or a substitute tickler. Keep in mind that the other person may be more ticklish than you, so even this isn’t a definitive test of the appropriateness of the tickling.

Finally, you should consider that your victim’s experience with tickling may carry over into later relationships. Your child may resent you, and you may not know why. He may grow up to be bigger than you and find ways to retaliate. She may have a hard time trusting male partners, fearing that they may turn out to be abusive ticklers.

Abusive tickling is not funny. Make sure your motives and methods are pure before giving in to the urge to tickle someone.

Benefits to Using Apple Cider Vinegar for Your Dog’s Health

I am sure you have heard of using apple cider vinegar for natural remedies in people, but have you heard of using it for your dog’s health? Apple cider vinegar can help with digestion, gas, constipation, bladder stones, and urinary tract infections. It is used to deter insects such as mosquitoes, fleas and tics. It can relieve skin conditions, and even take away the odor of skunk.

Many herbalists recommend the use of vinegar. It is recommended that you buy vinegar made from cold pressed, organically grown whole apples to get the benefit of the naturally occurring enzymes.

In it’s natural form apple cider vinegar is a natural antibiotic, antiseptic, and deodorant. It helps to remove tooth tartar; prevents tooth decay and hair loss (even mange), prevents and heals gum disease.

Have I listed enough benefits to using apple cider vinegar, yet?

There are many other benefits to using apple cider vinegar. It is known to reduce common infections, aid whelping, improve stamina, prevent muscle fatigue after exercise, increase resistance to disease, and protect against food poisoning. Cider vinegar is rich in the vitamins, minerals, and trace elements found in apples, especially potassium; it normalizes acid levels in the stomach, improves digestion and the assimilation of nutrients, reduces intestinal gas and fecal odors, helps cure constipation, alleviates some of the symptoms of arthritis and helps prevent bladder stones and urinary tract infections.

You can feed apple cider vinegar daily to your dog to keep him healthy. Add to the food or water. You may need to gradually increase the amount. Start with a few drops and slowly increase each day until reaching the recommended daily dose below.

The approximate amounts recommended :

1 teaspoon – dogs up to 14 pounds
2 teaspoon – medium dogs -15 to 34 pounds
1Tablespoon – large dogs-35 to 84 pounds

By mixing in the food or water of your dog, apple cider vinegar will restore the acid/alkaline balance of his digestive tract, getting rid of the brown spots in the lawn. A correct PH balance also helps keep away the fleas, black flies, ticks, and other external parasites. Your dog will have less chance of getting ringworm, staph infections, streptococcus, and mange. If your dog already has these problems sponge your dog’s skin with a mixture of equal parts of apple cider vinegar with equal amounts of warm water. If you prefer, you can use this mixture in a spray bottle to thoroughly wet your dog.

A NOTE OF CAUTION: Do not use apple cider vinegar if your dog is sensitive or allergic to yeast or if he has a chronic yeast infection. Also, do not give to dogs with irritated intestines.

Gastrointestinal Drugs, Know the Danger of Drugs – Part 1

Gastrointestinal Drugs – Part 1

Considering the average diet of most Americans, it is no wonder the country is prone to stomach chaos, indigestion woes, gas attacks and ulcer pains. Doctors suggest healthier changes in diet for better gastrointestinal performance, but instead of giving up bad habits, the majority of people continue to give their stomachs good reason for upset. Rather than choosing good nutrition, they depend on gastrointestinal drugs to calm their troubled insides only to continue taking poor dietary choices. It is an endless cycle plagued with a plethora of potential problems from unpleasant side effects to irreversible damage to one of the body’s most vital systems. Gastrointestinal drugs – such as antacids and anti-flatulents, laxatives, stomach acid blockers and ulcer drugs – may help the junk addict rationalize a substandard diet, but the body is not so easily fooled by these chemical dangers.

Antacids and Antiflatulents (Anti-gas)

An antacid is a common follow-up to a disagreeable meal, carelessly consumed as if it were a mere after dinner mint. However, the contents of antacids deserve cautious consideration. Many antacids feature aluminum hydroxide, an ingredient used to treat stomach acid and other antacids contain a combination of aluminum hydroxide, magnesium hydroxide and simethicone. Unfortunately, aluminum can cause bone damage, and the magnesium found in antacids can cause severe diarrhea. Doctors strongly discourage older adults with severe kidney disease from using magnesium antacids. Other adverse side effects caused by antacids ingredients include painful urination, dizziness, irregular heartbeat, mental changes, muscle weakness, diarrhea, vomiting and stomach cramps.

Not only found in antacids, the combination of magnesium hydroxide, aluminum hydroxide and simethicone is also taken as an antiflatulent (anti-gas) drug. But, according to physicians, there is no evidence that simethicone alone or combined with other ingredients effectively treats excess gas. In fact, physicians believe that treating excess gas is by and large a futile process. Suffers from excess gas may actually have a bloated feeling from overeating or discomfort from eating the wrong food. In this case, no anti-gas drug will help because the problem has nothing to do with gas. In general, the passing of gas is no cause for medical concern, but rather, a cause to improve diet.


Every year, Americans spend $725 million on laxatives (constipation 1). As with antacids and antiflatulents, many people take laxatives far more frequently than necessary. This is dangerous for several reasons. First, laxatives can cause lasting damage to the intestines and can interfere with the body’s use of nutrients. Second, they can be habit forming. Of taken for long periods, they inhibit the body’s natural ability to digest food properly, causing consumer dependency. The unpleasant side effects are numerous and scientists are continually discovering additional causes for concern. For example, the laxative ingredient danthron was recently recalled in the United States because of its cancer-causing possibilities. According to physicians, laxatives should not be used to “clean out the system” or to promote intestinal regularity, a process the body generally controls naturally.

Unfortunately, even those with healthy diets are not immune to occasional constipation. Although it may be bothersome, according to physicians, constipation itself usually is not serious. For most people, dietary and lifestyle improvements can lessen the chances of constipation. A well-balanced diet that includes fiber-rich foods, such as unprocessed bran, whole-grain breads and fresh fruits and vegetables, is recommended. Drinking plenty of fluids and exercising regularly also help to stimulate intestinal activity.

Is Mastic Gum Effective Against H Pylori?

Mastic gum is a tree resin obtained from the Pistacia lentiscus tree, which is grown on the island of Chios in Greece. Of all the natural products used to treat H pylori, mastic gum is probably the best known.

Several studies support the contention that mastic gum has an anti-bacterial action against H pylori. However these studies are often performed in vitro, which means in a test tube or petri dish, not inside the human stomach. We must always acknowledge that these studies do not necessarily represent exactly what happens in the stomach and intestines!

When I had H pylori, the natural treatment protocol I originally learned in my functional medicine training involved the use of mastic gum for 60-days at a relatively high dose (4-6 capsules per day).

This treatment method works very well for many people as long as the dosage guidelines and program duration are followed accurately. All too often, people do not take large enough doses and they often believe that just a few days of taking mastic gum is enough. This is not the case.

However this method of H pylori treatment did not work for me. Instead, I used Matula Herbal Formula for 30-days and this program resolved all my symptoms very quickly.

But don’t let that put you off using the gum as H pylori treatment because it DOES work for many people. Despite my poor reaction to the mastic gum program, there is quite a large body of research demonstrating its efficacy against H pylori and mastic gum has been shown to kill H pylori in vitro.

As well as taking mastic gum at a high enough dose to be effective and for a long enough duration, it is also important to choose products that contain only the highest quality mastic gum.

