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Lifelong Supplements


- Dr. James Meschino, DC, MS, ROHP

Lifelong Supplement Number 1: High Potency Multi-Vitamin And Mineral

As should be clear after reading Step 1, following a healthy diet is the foundation upon which you should provide your body with vitamins, minerals and other protective nutrients to help prevent many degenerative diseases. However, numerous research studies have shown that in order maximize your defenses against cancer, heart disease, dementia, immune system weakness, cataracts and other degenerative diseases, as well as to slow the aging process, it is mandatory to supplement your diet with certain vitamins and minerals at levels beyond which can be provided by a healthy diet alone. The growing awareness of the value of nutritional supplements has led to the increased use of vitamins and other supplements by the general public.

In fact, sixty percent of adults in North America are presently taking vitamin supplements each day. Of these, multiple vitamin and mineral supplement products are used most frequently. The primary reasons cited for taking a daily multiple vitamin and mineral supplement include:

In fact, sixty percent of adults in North America are presently taking vitamin supplements each day. Of these, multiple vitamin and mineral supplement products are used most frequently. The primary reasons cited for taking a daily multiple vitamin and mineral supplement include:

  • to enhance energy and well-being
  • to help defend against degenerative diseases such as cancer, heart disease, osteoporosis and dementia
  • to help manage existing health conditions such as arthritis and diabetes
  • to slow the aging process

However, some people still argue that we can get all the vitamins and minerals we need from food alone in order to attain the Recommended Daily Allowances (RDAs) for each nutrient, therefore supplements are not necessary. Individuals who have done their homework on this subject know that 80 to 91% of the population do not achieve the RDAs for each vitamin and mineral each day, nor do they even come close. In fact marginal nutrient deficiencies are present in as much as 50% of non-users of multiple vitamin and minerals. As well, the RDA levels, set out by the government, for each nutrient are only intended to guard against severe nutrient deficiency diseases such as scurvy (Vitamin C), pellagra (Niacin), and beriberi (Vitamin B1), but are not intended to serve as levels of vitamin and mineral intake that are optimal in regards to preventing degenerative diseases, slowing the biological processes of aging and maximizing our well-being and longevity. As part of an overall wellness/anti-aging program, taking a high potency multivitamin and mineral each day is absolutely mandatory from my vantage point. However, knowing what to look for in a multiple vitamin is crucial in terms of deriving the best available benefits. Most multiple vitamin products include all vitamins and minerals from A to zinc, but often at insufficient doses to provide the disease prevention and anti-aging benefits you should be seeking. I will explain the exact dosages of each vitamin and mineral that should be present in a high potency multivitamin and mineral, but first I want to share with you the studies that illustrate that vitamin and mineral supplementation is a key daily step in anti-aging and health-promotion

Free radicals And Antioxidants

The story of vitamin and mineral supplementation begins with an understanding of free radicals and antioxidants. It is widely accepted in the scientific community that substances known as free radicals cause cancer, accelerated aging, and contribute to the development and progression of heart disease and stroke, Alzheimer’s disease and age-related cognitive decline, cataracts and macular degeneration of the eye, weakening of the immune system, skin cancer, wrinkles and other degenerative conditions. In fact, free radicals are believed to play a role in more than sixty different health conditions.


So what are free radicals? A free radical is a molecule that possesses an unpaired electron, which must attempt to become whole and stable by stripping an electron from a neighboring molecule, as electrons spin around (orbit) the nucleus of an atom in pairs; one spinning clock-wise and the other spinning counter-clock wise. Thus, an atom or molecule with an unpaired electron will use what even means necessary to acquire the missing electron to spin in the opposite direction around the nucleus, to pair itself up.  If an atom or molecule is missing an electron (free radical state) it will strip an electron from a neighboring molecule, which was otherwise minding its own business. In turn, the molecule that has had an electron stripped away is now converted into a free radical and must now steal an electron from another nearby molecule, which in turn, converts the nearby molecule into a free radical and so on. This chain reaction of free radical propagation is known to cause damage to many cellular structures, including the cell membrane, enzymes, the DNA (genetic blueprints) and the mitochondria (energy factory) within the cell, to name a few important ones. Studies show that free radical damage of this nature can cause alterations to the DNA of the cell that lead to cancer. This is how cigarette smoking causes lung cancer, as cigarette smoke is loaded with free radicals that attack the DNA of lung cells creating cancerous mutations. Free radical damage to the cell also speeds up the aging process of the cell by damaging many of the structures, internal regulatory mechanisms, and the energy-producing machinery of the cell (mitochondria).


Where do free radicals come from? Well, cigarette smoke, as I mentioned, is loaded with free radicals, including second-hand smoke. This is why cigarette smoke has been shown to be responsible for approximately 30% of all human cancers. However, there are many other sources of free radicals. It may surprise you to learn that some of the oxygen we breathe in gets transformed into free radicals during the course of normal metabolism. These oxygen radicals cause damage to body cells and tissues. If you have ever cut open an apple and left it exposed to the air for a few minutes, you know that the exposed surface turns brown. This change in color is caused by oxygen free radical attack. The same kind of reaction occurs in the body. Many researchers have shown that this type of oxidizing over a lifetime produces much of the aging of our tissues. In other words, to a certain degree we don’t age, we actually are slowly rotting just like the apple. Fortunately we can slow down the rate of rotting (or aging) by taking higher dose of antioxidants, as I will explain. However, the point is that oxygen is a double-edged sword in that we need it to produce energy (without it we would die in three minutes or so), but at the same time, approximately 5% of the oxygen present in our cells gets converted into very aggressive free radicals (oxygen free radicals). In fact, cancer expert, Dr. Bruce Ames, estimates that each cell in the body endures 10,000 free radical hits per day just from oxygen free radicals. The cumulative effect of free radical attack over our lifetime is responsible for a large degree of the aging process, the age-related weakening of our immune system and the age-related increase in cancer incidence and other degenerative diseases.

In addition to cigarette smoke and oxygen there are many other environmental and food-borne free radicals that can enter the body, which can greatly increase free radical damage to our bodies. Here are examples of some other dangerous, yet common, free radicals:

  1. 1
    Alcohol – alcohol generates many free radicals and is responsible for approximately 3% of all human cancers in North America
  2. 2
    Heterocyclic amines – these are formed when you char meat on a Bar BQ or eat blackened or Cajun-style proteins (meat or fish)
  3. 3
    Polycyclic aromatic hydrocarbons (PAH) – these are formed when the fat in meat drips on to the Bar BQ coals and smoke rises into the meat or fowl. The smoke contains PAH, which then rises into the food on the grill. This is why smoked meat and fish are known to contain high levels of PAH, and regular consumption of these foods are associated with increased incidence of stomach and esophageal cancers.
  4. 4
    Pesticides (e.g. DDT)
  5. 5
    Nitrosamines – these are formed when you consume foods (often cold cuts) that contain nitrate and nitrite salts. Once in the intestinal tract nitrates combine with amines (derivatives of protein digestion) to form nitrosamines, which are associated with cancer of the colon, rectum and other tissue sites.
  6. 6
    Ultra-violet light (from the sun and tanning beds) – UV-light penetrates the skin and converts oxygen within skin cells into free radicals by injecting them with an unpaired electron from the photon energy in UV-light waves. These free radicals then go on to cause skin accelerated skin aging and increase risk of skin cancer. UV-light can also reach deep into the dermal layers and cause cross-linking of collagen fibers, which results in skin wrinkling.
  7. 7
    X-Rays – radiation beams fired through the body initiate free radical formation in the our cells to a significant degree in much the same way that UV-light initiates free radicals in skin cells.
  8. 8
    Air Pollution – contains many free radicals of which nitrous oxide and polycyclic aromatic hydrocarbons are important ones.
  9. 9
    Occupational Free Radicals – these include substances such as carbon tetrachloride, asbestos, vinyl chloride and heavy metals like mercury, cadmium and lead.

As you can see, your body comes into contact with a great number of free radical insults over your lifetime. Reducing your exposure to free radical as much is possible is an important way to reduce disease risk and slow aging, but it is also vital to optimize your antioxidant defenses, as antioxidants quench and neutralize free radicals and thereby minimize free radical damage to your body.

Antioxidants To The Rescue

The unique feature about antioxidants is that they quench, intercept and neutralize free radicals, converting them into stable, non-harmful substances and thus, prevent or halt free radical damage to your tissues. Antioxidants are able to neutralize free radicals because they have the ability to donate an electron or absorb an electron from a free radical molecule, without being converted into a free radical themselves. Fortunately, the body makes several antioxidant enzymes such as glutathione peroxidase, catalase and superoxide dismutase to help reduce free radical damage to the body. Without these enzymes to protect us from the damaging effects of oxygen free radicals alone, we would all be dead within hours. The fact that our bodies synthesize these antioxidant enzymes is what enables us to live in the earth’s atmosphere of 21% oxygen, and to use oxygen to power the energy production pathways in our cells. However, the antioxidant enzymes that the body makes require activation by certain minerals including manganese, magnesium, zinc, copper and selenium that we get from food and supplements. As well, our bodies require additional antioxidant protection from nutritional antioxidants such as vitamin A, vitamin C, vitamin E, Beta-carotene, lycopene, lutein and zeazantin, and bioflavonoids. Studies conducted over the past 25 years have provided evidence that supplementing with many of these nutritional antioxidants, at levels beyond what food alone can provide, can have a significant impact on preventing many degenerative diseases, and slow the aging process. This is why I strongly recommend that you take an antioxidant enriched, high potency, multi-vitamin and mineral each day. In general, part of your life long wellness/anti-aging plan must include reducing your exposure to unnecessary free radicals and maximizing your defenses against free radical damage by consuming at least 5 servings per day of fruit and vegetables, and by acquiring additional antioxidant protection from an antioxidant-enriched, high potency, multi-vitamin and mineral supplement each day.

Antioxidant Supplements Can Save and Prolong Your Life

Now that you know the damage that free radicals can do to your body, as well as many of the sources of free radicals, I want to clearly state that the emerging scientific evidence suggests very strongly that taking the right dosage of antioxidant supplements each day can not only slow the aging process, they can save your life and likely will prolong it. Let’s get more specific and examine the research that shows that antioxidant supplementation prevents degenerative diseases and improves your overall health status:

Antioxidants Reduce Cancer Risk

Numerous studies indicate that higher intakes of various antioxidants from food and supplements help to reduce risk of many human cancers. Several prospective studies that began during the 1980’s, particularly ones done in Finland and in Basel, Switzerland, provided some of the first convincing evidence that people who have higher intakes of vitamin C and beta-carotene and who maintain appreciable blood levels of these nutrients through their lives, have a significantly lower risk of many cancers, than do individuals with lower intake and/or blood levels. Antioxidants, like vitamin C, beta-carotene, vitamin E and others, quench free radicals that can cause cancerous mutations to the genetic material (DNA) of our cells.

 

Population studies show that the frequent ingestion of orange-yellow fruits and vegetables, and dark green vegetables, which provide many antioxidant vitamins, is associated with reduced cancer risk. As reported by Ziegler, a number of studies have shown that a high total carotenoid intake (e.g beta-cartoene, lycopene lutein etc.) is associated with a significant reduction in risk of cancers of the lung, stomach, breast, bladder and colon, as well as a several other tissue.

 

As reported by Gladys Block, approximately 90 epidemiological studies have examined the role of vitamin C or vitamin C-rich foods in cancer prevention. According to these findings, evidence is strong that vitamin C may protect against cancers of the esophagus, oral cavity, stomach, and pancreas and is substantial for cancers of the cervix, rectum, breast and lung. As for vitamin E, the association between serum vitamin E levels and subsequent cancer risk has been examined in at least 12 longitudinal studies. Overall, the studies showed, on average, a 3% lower blood vitamin E levels among individuals who later developed cancer. In particular, vitamin E appears to be protective against cancers of the stomach, pancreas, colon and rectum, and with selenium may reduce risk of reproductive organ cancers in women (e.g breast cancer). Many of these preliminary studies were summarized in The American Journal of Clinical Nutrition supplement to volume 54, in December, 1991. Since these early reports many studies have been performed over the past 13 years that have more closely examined the relationship between antioxidants and cancer prevention.

Don’t have time to read the whole book right now?

No worries. Let me send you a copy so you can read it when it’s convenient for you. Just let me know where to send it.

LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

Colon Cancer

A number of antioxidants, including vitamin C, vitamin E, and selenium have been shown to be important in the prevention of colon cancer.


Selenium is a trace mineral that is known to prevent chemically-induced colon cancer in many animal studies. In one study with rats that were fed a known cancer causing chemical, the rats whose diets were supplemented with selenium had a tumor yield of only 3%, whereas the rats who received no selenium supplementation had a 29% tumor yield. Other animal studies have shown that selenium supplementation can reduce the incidence of intestinal tumors by 50% compared with rats given the cancer causing agent without selenium supplementation.

 

Human observation studies are equally as impressive. For example, areas in North America with low soil and crop selenium concentrations, show higher rates for colon and rectal cancers. Other human studies demonstrate that lower blood levels of selenium are associated with an increased risk of developing colon cancer. In a study of U.S. veterans, blood levels of selenium were measured in subjects with colorectal cancer and those free from colon cancer. The results demonstrated that subjects with blood selenium levels below 128 micrograms per liter were 4.2 times more likely to have one or more cancerous polyps.

 

In a clinical trial using selenium to reduce risk of skin cancer 1,312 subjects were given either 200 micrograms of selenium or a placebo for almost five years. The subjects taking the selenium experienced a 58% reduction in colon and rectal cancers compared with subjects taking the placebo pill.

 

More recently, a study by Dr. Mark Russo and associates at The University of North Carolina (Chapel Hill) showed further supported for the role of selenium in the prevention of colon and rectal cancers. In their study, patients who were referred for a colonoscopy assessment, also had blood tests performed. As reported by these authors, lower blood levels of selenium were associated with multiple cancerous lessons in the colon. The average blood level for patients with cancerous lesions was 107 micrograms per liter compared to 120 micrograms per liter, for the cancer free subjects.

 

The authors conclude that this data support a protective effect of selenium against colon and rectal cancers after adjustments for possible confounding factors such as smoking, alcohol intake, use of dandruff shampoo (which contains selenium), vitamin E intake, vitamin C intake, iron intake, fat intake, and fiber intake. The researchers state, "Our results demonstrate that individuals with high plasma (blood) selenium levels are at a decreased risk for colorectal adenomas (cancerous lesions)". An increase of 30 micrograms per liter in blood selenium level was associated with a 50% reduction in risk of colon cancer lesions. It is important to note, that other human studies by Dr. Willett, and Dr. Solonen , also reported, a 2 and 3 fold increased risk for colon and intestinal cancer respectively, in patients presenting with low blood selenium levels when compared to patients with higher blood levels.

 

There are several ways that selenium is thought to reduce cancer risk. Selenium may act as an antioxidant by increasing activity and levels of a powerful antioxidant enzyme called glutathione peroxidase.

 

Glutathione peroxidase is considered a strong anticancer agent within the body.