One of the biggest problems with the natural supplement market is that there are many different versions of the same products, with each company claiming that their product is best. So which one do you choose?

I recommend that you DO NOT go for the cheapest products, no matter how attractive it may be. Generally, you get what you pay for.

The cheaper supplements are generally of significantly lower quality and this can actually cause you to spend MORE money in the long run. It may also take you a lot longer to deal with your symptoms. Don’t waste energy, time and money on cheap supplements. It won’t serve you in the long run.

The mastic gum products we recommend in our practice are Gastromend-HP by Designs For Health and Mastika by Allergy Research Group. These are available from distributors in North America and the UK.

In our experience, you can make mastic – and all other natural treatments – more effective by changing your diet. Avoidance of key foods like milk, gluten and soy can reduce stomach and intestinal inflammation. This allows the natural products to work more effectively against H pylori.

As with everything that you put in your mouth, mastic gum has the potential to cause a reaction.

Just as foods like gluten, milk, lactose and a whole host of other foods can cause problems in individuals as well. I’m sure you heard of people who had serious reactions to seemingly harmless foods like peanuts, crab and strawberries?

We also know that medical drugs – including antibiotics and antacids – can cause side effects for some people as well. Just because mastic gum is a ‘natural’ product, it doesn’t mean that it will not cause problems for some people.

Unfortunately we don’t have a crystal ball to predict what will happen, so the only way to know whether mastic gum or any other product suits you is to try it.

If you feel any adverse effects whatsoever, stop taking the product and seek professional guidance on alternatives.

H Pylori Infection Causes Gastritis

My Mother died aged just 60. When doctors performed her autopsy, they reported that she had been suffering severe gastritis and bleeding of the stomach and small intestine. In ten years of medical care, nobody had bothered to check her stomach for the presence of damage.

My Mother died as a result of septicemia: an infection developed in her psoas muscle, burst and allowed the infectious bacteria to enter her brain. It is fairly clear to me that the infectious organisms that caused the sepsis broke into her circulation through her damaged stomach and intestine.

This is a serious topic!

Gastritis simply means “inflammation of the stomach”. H pylori infection is the leading – but not the only – cause of gastritis.

In fact, any word that ends in ‘itis’ means inflammation. For example, colitis is inflammation of the colon, arthritis is inflammation of joints, uveitis is inflammation of the eyes.

Most of the pain people experience is caused by inflammation. If tissues in your body are inflamed, you’ll tend to feel pain there.

However, inflammation does not always cause pain and this is one of the most important lessons you can learn regarding your health because “silent” inflammation causes most of the diseases that afflict the Western population.

Chronic, long term inflammation can lead to cancer, heart disease, diabetes, depression, IBS, autoimmune disease and many other disease processes. These diseases don’t appear over night, they are the result of a long term process.

H Pylori, Gastritis & Stomach Pain

H pylori infection always causes inflammation. This inflammation is generally located in the stomach and small intestine, where it is known as gastritis and duodenitis, respectively.

In some folk, gastritis and duodenitis will cause them to experience pain consciously, but other folk will not feel this pain. This is similar to the situation in celiac disease, where some people feel extreme pain upon eating gluten, whereas others feel no discomfort whatsoever, even though the gluten causes huge amounts of inflammation in the intestine.

Individual differences in the way we react to the H pylori infection, in addition to the specific strain of H pylori involved, seem to be the primary reasons why some folk develop stomach pain, heartburn and other uncomfortable symptoms while others do not.

The most common symptom of gastritis is a burning pain that occurs between the breastbone and the bellybutton. The pain can either be worsened or made better by food.

Nausea, loss of appetite, bloating and other common digestive symptoms may also be signs of gastritis. Severe gastritis can lead to stomach ulcers or bleeding, both of which must be treated by a medical professional.

If you have severe pain, burning, nausea, vomiting – especially if you vomit blood or coffee-like granules – or if your bowel movements are unusually dark, seek medical attention immediately as you may have bleeding in your stomach or intestines.

Three Main Causes Of Gastritis

There are three major causes of gastritis:

First, H pylori infection is believed to be the number one cause of gastritis.

Second, NSAIDS such as Aspirin, Ibuprofen (Motrin, Advil), Naxopren (Aleve, Naprosyn) are used to treat pain syndromes such as arthritis and headaches. They are available over the counter, without prescription.

They work by decreasing the formation of some of the body’s pain signalling chemicals, known as prostaglandins. Gastritis and bleeding of the stomach are known to be side effects of using NSAIDS. For example, in one study it was found that the use of one adult strength aspirin per day triples a person’s risk of being hospitalised for a major gastrointestinal bleed.

Third, several diet and lifestyle factors may cause or contribute to the development of gastritis. Here are some of those factors:

• Alcohol consumption (alcohol is a major irritant of the GI tract)

• Cigarette smoking

• Dehydration

• Eating smoked, pickled and processed foods, for example bacon, salami, pickles, vinegar). Processed meats that contain nitrates and nitrites are preservatives are especially problematic.

• Spicy foods such as chilli

• Greasy foods containing processed vegetable oils

• Consuming gluten-containing foods (from wheat, rye and barley)

• Cow’s milk products, especially when they are pasteurised

• Sugar consumption

• Coffee drinking

• Food allergies: common triggers include cow’s milk, wheat, corn, yeast, nuts, eggs

• Stress (yes, stress has been shown to directly cause inflammation)

Overcoming Gastritis

Overcoming gastritis is not difficult. If you have digestive pain above your bellybutton, the chances are that you have gastritis.

So first, check your lifestyle against the factors listed above and correct any of these that need correcting. Remove problematic foods, stop smoking and talk to your doctor about whether you need NSAIDs.

If this does not relieve your symptoms, make sure that get a test for H pylori. You can get a test from your doctor. We recommend that you two tests: a stool antigen test and a urea breath test.

If H pylori is detected in your testing, you must take steps to eradicate the infection using triple therapy antibiotics or a well-designed herbal protocol such as the one I used when I had H pylori.

Once H pylori has been successfully eradicated, substances that are helpful in healing a damaged stomach and intestinal lining include DGL, zinc-l-carnosine, l-glutamine, cysteine or n-acetyl cysteine, gamma-oryzanol, colostrum and probiotics.

If you are experiencing very severe symptoms, I recommend that you ask for an endoscopy examination from your doctor or specialist. The endoscopy procedure can help you identify how severe your gastritis is. It can also determine whether you have developed stomach, or peptic ulcers, Barrett’s esophagus, atrophic gastritis and other conditions, including cancer. A biopsy can also be taken during the endoscopy procedure to identify H pylori infection.

Do not underestimate your body’s messages. If you have pain in your digestive system it means there is something wrong. H pylori can cause stomach cancer if it is left untreated. So what begins as simple gastritis can end up causing very serious problems.

Please don’t take chances. Alter your diet and lifestyle habits and, if this does not bring relief, seek medical attention immediately.

What Are the Common Symptoms of Gastritis?

Symptoms of Gastritis cover a large range. Know them to be able to identify Gastritis. Gastritis is not a disease, it is a condition that can be caused due to many reasons.

What is gastritis? Gastritis refers to the irritation or inflammation suffered in the stomach lining. It can be an acute or a chronic condition. Sometimes it is a part of other diseases or conditions.

The symptoms of gastritis can be very misleading. Sometimes a very minor inflammation can cause severe symptoms and at the same time severe inflammation may cause minor symptoms. The severity of the condition can only be judged after an endoscopic examination of the stomach has been performed by the doctor. An endoscope is a like an optical fiber with a minuscule camera at its end, which is introduced into the patient’s stomach to view the conditions inside.

This is especially so in the case of elderly patients. They may come into hospital with internal bleeding of the stomach without ever having suffered from any symptoms of gastritis before this particular incident.

Gastritis is a very common condition and it has been observed that almost 10% of the patients brought into emergency for abdominal pain are suffering from it.

One of the first symptoms that alert a person is discomfort or pain in the upper abdominal region.

The pain that one suffers due to gastritis is very typical. It may be felt in the pit of the stomach. People have described the feeling as cutting pain from front to back. The pain has been described as soreness, gnawing, aching or even burning sensation. It may feel as if it is cutting, stabbing or gnawing at you.

The other symptoms of gastritis include belching, nausea accompanied with vomiting, blood in the vomit, bloating, and an uncomfortable feeling of fullness and burning in the stomach.

The vomit could be clear, yellow or green. If the case is severe we may expect a bloody vomit and in moderate cases streaks of blood.

If the gastritis is particularly bad, there may be bleeding in the stomach too. This is marked by symptoms like sudden sweating, pallor or racing heart beat. Other symptoms could be feeling of faintness, short breath, and severe pain in chest or stomach. The characteristic symptom is vomiting blood. The patient may also suffer from bloody stools or sticky foul smelling stools.

The other symptoms that the patient might suffer from are black stools, a significant loss of appetite, stomach cramps, persistent fever, and lethargy, fetid taste in mouth, indigestion, diarrhea, and belching.

These symptoms of gastritis may or may not be present in a person suffering from gastritis. Sometimes the patient will realize this condition only when it has reached a severe state, where bleeding has begun. This is a marked aspect of patients on the wrong side of sixty. This condition may sometimes be caused due to excessive drinking or even because of aspirin consumption. It can be a part of other medical conditions too.

Tear Gas Orthochlorobenzylidenemalononitrile

Agent CS (Orthochlorobenzylidenemalononitrile) was first prepared in 1928 by two American chemists, Ben Corson and Roger Stoughton. (The CS initials were taken from the first letters of the names of the discoverers). However, it remained until 1956 for the British CBW laboratory at Porton Down, the Chemical Defense Experimental Establishment, to develop CS as a riot control agent. CS was first used on a large scale by the British in the Cyprus riots. In 1960, CS was officially adopted by the United States Army for use in riots.

CS in its pure form is a white crystalline powder resembling talcum powder. It is classified as an irritant agent and lachrymator. Since it is made of solid particles, it must be carried through the air by an agent or expelled in a fine dust. The odor is rather pungent.

CS causes burning and lacrimation of the eyes as well as irritation of the skin and respiratory system. The burning effects of the eyes and skin will be similar to CN and the irritation of the respiratory system will result in sneezing. It could take many seconds before the effect of CS is realized. CS is most irritating in a humid climate and on a moist skin surface. Anyone who has lost his sense of feeling because of the influence of narcotics or alcohol will not be affected by CS.

CS is a lachrymator and sneeze producer at levels as low as 0.05 mg/m3. The powder CS is designated CS1 and is much more durable than the aerosol form of the agent. As a further refinement, CS1 is coated with silicone to extend its field persistence up to several weeks; the weatherproofed variety is called CS2.

Being extremely persistent, CS causes a severe area decontamination problem. Particles disseminated by any of the standard means of dispersion will adhere to the person, clothing, furnishings, or fixtures for long periods. Humid conditions will cause the odor and irritant effect to linger indefinitely.

Decontamination is achieved by using an alkaline solution. A solution of water and 5% sodium bisulfite is usually employed for decontamination.

CS is less toxic than CN and has only transient effects on the eyes. However, both CS and CN cause dermatitis and are sensitizers that may cause very serious allergic reactions upon repeated exposure. Toxicological tests demonstrated that animals dying after exposure to CS show increased counts of goblet cells in the respiratory tract and conjunctiva (the mucous membrane in the eyes, lining the eyelid and covering part of the eyeball), necrosis (the death of cells) in the respiratory and gastrointestinal tract, pulmonary edema (lungs filled with fluid), and hemorrhage in the adrenal. Death results from impaired oxygen transfer to the blood stream as a result of edema, hemorrhage, and obstruction of the air passages in the lungs. In the case of a substance such as CS, attention must be directed to the breakdown products that will occur in the human body. Cleavage or hydrolysis into malononitrile and ortho-chlorobenzaldehyde is a reaction that is 50% complete in about ten minutes. The malononitrile is believed to suffer degradation to cyanide and thiocyanate whereas the remainder of the molecule is combined with glycine and excreted as ortho-chlorohippuric acid. Therefore malononitrile is a highly toxic substance found in CS. The mortal dose for a 150 pound person is estimated to be about a gram or less.

The Cholesterol Conspiracy – The Truth About Statins And Nutritional Supplementation

“All truth passes through three stages.

First, it is ridiculed.

Second, it is violently opposed.

Third, it is accepted as being self-evident.”

Arthur Schopenhauer

(1788 – 1860)

What is the true cause of heart disease, and how can we truly reduce the risk of death?

Atherosclerosis, or Coronary Artery Disease (CAD), is the leading cause of death in both men and women. In the U.S. alone, there are more than one million heart attacks every year, one third of them resulting in death. The majority of men and women currently have, or are actively developing, atherosclerosis. By age 20, most people already have a 15-25% narrowing of their arteries due to plaque formation. By age 40, there is a 30-50% clogging of their arteries.

In the beginning of the Twentieth Century, congestive heart disease (CHD) was mostly a result of rheumatic fever, which was a childhood disease. However by the year 1936 there was a dramatic change in the main cause of heart disease. Cardiovascular disease caused by atherosclerosis, or plaque buildup, took first place as the primary cause of heart disease, making congestive heart failure a distant second.

During the 1950’s, the autopsies conducted on men who died of heart disease that revealed plaque-clogged arteries concluded that cholesterol was the cause of hardening of the arteries (atherosclerosis) and coronary artery disease. Cholesterol, not calcium, was considered the “cause” of heart disease, despite plaque consisting of 95% calcium and a relatively small percentage of cholesterol. By 1956 there were 600,000 deaths annually from heart disease in the U.S. Of those 600,000, 90% were caused by atherosclerosis, or clogged arteries. In fewer than 25 years, the number one cause of death in the U.S. had changed dramatically …from congestive heart disease to coronary artery disease.

Because cholesterol was dubbed the “cause” of atherosclerosis, the effort to lower cholesterol by any means began in earnest. Both the food industry and the pharmaceutical industry seized upon this opportunity to cash in on a cholesterol-lowering campaign by creating foods and drugs that would supposedly save lives. Diets, such as the Prudent Diet, were established to lower the amount of cholesterol intake from food. There was no doubt that both polyunsaturated oils and drugs reduced cholesterol, but by 1966 it was also apparent that lowering cholesterol did not translate into a reduced risk of death from heart disease.

As there was so much money to be made from pharmaceutical development, the campaign to produce cholesterol-lowering drugs kicked into high gear, despite the lack of evidence showing that the lowering cholesterol reduced the risk of untimely death from heart disease.