 

Selenium supplementation also decreases the formation of the cancer permissive prostaglandin hormone known as prostaglandin series-2, which I will discuss in more detail in the next section. Selenium metabolism itself may initiate changes that lead to programmed-cell death of cancer cells and pre-cancerous cells. Selenium is an essential nutrient for humans; it fulfills the physiological requirements for more than 13 human enzymes and proteins.

 

The average intake of selenium from food sources is shown to be between about 50 micrograms daily. Is it adequate? This is not sufficiently adequate to maximize out cancer defenses according to the available research. The truth is that selenium consumed as a dietary supplement, beyond levels attainable from food, at 100-200 micrograms (mcg) per day, has been shown to reduce the incidence of lung, colorectal and prostate cancer in humans. As reported by B Combs and fellow researchers, selenium blood levels of approximately 120 ng/ml (1.5 umol/ml) may be optimal for cancer prevention in general. The most recent estimates suggest that women require a minimum of 96 micrograms per day and men require at least 120 micrograms per day to support plasma levels at 120 ug/ml (micrograms per milliliter). As for safety, toxicity of selenium begins at doses starting at 1,000 micrograms per day, so 100-200 mcgs of selenium supplementation from multiple vitamin is extremely safe.

 

Vitamin E has also been shown to reduce risk of colon cancer. On July 16, 1997, W.L.Stone and A.M.Papas reviewed the world-wide scientific evidence related to vitamin E in the prevention of colon cancer (Journal of the National Cancer Institute).

 

Previous studies dating back to 1982 demonstrated that 400 mg of vitamin E and 400 mg of vitamin C, when taken daily, were able to dramatically reduce the formation of cancer-causing agents (fecal mutagens) in the colon of test subjects.

Like selenium, Vitamin E also inhibits the formation of a dangerous prostaglandin hormone known as Prostaglandin E2. High levels of Prostaglandin E2 are linked to increased risk of colon cancer because it encourages the rapid division and growth of tumor cells and it helps cancer cells escape surveillance by the body's immune system that would otherwise kill these cancer cells in the normal course of events. By suppressing the formation of Prostaglandin E2, vitamin E helps prevent tumor cells from growing and spreading and enables the immune system to function more effectively to identify and destroy cancer cell that may emerge.

 

All of the animal studies reviewed by Dr. Prasad and fellow researchers, suggest strongly that colon cancer is reduced when animals are supplemented with vitamin E, after being exposed to known cancer-causing agents.

 

Animal and human studies are highly suggestive that vitamin E and selenium work synergistically to reduce risk of colon cancer.

 

More recently, the Iowa Women's Health Study demonstrated a very strong protective effect for vitamin E in the prevention of colon cancer. The Iowa Women's Health Study was a large-scale study of 35,000 women between 55 and 66 years of age who had no previous history of cancer.

 

This 4-year study provided convincing data that a high intake of vitamin E was associated with a reduced risk of colon cancer. Women in the top 20% level of vitamin E intake had a 66% lower risk of developing colon cancer than women ingesting vitamin E in the lowest 20% intake range.

 

In almost all cases, the women with a high intake of vitamin E were taking supplements containing Vitamin E.

 

Results from the Alpha-Tocopherol, Beta-Carotene, Cancer Prevention Study of 29,000 male smokers from Finland also indicated that a daily supplement of 50 mg of vitamin E helped to prevent the subsequent development of colon and rectal cancer.

 

From a practical standpoint, I recommend that adults ingest 400 I.U. of vitamin E per day, from a high potency multi-vitamin and mineral, as a means to help prevent colon cancer, and other cancers. In fact, Vitamin E plays a role in the prevention of many degenerative diseases, as I will outline in this section. Vitamin E is fat-soluble, so you must take it with a meal that provides some fat in order for it to be absorbed from your intestinal tract into the blood stream. The same is true for Vitamin A, beta-carotene, lycopene, lutein, (other carotenoids) Vitamin D and Vitamin K.

 

Vitamin C, in a number of different types of studies, has consistently been shown to be associated with a reduced risk of colon cancer. Vitamin C acts as an antioxidant in the intestinal tract and when supplemented, has been shown to decrease the concentrations of cancer-causing chemicals in fecal matter. Vitamin C also blocks the formation of cancer-causing nitrosamines within the entire intestinal tract. Vitamin C supplementation was also shown to reduce the recurrence of colon polyps by 35% compared to only 23% in the placebo group, in a 2.5- year study of polyp sufferers.

Prostate Cancer

One of the proposed mechanisms for the development of prostate cancer involves free radicals, as a number of studies suggest a link between free radicals (oxidative stress) and tumor development within the prostate

 

In several studies higher intakes and/or blood levels of the antioxidants vitamin E, selenium and lycopene have been associated with decreased prostate cancer incidence.

In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, long-term supplementation with vitamin E was associated with a 32% decrease in the incidence of prostate cancer compared with those not receiving vitamin E supplementation. Moreover, death from prostate cancer was 41% lower among men receiving the vitamin E supplement. The length of this supplementation study was 5-8 years and the dosage of vitamin E was 50 mg (alpha-tocopherol).

Previous studies have observed that low blood levels of vitamin E in smokers are associated with an increased risk of prostate cancer.

Many researchers believe that antioxidant function is an important means to prevent prostate cancer initiation and promotion. This contention is further supported by the work of Clark and fellow researchers, who demonstrated that supplementation with the mineral selenium (mean time period 4.5 years) was associated with a 63% lower incidence of prostate cancer. Blood levels of selenium have been reported to be low in patients with prostate cancer. In preliminary reports, people with the lowest blood levels of selenium had between 3.8 and 5.8 times the risk of dying from prostate cancer compared with those who had the highest selenium levels.

 

The Health Professionals Follow-up Study also supports the hypothesis that antioxidant function can prevent prostate cancer. In this study of nearly 48,000 subjects E. Giovannucci and fellow researchers reported that a significant decrease in risk of developing prostate cancer was associated with higher intake of lycopene. Lycopene is found in tomatoes and certain tomato products and is known for its potent antioxidant properties. It is interesting to note that the highest concentrations of lycopene occur in the testes, adrenals, and prostate gland. It is estimated that a minimum 4-6mg daily intake of lycopene is needed for prostate protection. An intake level of at least 6 mg per day or more of lycopene was associated with approximately a 21% reduction in prostate cancer incidence in The Health Professionals Follow-up Study, compared with men consuming less than 2.3 mg per day.

 

Lycopene is the most effective quencher of singlet oxygen (a very aggressive and harmful oxygen free radical) of the major carotenoids (beta-carotene-like compounds) and is the primary carotenoid in the blood and various tissues, including the prostate gland.

 

Taken together, the emerging research suggests that vitamin E, selenium and lycopene supplementation, at specific dosages, may significantly reduce the risk of prostate cancer.

Prostate cancer is the most common cancer in males in North America.

Other nutritional factors and supplements may also help to prevent prostate cancer and are discussed in more detail in Step 5.

Breast Cancer

Scientific investigation has revealed that vitamin E inhibits the growth of certain malignant cells, including certain human prostate and breast cancer cell lines.

 

In human populations, several epidemiologic (observational) and clinical intervention studies have suggested that vitamin E supplementation can inhibit the development of certain cancers. In particular, the studies by Knekt, Malvy and the Alpha-Tocopheral, Beta-Carotene Cancer Prevention Study Group have all provided evidence that vitamin E supplementation is associated with reduced risk of certain cancers, including breast cancer. For example, in the Nurses’ Health Study there was a 16% decreased risk of breast cancer in women within the top 20% of vitamin E intake compared to those in the lowest 20% range. Women in the top 20% intake range were taking vitamin E supplements in some form, to a large degree.

 

Vitamin E supplementation is also associated with reducing the spread and progression of breast cancer in women who have already had the disease. According to the study by A. Fleischauer and fellow researchers, vitamin E supplementation in breast cancer survivors is associated with 25-35% decrease in recurrence and mortality compared to non-users of vitamin E supplements. In fact, in women who have had breast cancer, a cocktail of various antioxidants was shown to be helpful in the study by K. Lockwood and fellow researchers.

 

These researchers conducted an 18-month study, involving 32 women with breast cancer. These women were put on a nutritional protocol consisting of high dose antioxidants and accessory nutrients. The women were between 32 and 81 years of age and classified “high risk” because of tumor spread to the lymph nodes in the axilla (under the arm). The nutritional protocol, which was added to the normal surgical and therapeutic treatments for breast cancer, consisted of a combination of the following antioxidants. Vitamin C, 2,850 mg; vitamin E, 2500 IU; beta-carotene, 32.5 IU selenium, 387mcg, plus secondary vitamins and minerals, essential fatty acids (1.2 gm gamma linolenic acid and 3.5 gm omega-3 fatty acids) and coenzyme Q10, (90-390 mg per day). Biochemical markers, clinical condition, tumor spread, quality of life parameters, and survival were followed during the 18-month trial. Compliance was excellent. The main observations were: none of the patients died during the study period (the expected number was four); none of the patients showed signs of further distant metastases; quality of life was improved (no weight loss, reduced use of painkillers); and six patients showed apparent partial remission.

 

This study indicates that various antioxidants and other nutrients can work synergistically to help contain and prevent cancer to some degree.

Don’t have time to read the whole book right now?

No worries. Let me send you a copy so you can read it when it’s convenient for you. Just let me know where to send it.

LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

Cervical Cancer

Antioxidants, such as vitamin E, beta-carotene and other carotenoids have been shown to protect against cervical cancer in certain studies. In several, but not all studies, elevated blood levels of folic acid, beta-carotene, lycopene, and vitamin E have been found to protect against cervical dysplasia (a precancerous condition of the cervix) In a recent study of 32 black women, by P. Kanetsky and fellow researchers, women with higher intake and blood levels of lycopene were one-third as likely to have cervical dysplasia as were women with the lowest one-third of lycopene blood levels. In addition, they were one-fourth as likely to develop the dysplasia if they had higher intake and blood levels of vitamin A, than were women with the lowest one-third of vitamin A blood levels. Vitamin A is also an antioxidant vitamin and has other anti-cancer properties.

 

Smoking is a known risk factor for the development of cervical dysplasia and beta-carotene has been shown to be effective against smoking-related cervical dysplasia and cervical cancer. This was documented in studies by HC de Vet and fellow researchers, and W Jr. Winkelstein.

 

In general, evidence suggests that low vitamin status of these antioxidants, folic acid (a B-vitamin), cigarette smoking and human papillomavirus infection combine to contribute to the risk and progression of cervical dysplasia.

 

In a study of patients with mild or moderate cervical dysplasia, 30 patients were treated with 30mg (50,000 I.U.) of beta-carotene orally for up to six months. More than 70 percent of patients showed reversal of their condition by six months. However, only three months were required to realize optimal reversal of this condition, according to biopsy studies of shed cervical cells.

 

At this time there is sufficient evidence to suggest that nutrition and antioxidant supplementation play a vital role in the prevention of cervical dysplasia and, in some cases, can reverse this condition in its early and moderate stages.

Stomach

Stomach cancer and colon cancer have been shown to susceptible to the influence of a carcinogen known as nitrosamines. Nitrosamines represent an important group of environmental carcinogens. On average, individuals consume approximately 74 mg per day of nitrates in North America. Processed meats that are treated are preserved with nitrate and nitrite salts are a major source of these carcinogens. Many alcoholic beverages contain nitrates, and soils treated with nitrogen fertilizers give rise to many plant foods that now contain more nitrates than was the case before the use of nitrogen fertilizers. Thus, all of us are exposed to some background levels of nitrates entering the body. Within the stomach and intestinal tract nitrates can combine with protein (amino acids) to form cancer-causing nitrosamines. Both vitamin C and vitamin E have been shown to block the formation of nitrosamines when taken as supplements with, or shortly after, a meal containing nitrates and protein. For optimal protection, taking 500 mg of vitamin C, twice per day has been shown to block as much as 85-100% of nitrosamines formation under conditions of a high nitrate intake. A number of different types of studies have consistently shown a strong protective effect of vitamin C against stomach and colon cancer. The same is true regarding vitamin E. For vitamin E, a daily dosage of 400 IU can help block the formation of nitrosamines.

Antioxidants Reduce Heart Disease Risk

There is a substantial body of evidence showing that Vitamin E and Vitamin C supplementation can reduce risk of heart disease and other cardiovascular conditions. Remember that cardiovascular disease accounts for nearly 50% of all deaths in our society, so the following information can truly be life-saving.

In 1987 F Gey and fellow researchers, published the results of a large cross-sectional study performed in different regions throughout Europe. The researchers collected blood samples from healthy men who lived in areas with high heart disease mortality (Southwest Finland, North Karelia, and Scotland), medium mortality (Northern Ireland) and low mortality (Switzerland and Southern Italy). The average blood vitamin E levels were found to be significantly higher in regions with low heart disease mortality compared with vitamin E blood levels in regions with higher rates. In a subsequent, more detailed study of 16 European regions (the Monica Study), F Gey and fellow researchers again reported a remarkably strong relationship between higher blood vitamin E levels and lower rates of heart disease mortality.

A number of other studies have also reported that low blood vitamin E levels are associated with an increased risk of heart and cardiovascular disease.

In patients with angina, Riemersma and fellow researchers, in a case-control study, found lower vitamin E levels in newly documented angina patients (105 patients) compared with normal subjects (382 control subjects). Individuals with the lowest 20% blood levels of vitamin E had a 2.7 times higher risk of developing angina.

Kok and fellow researchers followed 10,532 people in a Dutch nested case-control study. After 9 years, 68 cardiovascular deaths were documented (mostly heart disease). In this study subjects with the lowest 20% of vitamin E blood levels had a 1.5 times greater risk of cardiovascular disease mortality.

 

In Washington County MD Study, individuals with the lowest 20% blood levels of vitamin E had a 1.4 times greater risk of heart disease.

 

In a 14-year study of 5,133 Finnish men and women aged 30-69, Knekt found that individuals consuming the most vitamin E (top 1/3 intake level) had the lowest rates of heart disease.

In the Nurses’ Health Study, which has followed 87,245 US female nurses aged 34-59 years old, since 1980, women who were free from cardiovascular disease and cancer at the beginning of the study showed a 41% reduction in risk of heart disease in those who consumed vitamin E supplements (greater than/or equal to 100 I.U.) for at least 2 years, compared with other nurses, after 8 years of follow up. As with other studies this finding held true even after factoring in other heart disease risk factors.

 

In this same study, the risk of ischemic stroke was also reduced 29% in nurses using vitamin E supplementation at or above 100 I.U. per day.

 

Very similar findings were seen in men in the Health Professionals Follow-up Study as reported by E Rimm and fellow researchers. This study enlisted 39,910 men aged 40-75 years old in 1986 who were free of cardiovascular disease, diabetes, or high cholesterol at the beginning of the study. Once again, the men using vitamin E supplementation showed the greatest reduction in risk of heart disease (46% reduction in risk) compared with non-supplement users. This fact remained unchanged after factoring in other known risk factors such as age, smoking, high blood pressure etc. The protective vitamin E supplementation dosage was found to be 100-350 I.U. per day in this study. As with the Nurses' Health Study, vitamin E supplementation below 100 I.U. per day did not provide significant protection against heart disease.