Heart disease kills 725,000 Americans annually, with women accounting for 2/3 or nearly 500,000 of those deaths. After thirty years of cholesterol-lowering medications’ failure to significantly lower the death rate from cardiovascular disease, in 1987 a new and more dangerous class of drugs was unleashed upon the world: the “statin” drugs. Cholesterol-lowering statin drugs are now the standard of care that physicians are indoctrinated into prescribing to reduce cardiovascular disease. Are statin drugs the best way to prevent heart attacks and death?

Before 1936 the most common type of heart disease was congestive heart disease (CHD). It rarely caused sudden death and could be treated with the drug digitalis. The incidence of CHD remained stable until 1987, after which the incidence of the disease skyrocketed. Interestingly, the timing of the increased incidence of congestive heart disease coincides with the introduction of cholesterol-lowering statin drugs. Could cholesterol-lowering statin drugs have something to do with the weakening of heart muscles and the increased incidence of congestive heart failure? We will see that lowering the body’s co-enzyme Q10 levels, a side effect of statin drugs, does indeed increase the risk of muscle damage, including the muscles of the heart.

Atherosclerosis is a disease characterized primarily by inflammation of the arterial lining caused by oxidative damage from homocysteine, a toxic amino acid intermediary found in everyone. Homocsyteine, in combination with other free radicals and toxins, oxidizes arteries, LDL cholesterol, and triglycerides, which in turn releases C Reactive Protein (CRP) from the liver-a marker of an inflammatory response within the arteries. Inflammation (oxidation) is the beginning of plaque buildup and ultimately, cardiovascular disease. Plaque, combined with the thickening of arterial smooth muscles, arterial spasms, and clotting, puts a person at a high risk of suffering heart attack or stroke.

For years, doctors have hyper-focused on cholesterol levels. First it was the total cholesterol; later the focus became the ratio of “good” HDL cholesterol to “bad” LDL cholesterol. In other words, how much of your cholesterol was good, and how much was bad? Of the two, the important parameter is the level of HDL cholesterol, not LDL cholesterol. HDL, or high-density lipoprotein cholesterol, is responsible for clearing out the LDL cholesterol that sticks to arterial walls. Exercise, vitamins, minerals, and other antioxidants, particularly the bioflavonoid and olive polyphenol antioxidants, increase HDL cholesterol levels and protect the LDL cholesterol from oxidative damage, and therefore do more to reduce the risk of heart disease than any medication ever could.

There is nothing inherently bad about LDL cholesterol. LDL cholesterol is critical to maintain life. LDL cholesterol only becomes “bad” when it is damaged, or oxidized by free radicals. Only the damaged, or oxidized form of LDL cholesterol sticks to the arterial walls to initiate the formation of plaque.

Let us look towards cigarette smoking for a simple example demonstrating that we really need to reduce oxidized LDL cholesterol to prevent atherosclerosis, as opposed to indiscriminately lowering LDL cholesterol with statin drugs. Everyone knows that cigarette smoking increases the risk of many chronic diseases, such as cancer, heart disease, and stroke. Smokers with normal levels of LDL cholesterol are at an even greater risk of developing heart disease than a non-smoker who has elevated levels of LDL cholesterol. Of course the reason why a smoker with normal levels of LDL cholesterol is at greater risk of disease is because his LDL gets excessively oxidized.

Cigarette smoke releases so many toxins and free radicals that the LDL cholesterol, the triglycerides, and the arterial walls are extensively oxidized. Homocysteine levels are also increased by cigarette smoking which further oxidizes LDL cholesterol and the arterial lining. Oxidation is the initiating cause of atherosclerosis. Therefore, the more and longer one smokes, the more oxidative damage he sustains and the greater his risk of developing heart disease. The degree of oxidation directly corresponds to the risk of heart disease.

If you are not taking vitamins, minerals, and antioxidants then your LDL cholesterol is being oxidized, it is sticking to your arterial walls, and you ARE developing heart disease EVEN IF YOUR CHOLESTEROL LEVELS ARE NORMAL! LDL cholesterol starts sticking to arterial walls before the age of 5.

Among the many free radicals that damage cholesterol, triglycerides and the arterial lining is homocysteine, a toxic intermediate biochemical produced during the conversion of the amino acid methionine into another important amino acid, cysteine. Both methionine and cysteine are non-toxic, but homocysteine is very toxic to the lining of the arterial endothelium. Homocysteine oxidizes LDL cholesterol, triglycerides and the arterial lining.

Homocysteine is an amino acid normally produced in small amounts from the amino acid methionine. The normal role of homocysteine in the body is to control growth and support bone and tissue formation. However a problem arises when homocysteine levels in the body are elevated, causing excessive damage to LDL cholesterol, as well as to arteries. Furthermore, homocysteine actually stimulates growth of arteriosclerotic plaque, which leads to heart disease.

Thyroid hormone controls the level of homocysteine, but numerous factors play a role in the elevation of homocysteine. Normal aging, kidney failure, smoking, some medications, and industrial toxins all elevate homocysteine levels. Interestingly, estrogen helps lower homocysteine.

Homocysteine becomes elevated in the blood with a deficiency of the B vitamins-B6, B12 and folic acid. Genetics also play a role. About 12% of the population has an undetected defect requiring higher levels of folic acid than the rest of population to help maintain homocysteine levels in a safe range (below 6.5). Therefore if you have high homocysteine levels (> 7.0) even though you are taking supplemental B complex vitamins, then you may be among the 12% who need more than 1000 mcg of folic acid per day. In addition, betaine, also known as trimethylglycine (TMG) lowers homocysteine.

Homocysteine is second only to cigarette smoking in its oxidative destruction. It causes small nicks or tears in the arterial lining, while also oxidizing and damaging LDL cholesterol. The damaged, or oxidized LDL cholesterol sticks to the homocysteine-damaged areas of the arterial lining. The combination of oxidized LDL cholesterol and a damaged arterial lining is what causes LDL cholesterol to stick to the arteries, whether or not the LDL cholesterol level is normal.

Cholesterol-lowering statin drugs are the standard for treating high cholesterol. This is dogma, and anyone who states otherwise is committing medical heresy. Many people find it hard to believe that pharmaceutical companies could ever succeed in paying medical researchers, medical associations, and doctors to recommend something detrimental to our health.

Most people do not know that pharmaceutical companies fund medical institutions, medical education, medical conferences, and still reward doctors and research institutions for providing favorable results on their drugs. Likewise, pharmaceutical companies often suppress negative results from studies done on their drugs. Money has the power to sweep negative results and serious side effects under the rug. Money has the power to influence the FDA to decide which drugs make it to market and which drugs become the “standard” of treatment.

Former editor of the New England Journal of Medicine (NEJM), Dr. Marcia Angell, warned of the problem of commercializing scientific research in her outgoing editorial titled “Is Academic Medicine for Sale?” Angell called for stronger restrictions on pharmaceutical stock ownership and other financial incentives for researchers. She said that growing conflicts of interest were tainting science, warning “When the boundaries between industry and academic medicine become as blurred as they are now, the business goals of industry influence the mission of medical schools in multiple ways.” She did not discount the benefits of research but said, “a Faustian bargain” now existed between medical schools and the pharmaceutical industry. Angell left the NEJM in June 2000 and has written a book, “The Truth About the Drug Companies: How They Deceive Us and What to Do About It.”

Two years later, in June 2002, the NEJM announced that it was going to begin accepting articles that were written by biased researchers, as there weren’t enough unbiased researchers left to write articles. In other words, most research institutions were now funded by one or more of the numerous pharmaceutical companies.

An ABC report noted that a survey of clinical trials revealed that when a drug company did not fund a study, favorable results regarding a drug were found only 50% of the time. In studies funded by drug companies favorable results about the drugs were reported an amazing 90% of the time. Money can and does buy the desired results. This is how most medical research and drugs are now developed and brought to market.

In 1977, the internationally-renowned heart surgeon, Dr. Michael DeBakey pointed out that only 30-40% of people with blocked arteries and heart disease have elevated blood cholesterol levels, and posed the logical question, “How do you explain the other 60-70%?”

Because lowering cholesterol did not reduce the risk of death from heart disease, the Cholesterol Consensus Conference in 1984 developed new guidelines to lower the “acceptable level” of cholesterol. High cholesterol would now be the diagnosis for any man or woman with a cholesterol level over 200. Doctors had to convince their patients that they had the disease and needed to take one or more expensive drugs for the rest of their lives.

However, when lowering total cholesterol levels below 200 did not translate into saving lives from heart attacks, the focus then turned to LDL cholesterol levels. The “disease” of high cholesterol was refined to the disease of high LDL cholesterol. The unfortunate patient who had an LDL cholesterol level above 130 was now condemned to a lifetime of expensive drugs. Though completely illogical, even when a person with normal LDL cholesterol levels suffered a heart attack, he would still be prescribed a cholesterol-lowering drug.

As we shall see, statin drugs reduce the risk of death by repeat heart attacks by as much as 30%, but interestingly enough, the mechanism of action in reducing the risk of death after a heart attack is not via statin drugs’ ability to lower cholesterol! It has been discovered that statin drugs have a modest anti-inflammatory and antioxidant effect. Yet, there are many natural antioxidants that reduce inflammation and oxidation of LDL cholesterol and the lining of the arteries, which may soon be discovered to be more effective in reducing the risk of death than “antioxidant drugs,” without toxic side effects.

The myth that high LDL cholesterol is the primary cause of heart disease, and that we must be on drugs to protect ourselves is dispelled by the evidence. If the premise were true that people with high levels of LDL cholesterol get heart disease, then we could assume that people with normal levels of LDL should not get heart disease, or at least very few should get it. However, as Dr. DeBakey observed, approximately 60% of those who die from heart disease have normal LDL cholesterol levels!

Furthermore, after over 45 years of doctors prescribing cholesterol-lowering drugs, heart disease and stroke still remain the number one cause of death in both women and men. This says that regardless of whether you have a high or a normal level of cholesterol, you have a 50% chance of dying from heart disease. If this is so, and it is, then why take a dangerous drug to attempt to lower your cholesterol in the first place?

In 2001, the target level of LDL cholesterol was lowered from 130 to 100, and overnight the number of people considered to be candidates for cholesterol statin drugs doubled. Many people such as myself bristled at the news, because we knew the effectiveness of vitamins, minerals, and antioxidants in preventing and reversing heart disease. Many of us could see the conspiracy for what it was.

The level at which LDL cholesterol is considered normal has continually been influenced by pharmaceutical companies, who pull the financial strings of research grants that keep medical schools and medical organizations in business. The lower they can establish the level at which LDL cholesterol is considered to be normal, the more people automatically become victims of the dreaded disease of “high cholesterol.” Therefore, more people will be persuaded that they need to be taking a statin drug, and voilà, more profit for the manufacturers. When you consider the size of the profits already received, let alone the potential profit from statin drugs over the next several years, the cholesterol conspiracy is one of the largest money making schemes ever perpetrated on the world.

In July 2004, the level of LDL cholesterol considered normal underwent another change. The new norm plunged from 100 to 70, virtually doubling again the number of people who are “infected” with the plague of high cholesterol. Why, it’s the epidemic of our time! Many enlightened people howled at this news, wondering if the masses would ever wake up and see who is behind this, and why. Why is the medical establishment ignoring the thousands of published medical studies that show the beneficial effects of nutritional supplements against heart disease? Why is the medical establishment down-playing the dangerous and deadly side effects of statin drugs?

The “updated” LDL cholesterol recommendations were published in the July 2004 issue of the American Heart Association’s publication, Circulation. A panel from the National Heart, Lung and Blood Institute, a division of the National Institutes of Health, which is endorsed by the American College of Cardiology, and the American Heart Association, were the ones who actually pronounced the new cholesterol level at which drugs should be prescribed. Sounds pretty official and reliable if these powerful medical institutions are backing up these recommendations, right?

The fact is eight of the nine panel members making the new LDL cholesterol recommendations were being paid by the statin-producing pharmaceutical companies. The panelists did not disclose their financial conflict of interest. This information was uncovered by Newsday, a Long Island, New York

newspaper (D. Ricks and R. Robins, Newsday, July 15, 2004). Seven of the nine panelists have financial connections to Pfizer, the makers of Lipitor®. Five of the nine served as “consultants” to Pfizer. So, what did the other two panelists do to deserve their money? Seven of the nine panelists also received money from Merck, the producers of Zocor®, with four of them serving as “consultants” to the company. Eight of the panelists who made the recommendations that would increase the prescribing of statin drugs have received either research grants or honoraria from Pfizer, Merck, AstraZeneca, Novartis, Glaxo Smith Kline, Johnson & Johnson, Bayer, and many other drug companies that produce statin drugs.

You would think that with all the advertising and recommendations from medical experts on the benefits of statin drugs, the medical community would possess overwhelming evidence that the drugs reduce the risk of death from cardiovascular disease. A hint of some of the smoke and mirrors in the pharmaceutical companies’ advertising can be seen in their TV commercials. Read carefully the small print on some of Crestor’s® commercial advertising. Their commercial states how much it lowers LDL cholesterol. However, in the same ad you can read, “…Crestor® has not been shown to reduce the risk of heart disease or heart attack.” If so, then why take it? Isn’t the bottom line to prevent death?

The system for reporting adverse effects from medications is tremendously flawed, so much so that many people are seriously harmed or killed by some medications before they are finally removed from the market. Most doctors do not know what symptoms or effects are due to the drug, what should be reported, or even to whom to report adverse effects. They assume that the research that went into developing the drug has already identified all the effects and that a drug brought to market is “safe.” However, only one in twenty side effects is ever reported to either hospital administrators or the FDA.

Statin drugs block cholesterol production in the body by inhibiting the enzyme called HMG-CoA reductase in the early steps of its synthesis in the mevalonate pathway. Cholesterol is one of three end products in the mevalonate chain. This same biosynthetic pathway is also used to create co-enzyme Q10, or co-Q10, as well as dilochol. Therefore, one unfortunate consequence of statin drugs is the unintentional inhibition of both Co-Q10 and dilochol synthesis.

The drug information insert of a statin drug states that it lowers co-enzyme Q10 levels. Most doctors have forgotten their biochemistry class in medical school, and forgotten about the importance of Co-Q10. Therefore they apparently are not concerned about such a statement on the drug labeling information sheet. They may even reassure their patients that lowering Co-Q10 is nothing to worry about, but at the same time warn them that the drug may cause liver damage and to have their liver enzymes checked every three to six months to make sure the drug isn’t killing them. They do not realize that it is the depletion of Co-Q10 that leads to liver damage and death.