 

In a most remarkable study, H Hodis and fellow researchers assessed the progression of coronary artery narrowing by using serial, quantitative coronary angiographic methods. He found that in 162 nonsmoking men aged 40-59 years old, men who took vitamin E supplements had a significant reduction in the narrowing of coronary arteries compared with non-supplement users. The apparent benefit was once again limited to those taking greater than 100 I.U. of vitamins E per day. In this study subjects receiving cholesterol-lowering medication, and those who also took vitamin E supplements, showed regression (reversal) in coronary artery narrowing. No other group demonstrated this finding. The ability to reverse heart disease by this form of combination therapy is indeed, a remarkable finding.

 

Other intervention trials using vitamin E supplementation have also shown it effectiveness for cardiovascular function. In a study of patients with severe claudication (severe leg cramps during walking) from atherosclerosis (narrowed arteries) in peripheral vessels, the improvement in symptom-free walking distance in the vitamin E supplemented group (n=24) was twice as great as the results achieved in the placebo group (n=9).

 

DeMaio conducted a study in 100 patients who underwent coronary angioplasty. They were given either a placebo (n=48) or vitamin E at 1,200 I.U. (n=52) for 4 months after the procedure. Among those given the placebo, 50% had significant restenosis (narrowing), whereas only 35% of those in the vitamin E group had significant restenosis.

 

Similar findings were observed by DuBroff and fellow researchers, in 440 patients with coronary angioplasty. The restenosis rate was only 15% in the vitamin E supplement users compared to 31% in those taking no supplements, and 32% in those taking vitamin C supplements only.

 

Overall, studies indicate that taking vitamin E supplementation every day at a dosage that exceeds 100 IU (I strongly recommend a dosage of 400 IU) is associated with a 40% reduction in risk for heart attack and other cardiovascular problems related to atherosclerosis (narrowing of arteries).

 

Our present understanding suggests that vitamin E reduces risk of cardiovascular disease through 3 primary mechanisms: antioxidant effects, inhibition of the proliferation of smooth muscle, and reducing the stickiness of blood platelets.

 

As an antioxidant, vitamin E travels in the bloodstream bound to cholesterol (LDL). As part of this cholesterol complex, vitamin E serves to intercept free radicals, which may otherwise damage cholesterol and its related unsaturated fats. Cholesterol that gets damaged by free radicals is much more inclined to stick to the walls of the artery and cause narrowing, obstructing blood flow.

 

Secondly, vitamin E regulates the rate at which smooth muscle, below the artery wall, will grow or proliferate. Narrowing of the arteries involves several events. As part of the progression of this process smooth muscle grows into the artery from above and below the artery wall. This event contributes to further narrowing of the blood vessel at the involved site. As the artery becomes more plugged up with smooth muscle fibers growing into the channel of the artery and damaged cholesterol accelerating the narrowing process, the risk of a heart attack or stroke is greatly increased. Vitamin E is important to prevent both of these events.

 

The third protective action of vitamin E involves its ability to reduce the stickiness of blood platelets. Platelets are the blood cells that clump together and form a clot in the event you cut yourself. Their ability to form a clot when necessary prevents us from bleeding to death each time we nick ourselves with a sharp object or develop a nosebleed. Thus, platelets are supposed to clot under certain conditions.

 

However, several common lifestyle factors encourage platelets to be excessively sticky and to form abnormal clots or mini-plugs inside our arteries. Environmental factors such as obesity, high saturated fat diet, smoking and a sedentary lifestyle contribute to excessive platelet stickiness. The clumping together of platelets at the site of artery narrowing is frequently the final event that precedes a fatal or non-fatal heart attack or ischaemic stroke. The platelet plug completes the total obstruction to blood flow. Ideally, platelets should clump together to save your life, not to end it. Vitamin E functions to regulate platelet stickness, helping to discourage platelets from clumping together abnormally inside the artery wall. As a result, platelets are less inclined to contribute to blood flow obstruction even when other lifestyle factors are present that would otherwise encourage excessive platelet stickiness.

 

As demonstrated by a number of prominent researchers, to achieve blood levels of vitamin E necessary to materially reduce free radical attack of LDL-cholesterol, inhibit smooth muscle growth into the channel (lumen) of the artery and reduce platelet stickiness, vitamin E must be provided at doses obtainable only through supplementation.

 

From the available data, it appears that at least 100 I.U. of vitamin E per day is necessary to obtain a cardio-protective effect. In my view a daily dosage of 400 I.U. of vitamin E is most ideal from the standpoint of prevention and anti-aging.

 

What about vitamin C and heart disease? Previously F. Gey demonstrated in the large MONICA study (a study involving 10 countries) that vitamin C blood levels above 50 micromoles per litre was associated with more than a 50% reduction in heart disease mortality rates. This reduction was experienced in contrast to populations where blood vitamin C levels averaged between 15-27 micromoles per litre. In the MONICA study, low blood levels of vitamin C and vitamin E (vitamin E below the range of 25-30 micromoles per litre) were stronger predictors of future heart disease mortality than was high blood cholesterol levels, smoking or high blood pressure, which are known cardinal risk factors.

 

In a 20-year follow-up study, analysis of mortality in patients in the United Kingdom, who were older than 65 years of age, showed that low vitamin C status (either dietary intake or blood levels) was strongly associated with increased subsequent risk of death from stroke. A Swiss study uncovered an identical finding, which was reported in 1993 in The Journal of Clinical Investigation by F.Gey, H. Stahelin and associates.

 

In a study by D. Harats, the group receiving 500 mg of vitamin C not only attained more optimal blood levels of vitamin C, but also demonstrated other favorable indicators related to a decreased risk for cardiovascular disease.

 

The subjects ingesting 500 mg per day of vitamin C showed decreased free radical damage to cholesterol. When blood cholesterol becomes damaged by free radicals, it has a greater tendency to stick to the walls of the artery causing narrowing and blockage.

 

D. Harats and fellow researchers compared cardiovascular risk factors in subjects consuming 50 mg of vitamin C with those who were later assigned a vitamin C supplement of 500 mg per day for a two-month period.

 

In the subjects receiving the vitamin C supplement, blood levels of vitamin C rose from 13.5 micromoles per liter to 51.7 micromoles per liter.

 

A number of prior studies have demonstrated that vitamin E protects blood cholesterol from free radical attack. It appears that vitamin C may share this important role as a water-soluble antioxidant circulating in the bloodstream. In fact, higher doses of vitamin C (500-1,000 mg) have been shown to actually lower blood cholesterol in high cholesterol patients receiving supplementation.

 

In another Finnish study Salonen found that low vitamin E status (from diet) was associated with increased risk of heart attack only if vitamin C status was also low. Because vitamin C is required to regenerate vitamin E, this finding could explain the lack of protective effect of vitamin E. With lower vitamin C status, vitamin E is used up faster and can not be recycled back to an effective antioxidant state to provide continual protection against heart disease. Thus, vitamin C and vitamin E appear to work together to help protect us against heart attack, stroke and other vascular diseases The recommended daily allowance for vitamin C is listed at 60 mg. This nominal amount of vitamin C is insufficient to raise blood levels into a more protective range, discouraging free radical damage to blood cholesterol and helping to lower the total amount of cholesterol in the bloodstream.

Unbelievably, 20-30% of U.S. adults fail to even attain 60 mg of vitamin C each day from their diet. Ingesting a total daily dosage of at least 1000 mg per day of vitamin C, in two 500 mg doses, is what I recommend for general prevention and anti-aging.

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Dr. James Meschino, 

DC, MS, ROHP

Antioxidants Reduce Alzheimer’s disease, and Dementia Risk

Free radicals are also strongly linked to the development of dementia and Alzheimer’s disease. As the brain uses at least 10% of body’s oxygen, at any give moment, brain cells are thereby exposed to significant levels of oxygen free radicals. Over a lifetime these free radicals can cause enough corrosive damage to brain cells (in a similar fashion as oxygen in the air will rust out your car over time) to interfere with their normal function and to contribute to their death if the damage is severe enough. Researchers have shown that many brain and nerve degenerative diseases involve free radical damage. There is convincing evidence to show that Alzheimer’s disease and age-related cognitive decline (senile dementia) are strongly linked to free radical damage. Moreover, evidence is accumulating to demonstrate that individuals, who take antioxidant supplements at protective dosages, have a much lower risk of developing these conditions as they age.

In the Chicago Health in Aging Project, the average annual decline in cognitive score was 34% less in those with the highest Vitamin E intake (mean of 299 I.U./day) compared with those in the lowest intake group (6.7 I.U./day.) A weak association was also seen for Vitamin C. This study included 6,000 persons aged 62-102, who were followed for three consecutive years. In 1998 MC Morris and fellow researchers showed that among a group of 633 persons, 65 years and older, none of the vitamin E or vitamin C supplement users developed Alzheimer’s disease during the 4.3 year follow up study.

In the Alzheimer’s Disease Co-operative Study, Alzheimer’s patients with moderately advanced disease were treated with 2,000 I.U. Vitamin E/day or a placebo. The results indicated that Vitamin E supplementation was able to significantly slow the functional deterioration of the brain in these patients, delaying the need for nursing home placement and retarding the progression of the disease. (Grundman, M., 2000). Laboratory studies reveal that Vitamin E inhibits free radical damage to brain cells induced by the Abeta-protein, which is a hallmark feature in Alzheimer’s disease (Butterfield, D.A., et al, 1999).

 

Previous studies have shown that supplementation with vitamin E was effective in slowing the progression of Parkinson’s disease Alzheimer’s disease and helps to control tardive dyskinesia (a condition involving involuntary repetitive movements of the face and head brought on by certain drugs that affect brain function) (Vatassery GT et al. 1999).

 

Overall there is substantial clinical and experimental data to suggest that the use of a daily antioxidant-enriched, multiple vitamin and mineral supplement offers significant protection against age-related cognitive decline and Alzheimer’s disease, brought on by cumulative free radical damage to brain cells.

Antioxidants Reduce Eye Disease Risk (cataracts and macular degeneration)

The leading cause of blindness in people over the age of 55 in North America is a condition known as macular degeneration. The evidence linking free radical damage to the development of age-related macular degeneration of the eye (AMD) is strong and consistent. In order for us to see, ultra-violet light from the sun travels through the pupil of the eye to reach the back of the eye, where waves in the visible light spectrum stimulate the optic nerve to enable vision to occur. However the ultra-violet light reaching the back of the eye also induces free radical damage, which in turn can lead to macular degeneration. In addition to the effects of ultra-violet light, other risk factors for AMD include smoking, advancing age, atherosclerosis and high blood pressure. Early studies showed that animals given certain antioxidants experienced a lower risk of visual problems in experimental studies. Certain antioxidants are known to concentrate in various parts of the eye. Some of the antioxidants that have been shown to protect against eye diseases include vitamin C, vitamin E, Beta-carotene, zinc, lutein and zeazanthin.

 

Preliminary studies in humans also provided evidence that more optimal status of antioxidant vitamins and minerals could reduce the risk of AMD. In one study, higher blood levels of antioxidants were shown to be related to a lower risk of developing AMD. Another investigation revealed that individuals in the top 20% blood levels of selenium, Vitamin C and Vitamin E had a 70% lower risk of developing AMD than did those with blood levels in the lowest 20%. In the Physicians’ Health Study male doctors taking Vitamin E supplements had a 13% reduced risk of AMD.

 

Dietary intake of lutein and zeazanthin (mostly dark green vegetables) and supplementation with these two carotenoids has been shown to significantly increase the amount of macular pigment in the back of the eye, which acts as a free radical shield, protecting the optic nerve from free radical damage. In fact the area around the optic nerve, in the back of the eye, is known as the macula lutea due to the high concentration of lutein, which creates a yellowish- tinge to this area of the eye when viewed with an ophthalmoscope (the instrument used by doctors to view the back of the eye) One study showed that adults with the highest intake of lutein had a 57% reduced risk of developing AMD than did those with low levels of this carotenoid.

 

The most convincing evidence to show that antioxidant supplements provide protection against AMD was provided by the Age-Related Disease Study, a multi-center, intervention trial involving 4,757 patients between the ages of 55 and 80 years old. In this study, conducted by the National Eye Institute (NEI), patients who were at high risk of developing more advanced stages of age-related macular degeneration (AMD), reduced their risk by approximately 25% when treated with a high-dose combination of Vitamin C, Vitamin E, Beta-carotene, and zinc. According to the NEI, antioxidant supplementation is the first effective treatment ever shown to successfully slow the progression of AMD. Participants in this double-blind, placebo-controlled clinical study, who suffered from varying degrees of AMD, were given one of four treatments. The best results occurred in those taking both antioxidant and zinc supplements at the following doses:

  • Vitamin C – 500 mg 
  • Vitamin E – 400 IU
  • Beta-carotene – 25,000 IU
  • Zinc – 80 mg

Although all the details as to the underlying causes of AMD are not fully understood, it has been shown that free radical damage from ultra-violet light (sunlight), and other sources (e.g cigarette smoke) reaching the macula at the back of the eye, are likely a significant contributing factor.

 

Two previous intervention trials, using a commercially available broad-based antioxidant formulas in patients with established AMD, demonstrated that supplementation halted or significantly slowed the further progression of the disease and, in some cases, vision actually improved. These studies were only 6 months and 18 months in duration, thus the research and medical community demanded a longer term, multi-center, double-blind, placebo-controlled study to confirm these findings. This was the impetus for the design and implementation of the Age-Related Eye Disease Study reviewed above. In these previous intervention trials the supplement formula contained Beta-carotene, Vitamin C, Vitamin E, zinc, copper, manganese, selenium and riboflavin.

In an intervention trial with 16 participants (13 with retinitis pigmentosa and 3 with other retinal degeneration problems), vision improved significantly after 26 weeks of supplementation with lutein (40 mg for 6 weeks, followed by 20 mg for 20 weeks). These researchers have shown similar results in small trials involving patients with AMD as well.

Antioxidant supplements have also been shown to prevent cataracts. Cataracts are white, opaque lesions that form on the normally transparent lens of the eye. They occur as a result of damage to the protein structure of the lens. Strong evidence indicates that free radical damage from ultra-violet light (sunlight) and radiation exposure induces free radical damage that contributes to senile cataract development. The lens of the eye has been shown to be devoid of the antioxidant enzymes, superoxide dismutase (SOD), catalase and glutathione peroxidase, and is thus, completely dependent upon nutritional antioxidants including Vitamin E, Vitamin C, selenium and carotenes for its antioxidant defenses. It should be noted that cigarette smoking, which also increases free radical stress to the body, is also a known risk factor for the development of cataracts.