Ubiquinone, or co-enzyme Q10, is a critical cellular nutrient created in the cell’s mitochondria, the “engines” that produce energy for the cell. Mitochondria use sugar, oxygen, and water to produce energy molecules known as ATP. Without ATP cells could do nothing. Damaged tissues could not be repaired. Cells could not divide or produce or utilize proteins, enzymes, or hormones. Death of cells, and indeed of the human body would occur if ATP could no longer be produced and utilized. Co-Q10 functions within the mitochondria as an electron carrier to cytochrome oxidase, our main respitory enzyme, which helps turn oxygen and sugar into energy. The heart requires high levels of oxygen, sugar, and Co-Q10 since it utilizes a lot of energy. A form of Co-Q10 called ubiquinone is found in all cell membranes, where it plays a role in maintaining membrane integrity, so critical to nerve conduction and muscle contraction. Co-Q10 is also vital for the formation of elastin and collagen, which make up the connective tissues of the skin, musculature, and the cardiovascular system.

The most common side effect of statin drugs is muscle pain and weakness. In fact, many patients who start on the statin drugs almost immediately notice generalized fatigue and muscle weakness. This is due to the depletion of Co-Q10 needed to support muscle function. Dr. Beatrice Golomb of San Diego, California, is currently conducting a series of studies on statin side effects. The pharmaceutical industry insists that only 2-3% of patients get muscle aches and cramps, when in fact in one study, Golomb found that 98% of patients taking Lipitor®, and one-third of the patients taking Mevacor® (a lower dose statin), suffered noticeable to significant muscle problems.

Some people on statin drugs lose coordination of their muscles. Some develop pain in their muscles, some are not able to write due to loss of fine motor skills. Many lose the strength to exercise. Others are falling more frequently as their muscles give out, still others have trouble sleeping due to muscle cramping and twitching. Even worse, many people are experiencing most of these side effects. The problems are so numerous, it is difficult to list all the symptoms people might experience. These problems do not come from the “disease” of high cholesterol, but the disease of ignorance in prescribing these drugs.

As we age, Co-Q10 levels decline naturally. From the age of 20 to 80, Co-Q10 levels fall by nearly 50%. Along with the natural decline of Co-Q10, comes a natural decrease in energy and an increase in the risk of heart disease, stroke, and cancer. If the natural decline of Co-Q10 levels increases the risk of fatigue, cancer, heart disease, and stroke, would it not make sense that accelerating the decline of Co-Q10 levels with statin drugs would have the same effect? They do indeed!

Demonstrating the importance of Co-Q10 to cardiovascular health, in a randomized, double blind, placebo-controlled study of people either taking or not taking statin drugs, supplementation with Co-Q10 reduced the risk of heart attacks and death in those with heart disease and prior heart attacks by 50%, regardless of whether they were on a statin drug or not. (Singh R, Neki N, Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Mol Cell Biochem. 2003 Apr; 246(1-2):75-82.)

Additionally, Co-Q10 was shown to increase blood levels of vitamin E and significantly increase the levels of protective HDL. As low HDL is a major risk factor for heart disease, increasing it is a definite benefit. Statin drugs were shown not to provide any benefit beyond that of supplementing with Co-Q10. Let me make this clear – in this study only the co-enzyme Q10 provided any benefit, not the drugs!

Cardiologist Dr. Peter Langsjoen of East Texas University reported the effects of Lipitor® among 20 patients who started with completely normal hearts. After six months on a low dose of 20 mg of Lipitor® per day, two thirds of the patients started to show signs of heart failure, as seen by abnormalities in the heart’s filling phase. According to Dr. Langsjoen, this malfunction is due to Co-Q10 depletion. Nine controlled trials using statin drugs in humans have been conducted thus far. Eight of these showed significant statin-induced Co-Q10 depletion leading to a decline in left ventricular function and other biochemical imbalances.

In the United States, the incidence of heart attacks over the past ten to fifteen years has declined slightly. But congestive heart failure and cardiomyopathy have risen alarmingly. Is it a coincidence that statin drugs were first marketed in 1987, and then from 1989 to 1997, deaths from congestive heart failure more than doubled? 38 It scares me that virtually all patients with heart failure are put on statin drugs, even if their cholesterol is already low. In my opinion, the worst thing to do for a failing heart is take a statin drug. The best thing is to take is a full range of quality nutritional supplements, …vitamins, minerals, fish oil, and other antioxidants, including Co-Q10.

Various antioxidants work synergistically, each contributing to the fight against free radicals in different areas and in different ways. In the blood stream, water-soluble antioxidants, such as vitamin C, and grape seed extract come in contact with and neutralize free radicals before they damage LDL-cholesterol. Other antioxidants saturate arterial walls and other tissues, and protect collagen and elastic fibers from free radical damage, reducing inflammation and plaque formation. The fat-soluble antioxidants, vitamin E, beta carotene, and co-enzyme Q10 ride along in the blood fat (triglycerides) and LDL cholesterol, protecting them and the endothelium from oxidation. Vitamin E sits on the surface of LDL cholesterol, protecting it from free radical damage. Beta carotene, grape seed extract and olive extract penetrate deeper inside the LDL cholesterol and arterial walls, adding more protection from oxidation. Quercetin and alpha lipoic acid work through nitrous oxide pathways to reduce high blood pressure, a major risk factor for heart disease.

A report published in the Archives of Internal Medicine in 2005 looked at 97 double-blind controlled studies comparing the efficacy of cholesterol-lowering statin drugs to fish oil. They found that cholesterol-lowering statin drugs reduced the risk of death from heart disease by only 13%, and

interesting enough it was NOT due to the effect of lowering cholesterol. The benefits, although small, were derived from the fact that statin drugs have a slight antioxidant effect.

Even more interesting, the salmon oil was shown to reduce the risk of death from heart disease by 23%, nearly double the benefit of statin drugs. Salmon oil is an omega-3 fatty acid that gets incorporated into cholesterol and triglycerides and prevents the oxidation of LDL cholesterol. Since LDL cholesterol is protected from excessive oxidation there is less plaque buildup and less risk of heart disease.

Inflammation is a well-known component in the formation of atherosclerosis. To keep it simple, think of inflammation and oxidation as the same process. The immune system’s response to inflammation is to

release peroxides that act like acid to break down damaged tissues, so that cells from the immune system, macrophages, can consume the molecules and clean up the site. But peroxides escalate the oxidation/inflammation process, thus damaging more tissue. The arterial walls become more inflamed, escalating the formation of plaque and scarring. The downward cycle continues until atherosclerosis is so advanced that the occurrence of a heart attack or stroke becomes imminent.

The liver’s response to inflammation is to release C reactive protein (CRP) into the blood. Other inflammatory causes can cause elevated CRP levels, including cigarette smoking, obesity, insulin insensitivity, diabetes, rheumatoid arthritis, infections, dementia, colorectal cancer, high blood pressure, and aging. Accordingly, elevated CRP levels are a direct indication of inflammation in the body and that atherosclerosis, including heart disease, is actively developing.

Homocysteine and high sensitivity CRP levels can and should be tested. Dr. Jialal, of the Universtity of Texas Southwestern Medical School at Dallas, is well known for his research correlating oxidized LDL cholesterol as the true cause of atherosclerosis, has also identified high sensitivity C reactive protein as a predictive risk factor for inflammation of arterial walls and plaque formation. Your doctor may not test for these routinely, but you should insist on getting these tests done. Both of these predictive values can be kept at “safe” levels. Vitamins, minerals, antioxidants, and omega-3 fatty acids can lower the levels of homocysteine and CRP. The B vitamins, along with betaine, or tri-methyl-glycine (TMG), change homocysteine into safer amino acids and reduce inflammation of the LDL cholesterol and the arterial lining.