Cataracts are the leading cause of blindness and impaired vision in the United States. Forty thousand Americans are blind due to cataracts, and cataract surgery is the most prevalent major surgery among Medicare recipients in the U.S. The Canadian Study by J. Robertson and fellow researchers, suggested that if all individuals over 55 years of age took a supplement of Vitamin C and Vitamin E each day, at appropriate doses, it would reduce cataract incidence by at least 50% and cut related health care costs in half. A number of intervention trials have demonstrated that 1000 mg of Vitamin C per day (or more) can reduce cataract development and/or halt or slow the further progression of cataracts, in the early stages. Other case-control and prospective studies have suggested that higher blood levels and/or intake levels of Vitamin C are associated with a significant reduction in risk of cataracts. For instance, in the study by P Jacques, plasma Vitamin C at 40 umol/L was associated with an 11.3 times greater risk of cataract development than occurred in subjects with a plasma level of 90 umol/L or higher.

Vitamin E supplementation has also been shown to be protective in regards to cataract prevention. Daily supplementation with 400 IU was shown to be effective in this regard, whereas a dosage of only 50 IU failed to provide protection against cataract development in a double-blind trial.

The body of evidence suggests that antioxidant supplementation can prevent early stage development of both cataracts and age-related macular degeneration and, thus has the potential to markedly reduce financial costs to the health care system and improve the quality of life for millions of individuals. Consuming more fruits and vegetables, dark green leafy vegetables, not smoking and implementing lifestyle behaviors to prevent or better manage diabetes should be emphasized as preventive measures. However, the use of antioxidant supplements at levels beyond which an individual can customarily consume from food alone, have emerged as an extremely important practice through which these eye conditions may be prevented and treated.

Antioxidants Slow Skin, Wrinkling and Reduce Skin Cancer Risk

Premature aging of the skin and genetic damage to skin cells, most commonly occurs due to the production of free radical damage induced by exposure to ultraviolet light from solar radiation (sunlight) and tanning beds. Free radicals generated from cigarette smoking and alcohol consumption can also damage the skin in a similar way. Free radical damage hastens the process of skin aging and wrinkling and create mutations that are known to lead to the development of skin cancer (basal cell carcinoma, squamous cell carcinoma and melanoma). Therefore, avoiding over exposure to sunlight, (and other known sources of free radicals), wearing protective clothing and using antioxidant-containing sun block creams and lotions are prudent strategies to minimize risk of premature skin aging and skin cancer.

In addition to these factors, recent studies have indicated that the use of antioxidant supplements can further help to protect the skin from free radical damage and age-related changes linked to premature wrinkling and cancerous mutations. A double-blind, placebo-controlled study in human subjects demonstrated that subjects taking the Vitamin C (2000 mg per day) and Vitamin E (1000 I.U.) supplements had significantly less free-radical damage to their skin after UV-light exposure than did the group not given the antioxidant supplement regime. They also showed significantly less sunburn reaction.

Intensive investigation in this area of study strongly suggests that the daily supplementation of Vitamins A, C, E, Beta-carotene, selenium and zinc, at levels above those typically consumed from food alone, provides the skin with additional and possibly essential antioxidant defenses to help slow skin aging and lends important support to other skin cancer prevention initiatives.

Antioxidants Strengthen Your Immune System

Many studies have shown supplementation with antioxidants can help maintain more optimal immune function as we age, and help to strengthen the immune system in individuals who are in an immune compromised state. As we age, the immune system tends to become weaker and less efficient at killing germs that can cause serious infections, as well less efficient at identifying and killing emerging cancer cells. It is essential to maintain a strong, efficient immune system throughout your lifetime and daily antioxidant supplementation is an important proactive strategy to attain this objective. Here is a brief review of some of the research trials on this subject.

Vitamin E supplementation has been shown to enhance some measures of immune-cell activity in the elderly. This effect is more pronounced with 200 IU per day compared to either lower doses (60 IU per day), according to double-blind research. Intakes under 200 IU per day have not boosted immune function in some reports.

Beta-carotene supplementation and other carotenoids have increased immune cell numbers and activity in animal and human research, an effect that appears to be separate from their role as precursors to vitamin A. Placebo-controlled research has shown positive benefits of beta-carotene supplements in increasing numbers of some white blood cells and enhancing cancer-fighting immune functions in healthy people at 25,000–100,000 IU per day.

In double-blind trials in elderly subjects supplementation with 40,000–150,000 IU per day of beta-carotene was shown to increase natural killer (NK) cell activity, which are immune cells that identify and destroy emerging cancer cells. Supplementation at these high levels may be important to individuals who have already encountered cancer or have severely compromised immune function (e.g. HIV- infection, Hepatitis).

Vitamin C has been shown to stimulate the immune system by both elevating interferon levels and enhancing the activity of certain immune cells. A combination of antioxidants vitamin A vitamin C, and vitamin E significantly improved immune cell number and activity, compared to placebo, in a group of hospitalized elderly people. Daily intake of a 1,000 mg vitamin C, plus 200 IU vitamin E for four months improved several measures of immune function in another study, involving human subjects.

B-Vitamins Also Prevent Cancer, Heart Disease And Dementia

In addition to antioxidants, a well formulated high potency multivitamin and mineral should also include a B-50 complex (includes 50 mg of most of the B-vitamins, as well as 400 mcg of folic acid, 50 mcg of vitaminB12 and 300 mcg of biotin), as research shows these vitamins participate in the prevention of many degenerative diseases. More specifically, optimal B-vitamin status has been shown to reduce risk of heart disease, certain inflammatory states, improve detoxification processes and maintain brain and cognitive function as we age. B- vitamins are also essential for the synthesis of red blood cells, normal cell replication, and many more crucial functions. Known for their anti-stress and anti-fatigue properties, a B-50 complex is an important component of a high-grade multiple vitamin and mineral formulation.

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LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

B-Vitamins Reduce Risk Of Cervical and Colon Cancer

The B-vitamins folic acid and vitamin B12 are required to help the body convert a compound called homocysteine to methionine. Once formed, methionine is readily converted to S-adenosylmethionine, which is necessary to form the DNA that makes up our genetic blueprints for life.

If folic acid level and/or vitamin B12 status become sub-optimal, then the amount of S-adenosylmethionine declines. This results in an inability to properly produce DNA as cells replace themselves from one generation to the next. The danger is that genetic errors become more common and genetic linkages become more fragile and prone to breakage with resulting mutations. These alterations to genetic structure provide the foundation for cancerous changes to occur in our genes. It is well established that our DNA is much more prone to cancerous mutations under conditions of sub-optimal intake of folic acid and vitamin B12.

Women in a marginal deficiency state of folic acid are known to be prone to cervical dysplasia and cervical cancer. This is related to the fact that cells that line the cervix replace themselves every 7-14 days and therefore, must continuously synthesize DNA. Studies have demonstrated that poor folic acid status can lead to DNA abnormalities with subsequent development of cervical dysplasia or megaloblastic features of cervical cells (large abnormal cell appearance). With respect to cervical dysplasia (a precancerous condition), folic acid, via its role in DNA synthesis and DNA repair has been shown to inhibit the ability of the human papillomavirus (HPV) from invading the DNA of surface cervical cells. HPV is strongly associated with cervical cancer, and thus, folic acid supplementation is an important step to prevent its invasion of cervical tissue. Women who have experienced multiple sex partners are most prone to infection with HPV, as contact with human semen is the way in which cervical cells are typically exposed to the virus

 

As well, oral contraceptives are known to increase the rate of cell division of cervical cells, thereby, increasing the need for adequate folic acid intake. Studies by Whitehead and fellow researchers, as well as Butterworth and fellow researchers, have demonstrated that folic acid supplementation can reverse cervical megaloblastic changes and cervical dysplasia, respectively, in patients using oral contraceptives. In fact, oral contraceptive use is a known risk factor for cervical dysplasia, primarily due to its effect on speeding up cell division rates.

In the study by Butterworth, patients with mild and moderate degrees of cervical dysplasia showed reversal of their condition over a 3-month trial period with folic acid supplementation.

In both studies the authors noted a statistically lower mean red blood cell folic acid concentration in oral contraceptive users compared with non-users, which was particularly marked in patients with cervical dysplasia.

Other population studies (epidemiological studies) consistently support the research showing that folic acid plays a protective role in the prevention of cervical dysplasia.

 

Unfortunately, up to 88 percent of the population consumes less then 400mcg per day of folic acid. This is the level that women should ingest to reduce the risk of spinal birth defect in their offspring.

As it turns out, the same level of folic acid intake appears to be sufficient to reduce the risk of cervical dysplasia. Ingesting a multiple vitamin and mineral containing 400 mcg is likely the most practical and effective means of ensuring adequate folic acid intake.

With respect to colon cancer, E Giovannucci and fellow researchers assessed dietary intake for a 1-year period for women of the Nurses' Health Study and for men of the Health Professional Follow-up study – using a semi-quantitative and food frequency questionnaire. Of the 25,474 subjects, 895 developed adenomatous polyps of the left colon or rectum.

A major finding of the study was that high folic acid intake was protective against colorectal cancer. Women in the top 20% intake level of folic acid demonstrated a 34% decreased risk of colorectal cancer compared with women in the bottom 20% intake level of folic acid. For men a 37% reduction in risk was observed for the highest 20% intake of folic acid versus the lowest 20% intake group.

Users of multiple vitamins demonstrated the greatest reduction in risk of colorectal cancer in this study. Much of this protective effect was shown to be due to folic acid. These findings are consistent with other epidemiological evidence indicating that folic acid reduces the risk of colorectal cancers. As colon cancer is the second leading cause of cancer death in North America, the ingestion of 400 mcg per day of folic acid from a multiple vitamin is one more strategy to employ to help reduce your risk of this disease.

In regards to the role of B-vitamins in the prevention of heart disease and stoke, in the mid to late 1960s several researchers first identified that high blood levels of homocysteine was associated with premature narrowing of arteries leading to heart attacks and related heart disease. Homocysteine is thought to increase the risk for heart disease through direct toxic effects to the cells that line our blood vessels. It increases the tendency for blood platelet cells to clump together in the bloodstream thus, obstructing blood flow. It also stimulates muscle fibers beneath the blood vessels to grow into the artery, further impairing the flow of blood. High blood levels of homocysteine is now considered to be a significant risk factor for stroke, heart attack, and reduced blood flow to fingers, toes and peripheral body parts.

 

Homocysteine is formed routinely by the cells of our body during the course of normal metabolism. Fortunately our bodies can eliminate homocysteine by converting it into other important amino acids such as methionine, cystathionine, serine, and cysteine. However, in order to convert homocysteine into these desirable, non toxic amino acids, our bodies require an adequate intake of the B vitamins – folic acid, B6 and B12. A number of recent studies have shown that individuals with high blood levels of homocysteine can reduce their levels by supplementing their diet with folic acid, vitamin B6 and/or vitamin B12.

 

Reporting in the Journal of the American Medical Association (Feb. 1988) E Rimm and fellow researcher. demonstrated that women who supplement their diet with a multiple vitamin had a 24% lower risk of non-fatal and fatal heart attacks.

During the 14-year follow-up they documented 658 incident cases of non-fatal heart attacks and 281 cases of fatal heart attacks among the 80,082 women from the Nurses' Health Study. After controlling for well known risk factors for heart disease they showed that high intake levels of folic acid (696 mcg/day) was associated with a 31% lower risk for heart disease episodes, compared with lower folic acid intake levels (158 mcg./day). For vitamin B6 there was a 33% lower risk for heart disease episodes in subjects ingesting 4.6 mg/day compared with subjects ingesting 1.1 mg/day. For individuals with high intakes for both folic acid and vitamin B6, they experienced a 45% reduced risk for fatal and non-fatal heart attacks.

A major conclusion of this study suggests that intake of folic acid and vitamin B6 above the current recommended dietary allowance, may be required to prevent heart disease. This means that taking a multivitamin and mineral supplement each day with extra B-vitamin protection is associated with a significant reduction in risk of heart disease.

Findings from the Health Professional Follow-up Study among male health practitioners demonstrated that high folic acid intake was associated with a significant reduction in heart disease risk, as well. Thus, for both men and women high levels of folic acid intake are strongly linked to the prevention of heart disease.

In the Nurses' Health Study each 100 mcg./day increase in folic acid was associated with a 5.8% lower risk of heart disease. It is estimated that 88-90% of the population has dietary intakes of folic acid below 400 mcg/day.

 

Presently, elevated blood levels of homocysteine is considered to be responsible for approximately 10% of all heart attacks each year in the United States.

The current recommended dietary allowance for folic acid is 180 mcg/day for non-pregnant women. The average dietary intake in the United States among women is approximately 225 mcg/day.

The overall evidence suggests that this level of intake is insufficient to minimize risk of neural tube defects (i.e. spina bifida), and possibly heart disease. As such, many experts are urging that the recommended dietary allowance (RDA) be reset to the earlier level of 400 mcg./day.

To obtain 400-700 mcg/day of folic acid is exceeding difficult to do without using a multiple vitamin supplement.

The potential for this one simple intervention (multivitamin and mineral supplement)to prevent life threatening problems is staggering when you weigh all the evidence.

B Vitamins Preserve Memory and Cognitive Function

Deterioration of mental capacities has long been considered an aspect of the normal aging process. In recent years, however, the emerging scientific evidence has demonstrated that certain natural health products and supplements are effective in their ability to prevent, reverse, or even better manage cognitive impairment problems in older individuals. The Boston Veterans Affairs Normative Aging Study is one of many studies investigating the influence of nutrition on various aspects of age-related disorders.

 

In March of 1996 Drs. Riggs and associates published results from this study in The American Journal of Clinical Nutrition. Their findings indicated that older individuals with low blood concentrations of vitamin B12, vitamin B6, and the B vitamin known as folic acid had the poorest scores of brain function measured by a battery of cognitive tests.

In previous studies clinical deficiencies of B vitamins have been implicated in brain-related disorders, including reversible dementia (vitamin B12 and possibly folate), depression (folate), and electrophysiological dysfunction, including convulsions (vitamin B6). In healthy older adults blood levels of B vitamins usually considered to be in the normal range were associated with poorer scores on tests of delayed recall, abstract reasoning, and selective attention. There is also good evidence that deficiencies of vitamin B12, folic acid, and vitamin B6 increase with age and are common in older adults.

Thus, there is growing support for the premise that optimal B vitamin status can prevent, slow or reverse the deterioration in memory and other mental capacities important to quality of life issues in older individuals.

The Normative Aging Study involved 70 male subjects, aged 54-81 years. The results of this study revealed that blood levels of vitamin B12 and folic acid appear to be related to cognitive performance in a different manner than vitamins B6 blood levels. Low blood levels of vitamin B12 and folic acid were associated with deficits in spatial copying. Higher blood levels of vitamin B6 were associated with better performance on two tests of memory.

Another interesting finding was that nearly one half of the subjects in this study had low blood levels of vitamin B6 (<30 umol/L).

This study is extremely important because B vitamins are known to participate in brain chemistry and physiology. Vitamins B12 and folic acid are required as coenzymes in the synthesis of the neurotransmitters (important brain chemicals), serotonin, catecholamines (adrenaline, norepinephrine). They are also required for the production of S-adenosylmethionine, which has known anti-depressant properties. Vitamin B12 deficiency may also result in de-insulation of nerve fibers (demyelination), which produces a constellation of neurological symptom. Vitamin B6 is a cofactor in the production of other brain chemicals (neurotransmitters) including dopamine, norepinephrine, serotonin, GABA, and taurine.