When you receive the results of your homocysteine test, do not accept the answer, “Your test was normal.” Ask for the actual number. The doctor and nurse usually know what is normal by what the lab slip states as the “normal range.” Most lab results report a normal homocysteine level as being below 10.4, when in fact, since the early 1990’s, researchers have known that a homocysteine count above 6.5 signals a rapid linear rise in the risk for heart disease.

Furthermore, with every 3 point elevation of homocysteine above 6.5, e.g., when homocysteine levels are 9.5, the risk of coronary artery disease (CAD) rises by an additional 35%! Yet you may be told that 9.5 is “normal and not to worry.” With a homocysteine level of 12.5, the increase in the

risk for heart disease exceeds 70%. The greater the homocysteine level, the greater the oxidation

of both LDL cholesterol and the arterial lining. The greater the inflammation, the higher the CRP. Is it any wonder that homocysteine and CRP levels are more predictive for risk of heart disease than cholesterol levels and ratios?

I need to emphasize that anyone whether they have a medical problem or not, should discuss this information with their physician before acting upon anything written here. The information provided is not meant to diagnose or treat any disease. It is for informational purposes only; and no one should make decisions about their medications without consulting with their physician. No one should come off a cholesterol-lowering statin drug in lieu of nutritional supplements without a thorough discussion with their physician who is keenly aware of all the pros and cons of both treatment modalities.

In summary, I recommend a full spectrum of quality nutritional supplements, along with a healthy diet and exercise, to help obtain and maintain optimal heart and arterial health. I believe all would agree that lifestyle changes are the most important factor for optimal health, …and many believe that quality nutritional supplements are key in protecting against the process that leads to, and accelerates the development of almost all chronic degenerative diseases, that of oxidation. To combat oxidation we need a full range of quality antioxidants.


Lack Of Happiness And Contentment In Life Causes Heart Disease

What is rarely mentioned in reports on heart disease and their contributing risk factors is one the most important discoveries ever made about man’s number one killer disease: The greatest risks of developing heart disease are job satisfaction and happiness rating. These unexpected risk factors turned up when American researchers looked once more at clues of what could cause heart disease.

If you ask a man in the street whether he is satisfied with his job and happy, depending on his answer, you will be able to make a prognosis about whether he is at risk of developing heart disease or not. It would be too simplistic to assume that heart disease is only caused by stress, cigarette smoking, overeating, alcohol abuse, etc. These risk factors are not the ultimate causes of a dysfunctional heart, but rather the effects or symptoms of plain dissatisfaction in life.

The cause behind the major causes of heart disease, which is nothing but the plain lack of happiness and contentment in life, may still be there after all the other risk factors or causes have been eliminated. A large number of people have died from heart attacks with perfectly clean arteries and no other tangible, physical reasons. Many of them have never smoked, abused alcohol, or led a particularly stressful life. However, they were unhappy within themselves.

One 1998 study by the Johns Hopkins School of Medicine has confirmed what 10 other surveys have found: Clinically depressed men are twice as likely to suffer heart attacks or develop other heart illnesses as those who are not unhappy or depressed. If the “heartache” is severe enough, there are several ways to shut down the arteries and, in fact, the entire energy system in the body.

DNA research has shown that the double strands of the DNA controlling the health of every cell in your body suddenly contract and shorten when you feel fear, frustration, anger, jealously, or hatred. It is as if the software of a computer program begins to malfunction and the computer does no longer perform properly. By applying the procedure of kinesiology muscling testing to a depressed or unhappy person, you find that all the muscles in his body are weak, especially while he ponders his personal problems. His discontent also affects the muscles of his heart and arteries. If unhappiness persists, disease is inevitable, and whatever part of his body is the weakest will succumb first to the chronic shortage of energy. If it happens to be the heart, then heart disease may result.

Even if such a person doses himself with antioxidants, which are believed to protect the arteries against oxygen radical attacks, they will neither be digested and assimilated, nor be successfully delivered to the damaged arteries. Lack of satisfaction in life paralyzes the body’s functions of digestion, metabolism, and elimination. This causes congestion, high toxicity, and damage to all cell tissues. People who have blocked coronary arteries are not just sick in the area of the heart, they are sick throughout the body. The most important determinant factor of disease appears to be the inability to live a happy, satisfying life.

The reason modern medicine is so helpless in providing lasting cures of heart disease is that there is not much in the current medical approach that can increase happiness in a patient. Yet there is hardly any other primary risk factor for disease, including coronary heart disease, other than its absence. It is the lack of lasting happiness and peace of heart and mind that makes a person feel stressed, take drugs, overeat protein and other foods, abuse alcohol and cigarettes, drink excessive amounts of coffee, become a workaholic, or dislike his job or himself.

Dyspnea and Cyanosis – Important Clinical Symptoms of Respiratory Disorders


Difficulty or shortness of breath associated with marked awareness of the effort of respiration is called dyspnea. In the left-sided heart failure and in hypoventilatory states, the patient becomes more dypsneic in the recumbent posture and considerable relief is obtained by sitting up. This is referred to as orthopnea. Attacks of severe breathlessness occurring during sleep at night may awaken the patient and assumption of the erect posture gives relief. This is termed paroxysmal nocturnal dyspnea. This is also characteristic of left-sided heart failure. Respiratory disorders that lead to dyspnea may fall into different groups.

• Central causes for dyspnea affect the respiratory center, e.g encephalitis or cerebrovascular accidents.
• Significant airways obstruction is a common cause for dyspnea. Obstruction to the airway may be mechanical as due to a foreign body or functional as due to spasm. Larger airways may be obstructed by aspirated foreign bodies. Diphtheritic membrane, tumors, blood or secretions. Obstruction to the larynx produces inspiratory stridor and in-drawing of the chest wall. Dyspnea is felt both during inspiration and expiration. Obstruction to the smaller airways occurs in asthma, emphysema, chronic bronchitis, and extensive bronchiectasis. In these conditions the difficulty is felt more for expiration and the characteristic expiratory wheeze may be heard.
• Disorders that impair the process of gas exchange eg, massive pulmonary collapse, pulmonary embolism, respiratory distress syndrome, fibrosing alveolitis, pulmonary fibrosis and extensive parenchymal diseases such as tuberculosis, cystic disease and malignancy.
• Disease that prevent expansion of the lung, eg, pneumothorax, pleural effusion, kyphoscoliosis, injury to the chest wall, paralysis of respiratory muscles etc.
• Dyspnea is commonly the first symptoms when the inspired air does not supply adequate amounts of oxygen to the individual. This happens when the oxygen tension is low as in high altitudes or in gas poisoning.
• Hysterical hyperventilation presents as dyspnea. In this, the subject voluntarily hyperventilates. Other traits of the hysterical personality may be evident. Excessive removal of carbon-dioxide due to overventilation leads to repiratory alkalosis and tetany.
• In diseases like pneumonia and pleurisy, painful restriction of respiratory movements leads to hypoventilation and dyspnea.