As well, higher blood levels of homocysteine often results from subnormal intakes of folic acid, vitamin B12 and vitamin B6. High blood levels of homocysteine are associated with increased risk of cardiovascular, cerebrovascular (narrowed arteries in the brain), and peripheral vascular disease (narrowed blood vessels in the arms, hands, legs and feet.

Narrowed arteries in the brain (cerebrovascular disease) have been shown to be associated with decrements in psychomotor speed and on tests measuring fluid and visual abilities.

 

Such cognitive dysfunction, therefore, may stem from high levels of homocysteine. As previously stated, vitamins B6, B12 and especially folic acid are key nutrients that prevent and reverse high blood levels of homocysteine.

 

In the Normative Aging Study subjects with high levels of homocysteine performed, on average, like patients with mild Alzheimer's disease. They also exhibited difficulty in copying the most complex spatial figures. For example, few subjects in the highest 25 percent range of homocysteine concentrations completed the cube (22%) and tapered box (17%) correctly. By comparison, these figures are mastered by 50% of school children by the age of 13 years old. Subjects with the lowest blood homocysteine levels demonstrated the best results on these tests.

 

Taken together the body of evidence continues to support the contention that B vitamin nutritional status is crucial to the development and preservation of mental capacities throughout our lifetime. The sad reality is that many midlife and older members of society have poor dietary intake and nutritional status of various B vitamins (vitamin B6, folic acid etc.). For this reason I continue to emphasize the multitude of benefits available from the daily use of a well formulated multiple vitamin and mineral supplement that contains a B-50 complex.

Bone Support Nutrients From A High Potency Multi-Vitamin and Mineral

In North America, at least one in four women currently develops osteoporosis by age 50 and one in eight men develop this condition after the age of 50. In women, complications of osteoporotic fractures cause more deaths each year than the combined mortality rate from breast and ovarian cancers. Osteoporosis is an extremely important problem that requires a lifelong strategy to prevent its development. Central to the prevention of osteoporosis is the adequate daily intake of calcium, Vitamin D, magnesium, copper and zinc, which together are the essential bone strengthening nutrients. Studies show that across the population most adults (including 11-24 year olds) are lacking at least 500 mg of calcium per day in their diet, on average to prevent the future development of osteoporosis. Vitamin D nutritional status is also sub-optimal (Vitamin D is necessary to absorb calcium) for a large segment of the population, as is the ingestion of zinc. Thus, a well designed multiple vitamin containing 500 mg of elemental calcium, 400 IU of Vitamin D, 15 mg of zinc, 200 mg of magnesium and 2 mg of copper, is an important lifelong strategy to help prevent osteoporosis.

Overall Benefits Of A High Potency Multi-Vitamin And Mineral Supplement

The simple truth is that it is impossible to acquire the optimal doses of every vitamin and mineral from food alone, in order to prevent degenerative diseases, maximize your health and well being, and slow the aging process. In my view it is absolutely necessary for all adults to take a high potency multi-vitamin and mineral every single day.

By this I mean a multi-vitamin and mineral supplement that is antioxidant enriched, contains a B-50 complex and contains proper doses of bone building nutrients (e.g. 500 mg of calcium). This formula can not only help defend your body and mind against degenerative conditions and slow the biological processes of aging, but can also help to improve the quality and texture of your skin, hair and nails, improve sleep quality, strengthen your immune system and enhance your daily energy level.

The following is the high potency multi-vitamin and mineral formulation I developed and recommend to my patients and to other health practitioners:

Multi Vitamin & Mineral (Amts for 4 caplets)

120/bottle

Beta carotene

Biotin

Calcium

Chromium

Citrus Bioflavonoids

Copper

Folic Acid

Iron

Lutein – 5%

Lycopene – 5%

Magnesium

Manganese

Molybdenum

10,000 I.U.

300 mcg

500 mg

50 mcg

50 mg

2 mg

400 mcg

6 mg

6 mg

6 mg

200 mg

5 mg

50 mg

Niacin

Pantothenic Acid

Selenium

Vitamin A

Vitamin B-1

Vitamin B-2

Vitamin B-6

Vitamin B-12

Vitamin C

Vitamin D

Vitamin E (all natural)

Zinc

50 mg

50 mg

100 mcg

2500 I.U.

50 mg

50 mg

50 mg

50 mcg

1000 mg

400 I.U.

400 I.U.

15 mg

Don’t have time to read the whole book right now?

No worries. Let me send you a copy so you can read it when it’s convenient for you. Just let me know where to send it.

LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

References For Multivitamin Section Step 2

Antioxidants And Cancer


Cancer In General:

 

Ames Bruce N, et al. Oxidants, Antioxidants, and the Degenerative Diseases of Aging; Proceedings of the National Academy of Science 1993 Sep;90:7915-22
Block G. Vitamin C and cancer prevention: the epidemiologic evidence. Am J Clin Nutr. 1991;53(1):270-282
Block G, et al. Fruits, Vegetables and Cancer Prevention: A Review of the Epidemiologic Evidence; Nutrition and Cancer 1992;187:1029
Gutteridge John M. Antioxidants, Nutritional Supplements, and Life-Threatening Diseases; British Journal of Biomedical Science 1994;31:288-95
Weisburger J. Nutriitonal Approach to Cancer Prevention with Emphasis on Vitamins, Antioxidants, and Carotenoids; American journal of Clinical Nutrition 1991;53:2265-2375
Zeigler, R. Vegetables, Fruits, and Carotenoids and the Risk of Cancer; American Journal of Clinical Nutrition 1991;53:2515-2595


Colon Cancer


Blot WJ, et al. The Linxian trails: mortality rates by vitamin-mineral intervention group. AM J Clin Nutr.; 1995;62:14245-65
Bostick R.M, et al. Reduced risk of colon cancer with high intake of vitamin E:the Iowa Women's Health Study. Cancer Res 1993;53:4230-7
Bussey HJR, DeCosse JJ, Deschner EE, et al. A randomized trial of ascorbic acid in polyposis coli. Cancer 1982;50:1434–9.
Clark L, Cantor K, Allaway W. Selenium in forage crops and cancer mortality in US counties. Arch Environ Health 1991:46:37-42
Clark L, Combs GF, Turnbull BW, Slate EH, Chalker DK, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. JAMA 1996;276: 1957-1964
Clark L, Hixson L, Combs G, Reid M, Turnbull B, et al. Plasma selenium concentration predicts the prevalence of colorectal adenomatous polyps. Cancer Epidemiol Biomarkters Prev 1993;2:41-45
DeCosse JJ, Miller HH, Lesser ML. Effect of wheat fiber and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J Natl Cancer Inst 1989;81:1290–7
Dion PW, et al. The effect of dietary ascorbic acid and alpha-tocopherol on fecal mutagencity.Mutat Res. 1982;102:27-37
Fiala E, Joseph C, Sohn O, El-Bayoumy K, and Reddy B. Mechanism of benzylselenocyanate inhibition of azoxymethane-induced colon carinogenesis in F344 rats. Cancer Res 1991;51:2826-2830
Greenberg ER, et al. A clinical trial of antioxidant vitamins to prevent colorectal adenoma. Ployp Prevention Study Group. N Engl J Med 1994;331:141-7
Greenburg ER, Baron JA, Tosteson TD, et al. A clinical trial of antioxidant vitamins to prevent colorectal adenoma. N Engl J Med 1994;331:141–7
Jacobs M. Selenium inhibition of 1,2-dimethylhydralyzine-induced colon carcinogenesis." Cancer Res 1983;43:1646-1649
Kiremidjian-Schumacher L, et al. Supplementation with selenium and human immune cell functions; II, effect on cytotoxic lymphocytes and natural killer cells. Bio Trace Elem Res 1994;41:103-114
Lanfear J, Fleming J, Wu L, Webster G, Harrison PR The selenium metabolite selenodiglutathione induces p53 and apoptosis." Carcinogenesis 1994;15:1378-1392
Langnecker MP, et al. Serum alpha-tocopherol concentration in relation to subsequent colorectal cancer; pooled data from five cohorts.J Natl Cancer Inst 1992;84:430-5
Lavender OA, et al. Bioavailability of selenium to Finnish men as assessed by platelet glutathione peroxidase activity and other blood parameters. AM J Clin Med 1983;37:887-897
McKeown-Eyssen G, et al. A randomized trial of vitamin C and E in the prevention of recurrence of colorectal polyps. Cancer Res 1988;48:4701-5
McKeown-Eyssen G, Holloway C, Jazmaji V, et al. A randomized trial of vitamins C and E in the prevention of recurrence of colorectal polyps. Cancer Res 1988;48:4701–5
Mutanen M, Bioavailability of selenium. Annals Clin Res 1986;18:48-54
Paganelli GM, et al. Effect of vitamin A, C and E. Supplementation on rectal cell proliferation in patients with colorectal adenomas. J Natl Cancer Inst. 1992;84:47-51
Ponz de Leon M, Roncucci L. Chemoprevention of colorectal tumors: role of lactulose and of other agents. Scand J Gastroenterol Suppl 1997;222:72–5
Reddy B, Rivenson A, Kulkarni N, Upadhyaya P, El-Bayoumy K. Chemoprevention of colon carcinogenesis by the synthetic organoselenium compound 1,4phenylenebis (methylene) selenocyanate. Cancer Res 1992;52:5635-5640
Reddy B, Tanaka T, El-Bayoumy K. Inhibitory effect of dietary p-methoxybenzeneselenol on azoxymethane-induced colon and kidney carcinogenesis in female 344 rats.: JNCI 1985;74:1325-1328
Russo MW, et al. Plasma selenium levels and the risk of colorectal adenomas:, Nutrition and Cancer 1997;28(2):125-129
Salonen, J, Alfthan G, Huttunen J, Puska P. Association between serum selenium and the risk of cancer. Am J Epidemiol 1984;120:342-349
Soullier B, Wilson P, Nigro, N Effect of selenium on azoxymethane-induced intestinal cancer in rats fed a high fat diet Cancer Lett 198;12:343-348
Stone, W.L. and Papas, A.M. Tocopherols and the Etiology of Colon Cancer.J Natl Cancer Inst. 1997;14 (89):1006-1014
The effect of vitamin E and beta-carotene on the incidence of lung cancer and other cancers in male smokers. The Alpha-Tocopherol, Beta-carotene Cancer prevention Study Group. N Engl J med 1994;330:1029-35
Thompson CD, et al. Effect of prolonged supplementation with daily supplements of selenomethionine and sodium selenite on glutathione peroxidase activity in blood of New Zealand residents. AM J Clin Nutr 1982;36:24-31
Virtamo, J, Valkeila, E, Alfthan, G, Punsar, S, Huttunen, J, et al.: "Serum selenium and risk of cancer: a prospective follow-up of nine years." Cancer 1987;60:145-148
Willett WC, Polk PF, Morris JS, Stampfer MJ, Pressel S, et al.: "Prediagnostic serum selenium and risk of cancer." Lancet 1983;2:130-134


Prostate Cancer


​​​​Grovannucci et al. Intake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst 1995; 87; 23:1767-76
Heinonen OP, et al. Prostate cancer and supplementation with Alpha-Tocopheral and Beta-Carotene : Incidence and mortality in a controlled trial. J Natl Cancer Inst 1998; 90; 6:440-446
Liehr JG. Androgen – Induced redox changes in prostate cancer cells: what are causes and effects? J Natl Cancer Inst 1997;1:3-6
Linehan WM. Inhibition of prostate cancer metastasis: a critical challenge ahead. J Natl Cancer Inst 1995; 87; 5: 331-32
Olson KB, et al. Vitamins A and E: Further clues for prostate cancer prevention. J Natl Cancer Inst 1998; 90(6):414-415
Rao VA, et al. Serum and tissue lycopene and biomarkers of oxidation in prostate cancer patients: A case-control study. Nutr and Cancer, 1999; 33(2):159-164
Sigounas G, et al. DL-alpha-tocopherol induces apoptosis in erythroleukemia, prostate and breast cancer cells., Nutrition and Cancer 1997;28(1):30-35


Breast Cancer


Fleischauer A, et al. Antioxidant supplements and risk of breast cancer recurrence and breast cancer-related mortality among postmenopausal women. Nutrition and Cancer, 2003;46(1):15-22 Lockwood K, et al. Apparent partial remission of breast cancer in 'high risk' patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. Mol Aspects Med. 1994;15 Suppl:s231-40 Sung L, et al. Vitamin E: The evidence for multiple roles in cancer. Nutrition and Cancer, 2003; 46(1):1-14


Cervical Cancer


B-carotene on the regression and progression of cervical dysplasia: a clinical experiment. J Clin Epidemiol 1991;44:273-293
Brock KE, Berry G, Mock PA, MacLennan R, Truswell AS et al. Nutrients in diet and plasma and risk of in situ cervical cancer. JNCI 1988;80:580-585
Buckley DI, McPherson S, North CQ, Becker TM. Dietary micronutrients and cervical dysplasia in southwestern American Indian women. Nutr Cancer 1992;17:179-185
Cuzik J, Stavola BL, Russell MJ, Thomas BS. Vitamin A, vitamin E and the risk of cervical intraepithelial neoplasia. Br J Cancer 1990;62:651-652
De Vet HCW, Knipschild PG, Willebrand D, Schouten HJA, Sturmans F. The effect of
De Vet, HCW, Knipschild PG, Grol MEC, Schouten HJA, Sturmans F. The role of B-carotene and other dietary factors in the aetiology of cervical dysplasia: results of a case-control study. Int J Epidemiol 1991;20:603-610
Di Masio P, Kaiser S, Sies H. Lycopene as the most efficient biological carotenoid singlet quencher. Arch Biochem Biophys 1989;274:532-538
Harris RWC, Forman D, Doll R, Vessey MP, Wald NJ. Cancer of the cervix uteri and vitamin A. Br J Cancer 1986;53:653-659
Knekt P. Serum vitamin E level and risk of female cancer. Int L Epidemiol 1988;17:281-286
La Vecchia C, Decarli A, Fasoli M, Parazzini F, Franceschi S et all Dietary vitamin A and the risk of intraepithelial and invasive cervical neoplasia. Gynegol Oncol 1988;30:187-195
Liu T, Soong S, Wilson NP, Craig CB, Cole P, et al. A case control study of nutritional factors and cervical dysplasia. Cancer Epidemiol Biomarkers Prev 1993;2:525-530
Slattery ML, Abbott TM, Overall JC, Jr., Robinson LM, French TK et al. Dietary vitamins A, C, and E and selenium as risk factors for cervical cancer. Epidemiology 1990;1:8-15
Van Eenwyk J., Davis FG, Bowen PE. Dietary and serum carotenoids and cervical intraepithelial neoplasia. Int J Cancer 1991;48:34-38
Wylie-Rosett, JA, Romney SL, Slagle NS, Wassertheil-Smoller S, Miller GL et al. Influence of vitamin A on cervical dysplasia and carcinoma in situ. Nurt Cancer 6, 49-57, 1984.
Ziegler RG, Jones CJ, Briton LA, Norman SA, Mallin K, et al. Diet and the risk of in situ cervical cancer among white women in the United States, Cancer Causes Control 1991;2:17-29