Bluish discoloration of the skin and mucous membranes due to the presence of excess of reduced hemoglobin in peripheral blood is called cyanosis. In extensive diseases of the lungs, central cyanosis occurs due to defective oxygenation of arterial blood or the development of functional arteriovenous shunts. In chronic bronchitis and emphysema, the main defects are those of ventilation and perfusion. In fibrosing alveolitis, the defect is mainly one of diffusion. Differentiation between respiratory and cardiac causes of cyanosis can be made on clinical grounds in many cases. In respiratory diseases inhalation of oxygen helps in clearing the cyanosis, whereas this is not so in cardiac lesions with right to left shunts.

Growing Rosemary – Set It and Almost Forget It

I love growing Rosemary! The narrow leaves which actually look like needles have a spicy, resinous fragrance. They are hardy, forgiving, and don’t require a lot of attention. This plant is close to ‘Set It and Forget It’ in the amount of attention it needs.

Contrary to popular belief, for the most part Rosemary can be grown outdoors all year. This is a hardy perennial evergreen and can with stand winter temperatures above 5°F or -15°C. In the Northeast and Northern Plains states it may need to be taken indoors during the winter or given protection.

My Rosemary plants are outdoor plants. They occasionally get a little frost bite on their tips when the temperature drops below 20°F. When this happens I wait until after the last hard spring frost and then prune the dead tips off. This also spurs new growth. This is also the time I will give it a little fertilizer.

You can cut the plant back each spring, and new growth will come from the bottom. Some gardeners like to do this to keep their Rosemary maintained. I only cut off the damaged branches.

I have several of these aromatic plants of different varieties, as they are used for culinary, medicinal, ornamental, and aromatic purposes. They can be moved around, dug up, and transplanted to a new area and will do fine if done with a little care.

I have a Rosemary Officinalis shrub that is 3′ tall and 12 years old and is surrounded with strawberry plants. They were planted at the same time and are companion plants. No, I don’t dig it up each fall and put in the greenhouse. It stays in the garden year-round and does quite well. The temperature does get down to zero occasionally but only lasts a few days and we do have intermittent snow throughout the winter.

Two years ago, the Rosemary plant was dug up and transplanted. The key is to dig deep and get as much of the root ball as you can without disturbing it. The herb garden it was in was soon to become the foundation for a house so it had to be moved along with the strawberries growing at its base.

I have a backhoe so it was easy to dig up the plant and move it. Unfortunately I didn’t have time to plant it for a few days. I had put a wet gunny sack (burlap like material) around its base and root ball. To be honest, I was so involved in learning how to dig a foundation with the tractor that I completely forgot about my Rosemary plant for 3 days.

When I was ready to plant it, I used my little Mantis tiller to dig and prepare the hole. Why the tiller instead of the backhoe – because I wanted to till, pulverize, and sift the soil as I dug the hole. Little tillers like the Mantis tiller are great for this type of work.

I live in the Pacific NW and the ground is rocky and turns into clay after digging down a good 18 inches. The little tiller does a great job of digging the hole and tilling up the soil at the same time. The hole was dug twice as wide and deep as the Rosemary’s root ball. Next a layer of my potting medium was placed in the hole and watered. After the water was absorbed the Rosemary plant with its companion strawberry plants was set in the hole and positioned to look its best for its placement in the yard. A little more water was added and when absorbed my potting medium was placed in and around the root ball, tamped in, and watered again.

You may think I overwatered the plant, no. The plant’s root ball was quite dry and needed the water that was put in the hole; this wasn’t overwatering. If the root ball had retained a fair amount of moisture, I wouldn’t have used as much water in the hole.

Rosemary prefers a light, sandy, well-drained soil and full sun. Full sun I have; the light sandy soil, I have to make. This is can be accomplished by mixing sand and compost into your soil and mixing it into a fine granular or pulverized medium.

You can do this with by:

  • Buying a planting medium of that type
  • Mixing the sand, compost, and soil together

I like to place the soil along with sand and compost in the front loader of my tractor or a large wheelbarrow and then use the little tiller to mix it up into a nice granular potting medium. This was used to plant the Rosemary.

I also pruned it back a little bit just to shape it. The Rosemary plant never suffered any transplant shock due to having its entire root ball dug up and protected until I had a chance to plant it. I should also note here that this was done in November which is the perfect time to move the plants as it is less traumatic on them. Fall is the time to move them; however cuttings and layering can be done in either the spring or fall.

My plant is thriving and likes its new home.

Rosemary also likes a PH around 5.0. I place a ring of coffee grounds about 5 inches from the main stem of the plant. This keeps the PH just right and also works as a slow release fertilizer and keeps the slugs off my plants.

Don’t be afraid to move your Rosemary around. Keep it pruned and it will put out new growth. Depending upon where you live give it extra protection in the winter. You can also grow Rosemary in a pot planted in the ground and in the fall dig up the pot and move it to a protected area. You can also plant trailing Rosemary in a hanging basket and move it to a protected area as needed.

I have a friend in Montana who covers their 5 foot tall plant with burlap and places several flakes of straw around the base of her plant before the first snow. She covers it with a blanket when the temperature and wind chill is extreme. She says this works and she hasn’t had any problems in 5 years.

The main problem with growing Rosemary is overwatering. Go easy on the water unless you live in the south or have a severe drought. This is one of the herbs which doesn’t seem to be affected by pests or diseases.

If you haven’t tried growing Rosemary, try it you’ll be surprised at how easy it is to grow and what a wonderful addition it makes to your landscape and garden. This is as easy as it gets.

Please visit Growing Rosemary for an in-depth look at this wonderful herb. Happy Gardening!

3 Colon Cancer Warning Signs You Should Never Ignore!

There are 3 particular colon cancer warning signs that are very important. They are signs you should not ignore at all.

Why are they important? Here’s why… A tumor that forms in either your colon or rectum normally grows quite slowly. Because of its slow growth, it doesn’t show any sign or symptom for a long period of time.

What happens more often than not is… when colorectal cancer is diagnosed, it is already at its advanced stage. This is unfortunate because colorectal tumor at stage 4 is extremely difficult to treat. It requires more than 1 treatment and the survival rate is poor. So, what signs should you look out for? Be aware of the following colon cancer warning signs like…

Persistent Fatigue

Fatigue is described as the physical feeling of extreme tiredness or weakness. It can mean other medical conditions but if it is persistent, it can mean cancer. It is one of the signs of late stage cancer of any type.

However, in colon cancer, fatigue can be an early symptom. In fact, it can be your only symptom.

How does this happen? Fatigue is caused by occult bleeding inside your colon or rectum. Occult bleeding is invisible — something you can’t see. Fatigue is also a symptom that is first noticed by you and nobody else. Thus, fatigue is a very important symptom. See your doctor if you feel very,very tired for more than a week even after going on a vacation.

Persistent Diarrhea

Persistent Constipation

Both are unusual changes in your bowel habits. Why are they considered as unusual changes?

Here’s why…Let’s say you move your bowel once a day regularly everyday. But now you move it either 2 to 3 times daily or 2 to 3 times in a week. This is abnormal particularly if diarrhea or constipation happens persistently.

What does persistent diarrhea or constipation mean? Persistent constipation alone means there might be a tumor at your rectum which is located next to your anus. A rectal tumor will cause an obstruction against the stool. You will experience difficulty in moving your bowel. Persistent diarrhea and constipation that occur alternately mean a tumor at the left colon which is the descending section.

Why is this so? The left section of the colon has a narrower circumference compared to the right section. The stool is semi-solid and the tumor if situated at the left section typically wraps around the colon. This leads to diarrhea and constipation.

These are just 3 of the signs you should be aware of. There are other important colon cancer warning signs — such as the color of your stool — you should know about.