Stomach Cancer


Block G. Vitamin C and cancer prevention: the epidemiologic evidence. Am J Clin Nutr 1991 Jan;53(1):270S-282S
Kyrtopoulos SA. Ascorbic acid and the formation of N-nitroso compounds:possible role of ascorbic acid in cancer prevention. Am J Clin Nutr 1987May;45(5):1344-50
Tannenbaum SR, Wishnok JS, Leaf CD. Inhibition of nitrosamine formatin by ascorbic acid. Am J Clin Nutr 1991Jan;53(1):247S-250S


Antioxidants And Heart Disease


Boscoboinik D, Szewczyk A, Hensey C, Azzi A. Inhibition of cell proliferation by a-tocopherol: role of protein kinase C. J Biol Chem 1991;266;6188-94
DeMaio SJ, King SB, Lembo NJ, et al. Vitamin E supplementation, plasma lipids and incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). J Am Coll Nutr 1992;11:68-73
Enstrom J E, Kanin L E, Klein M A. Vitamin C intake and mortality among a sample of the U.S. Population. Epidemiology 1992;2:194-202
Frei B. Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. Am J Clin Nutr 1991;54 (suppl):1113s-8s
Gey K F, Brubacher G B, Stehelin HB. Plasma levels of anti-oxidant vitamins in relation to ischemic heart disease and cancer. American Journal of Clinical Nutrition 1987;45:1368-1377
Gey KF, Brubacher GB, Stahelin HB. Plasma levels of antioxidant vitamins in relation to ischemic heart disease and cancer. AM J Clin Nutr 1987;45(suppl):1368-77
Gey KF, et al. Inverse correlation between plasma Vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am J Clin Nutr 1991; 53:326s-34s
Gey KF, Moser UK, Jordan P, Stahelin HB, Eichholzer M, Ludin E. Increased risk of cardiovascular disease at sub-optimal plasma concentrations of essential antioxidants: an epidemiological update with special attention to carotene and vitamin C. Am J Clin Nutr 1993;57(suppl):787S-97S
Gillilan RE, Mondell B, Warbasse JR. Quantitative evaluation of vitamin E in the treatment of angina pectoris. AM Heart J 1977;93:444-9
Ginter E, et al. The effect of ascorbic acid on cholesterolemia in healthy subjects with seasonal deficit of vitamin C. Nutr Metab 1970;12:76-86
Harats D, et al. Citrus fruit supplementation reduces lipoprotein oxidation in young men ingesting a diet high in saturated fat: presumptive evidence for an interaction between vitamin C and E in vivo.Am J Clin Nutr 1998Feb; 67:240-245
Hodis HN, Mack WJ, LaBree L, et al. Serial angioghaphic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. JAMA 1995;273:1849-54
Knekt P, et al. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am J Epidemiol 1994;139:1180-9
Knekt P, Reunanen A, Järvinen R Seppänen R, Heliövaara M Aromaa A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. AM J Epidemiol 1994;139:1180-9
Kok FJ, de Bruijn AM, Vermeeren R, et al. Serum selenium, vitamin antioxidants, and cardiovascular mortality: a 9 y follow-up study in the Netherlands. AM J Clin Nutr 1987;45:462-8
Paolisso G, et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll.Nutr.1995;14:387-92
Princen HMG, von Poppel G, Vogelezang C, Buytenhek R, Kok FJ. Supplementation with Vitamin E but not b-carotene in vivo protects low density lipoprotein from lipid peroxidation in vitro: effect of cigarette smoking. Arterioscler Thromb 1992;12:554-62
Puurunen M, Manttari M, Mannienen V, et al. Antibody against oxidized low-density lipoprotein predicting myocardial infraction. Arch Intern Med 1994; 154:2605-9
Riemersma RA, Wood DA, Macintyre CCA, Elton RA, Gey KF, Oliver MF. Risk of angina pectoris and plasma concentrations of vitamins A, C and E and carotene. Lancet 1991;337:1-5
Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC. Vitamin E consumption and risk of coronary heart disease among men. N Engl J Med 1993;328:1450-6.
Salonen JT, et al. Serum fatty acids, apolipoproteins, selenium and vitamins in relation to ischemic heart disease and cancer. American Journal of Clinical Nutrition 1987;45:1368-1377
Salonen R, Nyyssönen K, Porkkala E, et al. Low vitamin E status is associated with increased risk of myocardial infarction only if vitamin C status is low: a population study in men in Eastern Finland. Circulation 1995;91:933(abstr)
Stamfer MJ, Rimm EB, Epidemiologic evidence for vitamin E in prevention of cardiovascular disease. Am J Clin. Nut 1995;62;1365s-1369s
Stampfer MJ and Rimm EB Epidemiologic evidence for vitamin E in prevention of cardiovascular disease. AM J Clin Nutr 1995;62(suppl):1365S-9S
Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willet WC. A prospective study of vitamin E consumption and risk of coronary disease in women. N Engl J Med 1993;328:1444-9
Stampfer MJ, Rimm EB. A review of the epidemiology of dietary antioxidants and risk of coronary heart disease. Can J Cardiol 1993;9:14B-8B Steinberg D. Antioxidants and artherosclerosis. A current assessment. Circulation 1991;84:1420-5 (editorial) Steiner M, Glantz M, Lekos A. Randomized, double-blind study of vitamin D plus aspirin compared with aspirin alone for the prevention of recurrent strokes and transient ischemic attacks. Am J Clin Nutr 1995;62(suppl):1381S-4S Street DA, Comstock GW, Salkeld RM, Schuep W, Klag M. Serum antioxidants and myocardial infarction: are low levels of carotenoids and a-tocopherol risk factors for myocardial infarction? Circulation 1990;90:1154-61 Williams HTG, Fenna D, Macbeth RA. Alpha-tocopherol in the treatment of intermittent claudication. Surg Gynecol Obstet 19971;132:662-6


Antioxidants and Alzheimer’s Disease and Dementia


Grundman M. Vitamin E and Alzheimer disease: the basis for additional clinical trials. Am J Clin Nutr 2000Feb;71(2 Part 2):630S-636S
Yatim SM, et al. The antioxidant vitamin E modulates amyloid beta-peptide-induced creatine kinase activity inhibition and increased protein oxidation: implications for the free radical hypothesis of Alzheimer's disease. Neurochem Res 1999 Mar;24(3):427-35
Morris MC, et al. Vitamin E and vitamin C supplement use and risk of incident Alzheimer disease. Alzheimer Dis Assoc Disord 1998 Sep;12(3):121-6
Rivieire S, et al. Low plasma vitamin C in Alzheimer patients despite an adequate diet. Int J Geriatr Psychiatry 1998 Nov;13(11):749-54
Hake AM, Schere P. On the brink of the pandemic: epidemiology and risk factors for Alzheimer’s. World Alzheimer’s Congress 2000
Vatassery GT, et al. High doses of vitamin E in the treatment of disorders of the central nervous system in the aged. Am J Clin Nutri 1997: 70(5):793-801


Antioxidants and Eye Diseases


Atkinson D. Malnutrition as an etiological factor in senile cataract. EENT Monthly, 1952;31:79-83

Bouton S, et al. Vitamin C and the aging eye. Arch Int Med 1939;63:930-945
Brown L, et al. A prospective study of carotenoid intake and risk of cataract extraction in U.S. men. Am J Clin Nutr. 1999;70(4):517-524
Caselli L, et al. Clinical electro-retinographic study on the activity of anthocyanosides. Arch Med Int 1985;37:29-35
Chasen-Taber L, et al. A prospective study of carotenoid and vitamin A intakes and risk of cataract extraction in U.S. women. Am J Clin Nutr 1999;70(4):509-516
Chaundry PS, et al. Inhibition of human lens aldose reductase by flavonoids, sulindac and indomethacin. Biochem Pharmacol 1983;32;1995-1998
Corbe C, et al. Light vision and Chorioretinal circulation: Study of the effect of procyanidolic oligomers. J Fr Ophthalmol, 1988;11:453-460
Dagnelie G, et al. Lutein improves visual function in some patients with retinal degeneration: a pilot study via the Internet. Optometry 2000;71(3):147-164
DeFeudis FV (ed.). Ginkgo biloba extract (Egb-761): Pharmacological Activities and Clinical Applications. Elsevier, Paris; 1991
Eye Disease Case-Control Study Group. Antioxidant status and neovascular age-related macular degeneration. Arch Ophthalmol. 1993;111:104-109
Halliwell B., and Gutteridge, J. Free Radicals in Biology and Medicine (2nd edit.), Oxford University Press, 1991; 218-266
Hammond BR, et al. Dietary modification of human macular pigment density. Invest Ophthalmol Vis Sci 1997;38:1795-1801
Hammond, Jr. BR, et al. Density of the human crystalline lens is related to the macular pigment carotenoids, lutein and zeazanthin. Optom Vis Sci 1997;74(7):499-504
Jacques PF, et al. Epidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention. Am J Clin Nutr 1991;53(1):352-355 (suppl)
Jampol LM, et al. Age-Related Eye Disease Study Research Group (collective name-AREDS). A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta-carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no.8. Arch Ophthalmol 2001Oct;119(10):1417-36
Katz ML, Parker KR, Handelman GJ, et al. Effects of antioxidant nutrient deficiency on the retina and retinal pigment epithelium of albino rats: a light and electron microscopic study. Exp Eye Res 1982;34:339-59
Landrum JT, et al. Macular pigment stereomers in individual eyes. Invest Ophthalmol Vis Sci. 1995;38:1795-1801
Landrum JT, et al. The macular pigment: A possible role in protection from age-related macular degeneration. Adv Pharmacol 1997; 38: 537-556
Lebuisson DA, et al. Treatment of senile macular degeneration with ginkgo biloba extract: A preliminary double-blind versus placebo study. Presse Med 1986;15:1556-1558
Lyle BJ, et al. Antioxidant intake and risk of incident age-related nuclear cataracts in the Beaver Dam study. Am J Epidemiol. 1999;149:801-809
Mares-Perlmen JA, et al. Serum antioxidants and age-related macular degeneration in a population-based case control study. Arch Ophthalmol, 1988;113:1518-1523
Murray M, Pizzorno J. Encyclopedia of Natural Medicine (2nd edit) Prima Health 1998: 319-324
Murray M. The Healing Power of Herbs (2nd edit). Prima Publishing, 1995: 50-59
Murray M, Pizzorno J. Encyclopedia of Natural Medicine, 2nd edition. (Prima Publishing) 1998:319-24
Newsome DA, et al. oral zinc in macular degeneration. Arch Ophthalmol. 1988; 106: 192-198
Olson R J. Supplemental antioxidant vitamins and minerals in patients with macular degeneration. J Am Coll Nutr 1991;10:550/Abstract 52
Patient Risk Factors; Antioxidants and Maculopathy. Nurses” Drug Alert 23, 1999; 6:45
Proto F, et al. Electrophysical study of Vitis Vinifera procyanoside oligomers effects on retinal function in myopic subjects. Ann OH Clin Ocul 1988;11:453-460
Reiter RJ, et al. Oxygen radical detoxification process during aging: The functional importance of melatonin. Aging Clinical Exp Res 1995;7:340-351
Ringwold, A, et al. Senile cataract and ascorbic acid loading. Acta Opthalmol. 1985; 63: 277-280
Robertson J, et al. A possible role for Vitamin C and E in cataract prevention. Am J Clin Nutr. 1991:53(1):346-351 (suppl)
Rouhiainen P, et al. Association between low plasma Vitamin E concentration and progression of early cortical lens opacities. Am J Epidemiol. 1996;144: 496-500
Scharrer A, et al. Anthocyanosides in the treatment of retinopathies. Klin Monatsbl Augenheilked. 198;178:386-389
Seddon JM, et al. Dietary Carotenoids, Vitamin A, C, and E and advanced age-related macular degeneration. JAMA 1994; 272:1413-1420
Soyeux A, et al. Endotelon: Diabetic retinopathy and hemorrheaology (preliminary study) Bull Soc Ophthalmol Fr., 1987; 87: 1441-1444
Stur M, et al. Oral zinc and the second eye in age-related macular degeneration. Invest Ophthalmol 1996;37:1225-1235
Teikari JM, et al. Long-term supplementation with alpha-tocopherol and beta-carotene and age-related cataract. Acta Ophthalmol Scan 1997;75:634-640
Varma S. Scientific basis for medical therapy of cataracts by antioxidants. Am J Clin Nutr. 1991;53(1):335-345 (suppl)
Wegmann R, et al. Effects of anthocyanosides on photoreceptors: Cytoenzymatic aspects. Ann Histochim 1969;14:237-256
West S, et al. Are antioxidants or supplements protective of age-related macular degeneration? Arch Ophthalmol 1994;112:222-227
Young RW. Solar radiation and age-related macular degeneration. Surv Ophthalmol 1988;32: 252-59


Antioxidants and skin

 

Eberlein-Konig B, et al. Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E). J Am Acad Dermatol 1998;38(1):45-8
Emonet-Piccardi N, et al. Protective effects of antioxidants against UVA-induced DNA damage in human skin fibroblasts in culture. Free Radic Res 1998;29(4):307-13
Firkle T, et al. Antioxidants and protection of the skin against the effect of ultraviolet rays. Cas Lek Cesk 2000;139(12):358-60
Keller KL, Fenske NA. Uses of vitamins A, C, and E and related compounds in dermatology: a review. J Am Acad Dermatol 1998;39(4 Pt 1):611-25
Podda M, et al. UV irradiation depletes antioxidants and causes oxidative damage in a model of human skin. Free Radic Biol Med 1998; 24 (1): 55-65
Pugliese PT. The skin’s antioxidant systems. Dermatol Nurs 1998;10(6):401-16;quiz417-8
Shukla A. Depletion of reduced glutathione, ascorbic acid, vitamin E and antioxidant defense enzymes in a healing cutaneous wound Free Radic Res 1997; 26(2):93-101
Stahl W, et al. Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-induced erythema in humans. Am J Clin Nutr 2000 Mar;71(3):795-8


Antioxidants and Immune Function


Anderson R. The immunostimulatory, anti-inflammatory an anti-allergic properties of ascorbate. Adv Nutr Res 1984;6:19–45 [review]
Banic S. Immunostimulation by vitamin C. Int J Vitam Nutr Res Suppl 1982;23:49–52 [review]
Chew BP. Role of carotenoids in the immune response. J Dairy Sci 1993;76:2804–11. Bendich A. Beta-carotene and the immune response. Proc Nutr Soc 1991;50:263–74
Coodley GO, Coodley MK, Lusk R, et al. Beta-carotene in HIV infection: an extended evaluation. AIDS 1996;10:967–73
De Waart FG, Portengen L, Doekes G, et al. Effect of 3 months vitamin E supplementation on indices of the cellular and humoral immune response in elderly subjects. Br J Nutr 1997;78:761–74
Delafuente JC, Prendergast JM, Modigh A. Immunologic modulation by vitamin C in the elderly. Int J Immunopharmacol 1986;8:205–11
Fryburg DA, Mark RJ, Griffith BP, et al. The effect of supplemental beta-carotene on immunologic indices in patients with AIDS: a pilot study. Yale J Biol Med 1995;68:19–23
Fuller CJ, Faulkner H, Bendich A, et al. Effect of beta-carotene supplementation on photosuppression of delayed-type hypersensitivity in normal young men. Am J Clin Nutr 1992;56:684–90
Gerber WF, Lefkowitz SS, Hung CY. Effect of ascorbic acid, sodium salicylate, and caffeine on the serum interferon level in response to viral infection. Pharmacology 1975;13:228
Girodon F, Lombard M, Galan P, et al. Effect of micronutrient supplementation on infection in institutionalized elderly subjects: a controlled trial. Ann Nutr Metab 1997;41:98–107
Glasziou PP, Mackerras DEM. Vitamin A supplementation in infectious diseases: a meta-analysis. BMJ 1993;306:366–70
Hughes DA, Wright AJ, Finglas PM, et al. The effect of beta-carotene supplementation on the immune function of blood monocytes from healthy male nonsmokers. J Lab Clin Med 1997;129:309–17
Kazi N, Radvany R, Oldham T, et al. Immunomodulatory effect of beta-carotene on T lymphocyte subsets in patients with resected colonic polyps and cancer. Nutr Cancer 1997;28:140–5
Kennes B, Dumont I, Brohee D, et al. Effect of vitamin C supplements on cell-mediated immunity in old people. Gerontology 1983;29:305–10
Knodell RG, Tate MA, Akl BF, et al. Vitamin C prophylaxis for posttransfusion hepatitis: Lack of effect in a controlled trial. Am J Clin Nutr 1981;34(1):20–3
Meydani SN, Barklund MP, Liu S, et al. Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. Am J Clin Nutr 1990;52:557–63 Meydani SN, Meydani M, Blumberg JB, et al. Vitamin E supplementation and in vivo immune response in healthy elderly subjects: a randomized controlled trial. JAMA 1997;277:1380–6 Murata A. Virucidal activity of vitamin C for prevention and treatment of viral diseases. In Proceedings of the First Intersectional Congress of IAMS, vol 3. Science Council Japan, 1975, 432 Murata T, Tamai H, Morinobu T, et al. Effect of long-term administration of beta-carotene on lymphocyte subsets in humans. Am J Clin Nutr 1994;60:597–602 Penn ND, Purkins L, Kelleher J, et al. The effect of dietary supplementation with vitamins A, C and E on cell-mediated immune function in elderly long-stay patients: a randomized controlled trial. Age Ageing 1991;20:169–74 Santos MS, Leka LS, Ribaya-Mercado JD, et al. Short- and long-term beta-carotene supplementation do not influence T cell-mediated immunity in healthy elderly persons. Am J Clin Nutr 1997;66:917–24 Santos MS, Meydani SN, Leka L, et al. Natural killer cell activity in elderly men is enhanced by beta-carotene supplementation. Am J Clin Nutr 1996;64:772–7 Semba RD. Vitamin A, immunity, and infection. Clin Infect Dis 1994;19:489–99 [review]


B-Vitamins and Cancer

 

Butterworth CE Jr., Hatch KD, Gore H, Mueller H, Krumdieck CL. Improvement in cervical dysplasia associated with folic acid therapy in users of oral contraception. Am J Clin Nutr 1982;35:73-82
Butterworth CE Jr., Hatch KD, Macaluso M, et al. Folate deficiency in cervical dysplasia. JAMA 1992;267:528-33
Cravo ML, Mason JB, Dayal Y, et al. Folate deficiency enhances the development of colonic neoplasia in dimethylhydrazine-treated rats. Cancer Res 1992;52:5002-5006
Feinberg AP, Gehrke CW, Kuo KC, et al. Reduced genomic 5-methylcytosine content in human colonic neoplasia. Cancer Res 1988;48:1159-1161
Feinberg AP, Vogelstein B. Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Nature 1983;301:89-92
Freudenheim JL, Graham S, Marshall JR, et al. Folate intake and carcinogenesis of the colon and rectum, IntJ Epidemiol 1991;20:368-374
Giovannucci, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma. J. Natl Cancer Inst. 1993;85(11):875-83
Goelez SE, Vogelstein B, Hamilton SR, et al. Hypomethylation of DNA from benign and malignant human colon neoplasms. Science 1985;228:187-190
Hoffman RM. Altered methionine metabolism, DNA methylation and oncogene expression in carcinogenesis. Biochim Biophys Acta 1984;738:49-87
Lashner BA, Heidenreich PA, Su GL, et al. Effect of folate supplementation on the incidence of dysplasia and cancer in chronic ulcerative colitis. A case-control study, Gastroenteral 1989; 97:255-259
Nyce J, Weinhouse S, Magee PN. 5-Methylcytosine depletion during tumor development: An extension of the miscoding concept, Br J Cancer 1983;48:463-475
Sauberlich HE. Evaluation of folate nutrition in population groups. In: Folic Acid Metabolism in Health and Disease (Picciano MF, Stokstad ELR, Gregory JF, eds). New York: Wiley-Liss, 1990;211-235
Shivapurkar N. Poirer LA. Tissue levels of S-adenosylmethionine and S-adenosylhomocysteine in rats fed methyl-deficient diets for one to five weeks. Carcinogenesis 1983;4:1052-1057
Wainfan E, Dizik M, Stender M, et al. Rapid appearance of hypomethylated DNA in livers of rats fed cancer-promoting, methyl-deficient diets. Cancer Res 1989;49:4094-4097
Wainfan E, Poirier LA: Methyl groups in carcinogenesis: Effects of DNA methylation and gene expression. Cancer Res 1992;52:2071s-2077
Whitehead N, Reyner F, Lindenbaum J. Megaloblastic changes in the cervical epithelium: association with oral contraceptive therapy and reversal with folic acid. JAMA 1973;226:1421-4
Willet W. The search for the causes of breast and colon cancer. Nature 1989;338:398,394
Winkelstein W Jr. Smoking and cervical cancer – current status: a review. Am J Epidemiol 1990;131:945-57;(discussion:958-60)


B-Vitamins and Brain Function


Abou-Saleh MT, Coppen A. The biology of folate in depression: implications for nutritional hypotheses of the psychoses. J Psychiatr Res 1986;20:91-101
Berg S. Psychological functioning in 70-and 75-year old people. Acta Psychiatr Scand 1980;Suppl 288:1-47
Bohnen N, Jolles J, Degenaar CP. Lower blood levels of vitamin B12 are related to decreased performance of healthy subjects in the Stroop Color-Word Test. Neurosci Res Commun 1992;11:53-6
Botwinick J, Storandt M. Memory, related functions and age. Springfield, IL: Charles C Thomas, 1974
Dakshinamurti K, Paulose CS, Siow YL. Neurobiology of pyridoxine. In: Reynolds RD, Leklem JE, eds. Vitamin B6: its role in health and disease. New York: Alan R Liss, Inc, 1985;99-121.
Goodwin JS, Goodwin JM, Garry PJ. Association between nutritional status and cognitive functioning in a healthy elderly population. JAMA 1983;249:2917-21
Hertzog C, Schaie KW, Gribbin K. Cardiovasular disease and changes in intellectual functioning from middle to old age. J Gerontol 1978;33:872-83
Jacques PJ, Riggs KM. B vitamins as risk factors for age-related diseases. In: Rosenberg IH, ed. Nutritional assessment of elderly populations. Measure and function. New York: Raven Press, 1995.
Joosten E, van den Berg A, Riezler R, et al. Metabolic evidence that deficiencies of vitamin B12 (cobalamin), folate, and vitamin B6 occur commonly in elderly people. Am J Clin Nutr 1993;58:468-76
Leklem JE. Vitamin B6. A status report. J Nutr 1990;120:1503-7. 1987;83(suppl 5A):104-6
Levitt AJ, Joffe RT. Folate, vitamin B12, and life course of depressive illness. Biol Psychiatry 1989;25:867-72
Lindenbaum J, Rosenberg IH, Wilson PWF, Stabler SP, Allen RH. Prevalence of cobalamin deficiency in the Framingham elderly population. Am J Clin Nutr 1994;60:2-11
Martin DC. B12 and folate deficiency dementia. Clin Geriatr Med 1988;4:841-52
Riggs K, et al. Relations of vitamin B12, Vitamin B6, Folate, and homocysteine to cognitive performance in the Normative Aging Study. Am. J. Clin. Nutr. 1996; 63:306-14
Rinn WE. Mental decline in normal aging: A review. J Geriatr Psychiatry Neurol 1988;1:144-58
Sauberlich HE. Relationship of vitamin B6, vitamin B12, and folate to neurological and neuropsychiatric disorders. In: Bendich A, Butterworth CE Jr, eds. Micronutrients in health and in disease prevention. New York: Marcel Dekker, Inc 1991:187-218.
Selhub J, Jacques PJ, Wilson PWF, Rush D, Rosenberg IH. Vitamin status and intake as primary determinants of homocysteinemia in the elderly. JAMA 1993;270:2693-8.
Shane B, Stokstad ELR, Vitamin B12 folate interrelationships. Annu Rev Nutr 1985;5:115-41
Spieth W. Slowness of task performance and cardiovascular disease. In: Welford AT, Birren JE, eds. Behavior, aging and the nervous system. Springfield, IL: Charles C Thomas, 1965:366-400


Bone Support Nutrients


Chapuy MC,et al. Vitamin D3 and calcium prevent hip fractures in elderly women. N Engl J Med 1992;327:1637-42
Dawson-Hughes B, Dallal G, Tannenbaum S, Sahyoun N, Krall E. Effect of calcium supplements on postmenopausal bone loss. J Bone Miner Res 1989;4(suppl):109(abstr)
Dawson-Hughes B, et al. Effect of calcium and vitamin D supplementation on bone desnity in men and women 55 yers of age and older. N Engl J Med 1997; 337: 670-6
Dawson-Hughes B, et al. Rates of bone loss in postmenopausal women randomly assigned to one of two dosages of vitamin D. Am J Clin Nutr 1995;61:1140-5
Dawson-Hughes B. Calcium supplementation and bone loss: a review of controlled clinical trials. Am J Clin Nutr 1991;54:274(S)-280(S)
Devine AC, Rosen, Mohan S, Baylink D, Prince R. Effects of zinc and other nutritional factors on insulin-like growth factor I and insulin-like growth factor binding proteins in postmenopausal women. Am J Clin Nutr 1998; 68:200-6
Droke EA, Spears JW, Armstrong JD, Kegley EB, Simpson RB. Dietary zinc affects serum concentrations of insulin and insulin-like growth factor I in growing lambs. J Nutr 1993; 123:13-9
Elders PJJ, Netelenbos JC, Lips P, van Ginkel FC. Calcium supplementation reduces perimenopausal bone loss. J Bone Miner Res 1989;4(suppl):1128(abstr)
Ettinger B, Genant HK, Cann C.E. Postmenopausal bone loss is prevented by treatment with low-dosage estrogen with calcium. Ann Intern Med 1987;106:40-5
Harvey JA, Zobitz MM, Pak CYC. Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate. J Bone Miner Res 1988;3:253-8
Honley D. et al. Prevention and management of osteoporosis. Can Med Asso J 1996;155(7):921-23
Horowitz M. et al. Oral calcium suppresses biochemical markers of bone resorption in normal men. Am J Clin Nutr 1994;60:965-968
Kinyamu HK. Dietary Calcium and Vitamin D intake in elderly woman: effect on serum parnathyroid hormone and vitamin D metabolites. Am J Clin Nutr 1998;67:342-8
Kreiger N, et al. Dietary factors and fracture in postmenopausal women: a case-control study. Int J Epidemiol 1992:21953-8
Llyod TL, et al. Calcium supplementation and bone mineral density in adolescent girls. JAMA 1993;270:841-4
Optimal Calcium Intake: NIH Consensus Panel. JAMA, 1994;272(24):1942-48
Polley KJ, et alEffect of calcium supplementation on forearm bone mineral content in postmenopausal women: a prospective, sequential controlled trail. J Nutr 1987;117:1929-35
Reid IR, Ames RW, Evans MC, Gamble GD, Sharpe SJ. Effect of calcium supplementation on bone loss in postmenopausal women. N Engl J Med 1993;328:460-4
Smith EL, Gilligan C, Smith PE, Sempos CT. Calcium supplementation and bone loss in middle-aged women. Am J Clin Nutr 1989;50:833-42
Stepan JJ, Pospichal J, Prest J, Pacovsky V. Prospective trial of ossein-hydroxyapatite compound in surgically induced postmenopausal women. Bone 1989;10:179-85
Taking Supplements for osteoporosis: Advice for the Pharmacist. Jason Sit. mycefuge@ geacities.com
Windsor ACM, et al. The effect of whole-bone extract on 47 calcium absorption in the elderly. Age and Aging 1973;2:230-234 


Lifelong Supplement Number 2: Essential Fatty Acids

The second lifelong supplement that I highly recommend you take each day of your life contains specific essential fatty acids. These essential fatty acids play a vital role in the prevention of cancer and heart disease, help reduce and prevent inflammatory states (arthritis, Crohn’s disease, ulcerative colitis, eczema, psoriasis etc.), improve the softness and smoothness of your skin, and provide other health benefits, as I will explain.

In the body, essential fatty acids are important components of the outer skin (cell membrane) of every cell. The cell membrane determines which chemicals and nutrients will be allowed to enter and exit the cell. Thus, essential fats influence the health status of every cell in the body through their effects on supporting the structure and function of the cell membrane. As vital components of nerve cell membranes, essential fatty acids facilitate nerve conduction, which enables the brain to think, and facilitates the transmission of impulses to other nerves, muscles, and organs. Essential fats are also required for brain development and vision. However, the most unique function of essential fatty acids is that they are continually activated within the cell membrane and converted into prostaglandin hormones. Their conversion into prostaglandin hormones is the main reason that essential fatty acids can produce very powerful disease prevention and anti-aging effects on a wide range of tissues within the body

Unfortunately deficiencies and imbalances of essential fatty acids are common problems in today’s world due to modern day agricultural, livestock, food processing practices, and our typical style of eating. As such, it is virtually impossible to get optimal concentrations of the health promoting, anti-aging essential fatty acids into your body, unless you take a well-formulated essential fatty acid supplement every day, as I am strongly recommending.

Don’t have time to read the whole book right now?

No worries. Let me send you a copy so you can read it when it’s convenient for you. Just let me know where to send it.

LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

Prostaglandin Series-2 (PG-2) Promotes Many Health Problems

Prostaglandins are local tissue hormones that are produced from the different types of unsaturated fats (essential fatty acids) we consume from our diet, and from supplements. There are three main types of prostaglandin hormones (PG); PG-1, PG-2, and PG-3. Essentially PG-1 and PG-3 produce positive effects on our health while PG-2 produces very undesirable effects. Unfortunately, the dietary habits of most North Americans favors the production of PG-2, which encourages blood vessels to constrict and blood platelets to clot abnormally, restricting blood flow and increasing risk of heart attack, ischemic stroke, and high blood pressure. PG-2 also encourages inflammation, worsening arthritis, other joint, muscle and tendon conditions, as well as other inflammatory conditions (e.g. Crohn’s disease, Colitis). Animal studies and human observation and correlation studies reveal that PG-2 is associated with increased cancer risk in that it encourages more rapid cell division (when cells divide at a faster rate they tend to make more genetic mistakes and have less time to correct these genetic errors, enabling a cancerous mutation to occur). Higher Pg-2 levels are associated with an increased risk of breast, prostate and colon cancer, whereas the essential fatty acids that promote the formation of PG-3 are associated with a reduced risk of these cancers.

PG-2 formed within skin cells has also been shown to make the skin dry, rough, and scaly, and can aggravate a number of common skin disorders, including eczema and psoriasis, and possibly roscacea.

PG-2 is formed from the unsaturated fat known as arachidonic acid, which is found in rich concentrations in high fat meats and high fat dairy products. As well, the over-consumption of linoleic acid (an unsaturated fat found in corn oil, sunflower seed oil and safflower seed oil, and mixed vegetable oils) encourages the conversion of linoleic acid to arachidonic acid by the body, adding to the cell membrane concentrations of arachidonic acid. Higher cell membrane concentrations of arachidonic acid, from the over-consumption of these foods, tends to favor the synthesis of PG-2, contributing to inflammation, cancer development, cardiovascular disease, and drier, rougher, scalier skin. Unfortunately, the typical North American diet is a rich source of arachidonic acid and linoleic acid, and thus, most individuals produce too much PG-2, which greatly contributes to our high rates of cancer and heart disease, and aggravates arthritis, many skin conditions and other inflammatory conditions.

Lowering your tissue concentrations of arachidoninc acid is another reason that it is advisable to choose chicken, turkey, and fish instead of higher fat meat products, and choose non-fat or 1% milk and yogurt products, and exclude from your diet any cheese that is more than 3% milk fat. As well, the use of olive oil and canola oil instead of other vegetable oils in salad dressings, and to sauté vegetables is a proven way to prevent the over ingestion of linoleic acid. As I mentioned previously, peanut oil can be used for stir-fries if desired, but no oil can be safely used for deep-frying, which should be avoided. Note that olive oil and canola oil are good sources of monounsaturated fat (oleic acid; an omega-9 fatty acid), which does not participate in the formation of prostaglandin synthesis, and is known to help reduce cholesterol and support cardiovascular health in other ways (e.g raising HDL-cholesterol levels).

Supplementing With Healthy Essential Fatty Acids That Make PG-1 and PG-3

In addition to preventing the formation of PG-2 by making the appropriate dietary changes, it is highly useful to supplement your diet with essential fatty acids that promote the production of PG-1 and PG-3. These essential fatty acids support the optimal expression of good health by suppressing inflammation, dilating blood vessels, helping to prevent abnormal blood clotting, slowing the rate of cell division, and improving the smoothness and softness of the skin, as well as helping to heal various skin conditions.

 

PG-1


The key building block for PG-1 is an unsaturated fat known as GLA (gamma-linolenic acid), which is found in high concentrations in borage oil (22% yield, whereas the more well-known evening primrose oil is only a 9% yield). GLA can also be formed in the body from linoleic acid, but individuals with certain conditions (diabetes, eczema, PMS sufferers) have been shown to have a defect in the enzyme that converts linoleic acid to GLA (delta-6 desaturase enzyme). As well, the consumption of alcohol, refined sugars, and hydrogenated fats tends to inhibit the conversion of linoleic acid to GLA. The aging process itself also slows the conversion of linoleic acid to GLA as the delta-6 desaturase enzyme becomes more sluggish. As such, virtually everyone has sub-optimal cell membrane concentrations of GLA.

The simple and effective solution is to take borage oil (22% GLA) everyday as a supplement. It is an invaluable medicinal oil to help the body produce more optimal levels of PG- 1 hormones
Studies have shown that supplementation with GLA-containing oilse can reduce pain and swelling in arthritis (including rheumatoid arthritis), improve fibrocystic breast disease, PMS, and skin lesions, such as eczema, largely due to increased production of PG-1. Even if you don’t have these health conditions, it is still important to optimize your synthesis of PG-1 each day through supplementation with borage seed oil.


PG-3

 

PG-3 is formed in the body from the omega-3 unsaturated fat known as EPA (eicosapentaenoic acid), which is found in cold-water marine fish such as salmon, mackerel, anchovies, sardines, and tuna, and supplements containing EPA. The body can also convert the omega-3 fat ALA (alpha-linolenic acid) into EPA, increasing the production of PG-3. ALA is found in rich concentrations in flaxseed oil (58% yield). Fish oil also contains DHA (docosahexaenoic acid), which the body can convert into EPA and thus, PG-3, if required. DHA is also used to promote the development and function of the brain and is required for vision.

PG-3 is considered to be very important for total body wellness as it also reduces risk of heart attacks by dilating blood vessels and reducing abnormal blood clotting. PG-3 has been shown to reduce cancer risk by slowing down the cell division rates (more rapid cell division leads to increased genetic mutations and thus, increased formation of cancer cells, with less time for DNA repair enzymes to correct the mistakes). There is strong evidence to show that higher tissue concentrations of omega-3 fats significantly reduce risk of breast, prostate and colon cancer. This has also been shown to be true with respect to skin cancer in experimental studies, whereby higher PG-2 levels in skin cells produced a significantly higher yield of cancer development upon exposure to ultra-violet light, compared to skin cells that with higher PG-3 concentrations. PG-3 is also known to reduce inflammation (including skin inflammatory responses), a role it shares with PG-1. EPA and DHA (eicosapentaenoic acid and docosahexaenoic acid) are the omega-3 fats found in fish. EPA can be converted to PG-3. DHA is required for brain development, vision, immune function, and for synthesis of the myelin sheath, that insulates many nerves throughout the body. As stated earlier, DHA can also be converted into EPA and then into PG-3, if necessary.

Take My Advice And Supplement Your Diet With Borage, Flaxseed and Fish Oil

Unknowingly, most individuals suffer from an essential fatty acid deficiency or imbalance, which has been shown to contribute to numerous health disorders, including cancer, heart disease and stroke. A sub-optimal intake of the healthy essential fatty acids also promotes accelerated aging, and aggravates poor complexion problems, certain skin disorders, and inflammatory conditions. Thus, to ensure optimal essential fatty acid nutritional status I recommend take you take an essential fatty acid supplement each day that contains omega 3, 6 and 9 fatty acids, derived from equal amounts (e.g. 400 mg each) of GMO-free flaxseed oil, borage oil, and a high yield fish oil (30% EPA/20DHA). For general health maintenance, I suggest two to three 1200 mg capsules per day. This simple practice can produce significant effects on your health, your appearance, the rate at which your body will age, and your risk of future illness. (see reference section for product details).

Vitamins and Minerals As Co-Factors For Prostaglandin Synthesis

One final note is that certain vitamins and minerals are required as co-factors in the enzymatic reactions that allow the cells of your body to convert the healthy essential fatty acids (flaxseed, borage and fish oils) into PG-1 and PG-3. For example, the conversion of ALA to EPA requires optimal nutritional status of Vitamin B6, zinc, magnesium, and niacin (Vitamin B3), as coenzymes. The synthesis of PG-1 and PG-3 also requires optimal intake of Vitamin C, Vitamin E, and selenium. Thus, the use of a high potency multi-vitamin and mineral, as I described earlier in Step 2, is also a vital supplement to help your body make health-promoting prostaglandins, by stimulating the enzymes that convert these essential fats into PG-1 and PG-3.

References


Calder PC. Dietary modification of inflammation with lipids. Proc Nutr Soc. 2002 Aug;61(3):345-58
Dietary Supplement Information bureau (Dietary Supplement Education Alliance, U.S.A.) www.supplementinfo.org/omega-6 fatty acids, omega-3 fatty acids
DiGiacoma RA, Kremer JM, Shah DM. Fish-oil dietary supplementation in patients with Raynaud’s phenomenon: a double-blind, controlled, prospective study. Am J Med 1989;86:158–64
Galland L. Increased Requirements for Essential Fatty Acids in Atopic Individuals: A Review with Clinical Descriptions. J Am Coll Nutr. 1986;5(2):213-28
Garg ML, et al. Alpha-linolenic Acid and Metabolism of Cholesterol and Long-chain Fatty Acids. Nutrition. Jun1992;8(3):208-10
Geusens P, et al. Long-term Effect of Omega-3 Fatty Acid Supplementation in Active Rheumatoid Arthritis. A 12-month, Double-blind, Controlled Study. Arthritis Rheum. Jun1994;37(6):824-29
Gibson RA, Neumann MA, Makrides M. Effect of dietary docosahexaenoic acid on brain composition and neural function in term infants. Lipids 1996;31:177S–81S
Harris WS, Park Y, Isley WL. Cardiovascular disease and long-chain omega-3 fatty acids. Curr Opin Lipidol. 2003 Feb;14(1):9-14
Health Notes. www.puritan.com/Health Notes/Supp/EPA
Holland PA, et al. Drug Therapy of Mastalgia. What are the Options? Drugs. Nov1994;48(5):709-16
Horrobin DF, Manku M, Brush M, et al. Abnormalities in plasma essential fatty acid levels in women with pre-menstrual syndrome and with non-malignant breast disease. J Nutr Med 1991;2:259–64
Horrobin DF. Essential fatty acids in clinical dermatology. J Am Acad Dermatol 1989;20:1045–53
Horrobin DF. The importance of gamma-linolenic acid and prostaglandin E1 in human nutrition and medicine. J Holistic Med 1981;3:118–39
Isseroff RR. Fish Again for Dinner! The Role of Fish and other Dietary Oils in the Therapy of Skin Disease. J Am Acad Dermatol. Dec1988;19(6):1073-80
Joe LA, Hart LL. Evening primrose oil in rheumatoid arthritis. Ann Pharmacother 1993;27:1475–7 [review]
Keen H, Payan J, Allawi J, et al. Treatment of diabetic neuropathy with gamma-linolenic acid. Diabetes Care 1993;16:8–15

Kinsella JE, et al. Dietary n-3 Polyunsaturated Fatty Acids and Amelioration of Cardiovascular Disease: Possible Mechanisms. Am J Clin Nutr. Jul1990;52(1):1-28
Knapp HR, et al. The Antihypertensive Effects of Fish Oil. A Controlled Study of Polyunsaturated Fatty Acid Supplements in Essential Hypertension. N Engl J Med. Apr1989;320(16):1037-43
Kremer JM, Lawrence DA, Petrillow GF, et al. Effects of high¬dose fish oil on rheumatoid arthritis after stopping nonsteroidal antiinflammatory drugs. Arthritis Rheum 1995;38:1107–14.
Leventhal LJ, et al. Treatment of Rheumatoid Arthritis with Gammalinolenic Acid. Ann Intern Med. Nov1993;119(9):867-73
Maes M, Christophe A, Bosmans E, et al. In humans, serum polyunsaturated fatty acid levels predict the response of proinflammatory cytokines to psychological stress. Biol Psychiatry 2000;47:910–20
Makrides M, Neumann MA, Gibson RA. Is dietary docosahexaenoic acid essential for term infants? Lipids 1996;31:115–9
Manku MS, Horrobin, DF, Morse NL, et al. Essential fatty acids in the plasma phospholipids of patients with atopic eczema. Br J Derm 1984;110:643
Masuev KA. The Effect of Polyunsaturated Fatty Acids of the Omega-3 Class on the Late Phase of the Allergic Reaction in Bronchial Asthma Patients. Ter Arkh. 1997;69(3):31-33
Mate J, Castanos R, Garcia-Samaniego J, Pajares JM. Does dietary fish oil maintain the remission of Crohn’s disease: a case control study. Gastroenterology 1991;100:A228 [abstract].
Murray M. Encyclopedia of Nutritional Supplements. (Prima publishing, 1996):239-278
Pye JK, et al. Clinical Experience of Drug Treatments for Mastalgia. Lancet. Aug1985;2(8451):373-77
Stevens L, Zentall SS, Deck JL. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr. 1995;62:761-768

Lifelong Supplement Number 2: Flaxseed Powder (Groung Flaxseed)

One of the most multi-purpose natural agents that can help reduce the risk of many degenerative diseases and optimize health and well being for both adult men and women, is the daily ingestion of ground flaxseed (flaxseed powder).

Flaxseeds are an extremely rich source of a substance known as SLD (secoisolariciresinol diglycoside) that provides the body with the raw material from which the bacteria in the large bowel produce two powerful phytoestrogens (estrogen look-a-like compounds) . In fact, flaxseeds contain 800 times more SLD and related compounds (mammalian lignan precursors) than any other common food. Ingesting the equivalent of two heaping tablespoons of ground flaxseed (flaxseed powder) per day, or approximately 40-50 gm of ground flaxseed, helps support the health of female reproductive organs, as well as the male prostate gland. This level of daily intake has also been shown to lower blood cholesterol levels, support liver and gallbladder function, improve large bowel health, reverse fibrocystic breast disease, help support bone density and improve the texture and smoothness of the skin. Here is how and why flaxseed powder can provide such a multitude of health benefits:

Flaxseed and Breast Health

Enterolactone and enterodiol are classified as phytoestrogens (plant-based estrogens), which means they can bind to estrogen receptors on breast tissue, the endometrium of the uterus and cells on the cervix, toning down the over stimulation of the body’s more potent estrogens on these tissues. This is important because over stimulation of these tissues by the body’s endogenous estrogens (or hormone replacement therapy or the birth control pill) is linked to an increased risk of breast cancer, endometrial cancer and cancer of the cervix.

The phytoestrogens derived from flaxseed are so effective at protecting a woman’s reproductive tissues from estrogen over stimulation that a recently published Toronto-based hospital study demonstrated that flaxseed supplementation greatly improved symptoms in women who suffered from cyclical mastalgia (fibrocystic breast disease).

Other studies have demonstrated that flaxseed supplementation can help normalize estrogen production and reduce the build up of more cancer permissive estrogens (decreases synthesis of 16-alpha hydroxyestrone). Furthermore, flaxseed ingestion has been shown to directly slow down the breast cell division rate (antiproliferative), which is a factor in the prevention of breast cancer development. All indicators suggest that every adult woman (by age 16) should capitalize upon the benefits of flaxseed as it impacts the lifelong health of reproductive tissues.

Flaxseed and Prostate Health

The phytoestrogens derived from flaxseed also help preserve prostate health in various ways. These phytoestrogens (enterolactone and enterodiol) block the over production of estrone hormone within fat cells. With weight gain, fat cells become larger and tend to manufacture more estrone hormone, which encourages prostate cells to synthesize more dihydrotestosterone (DHT) and/or reduce its breakdown. The build up of DHT in the prostate, in turn, stimulates rapid cell division of prostate cells leading to prostate enlargement. DHT also promotes the growth of any existing prostate cancer cells. By age 50, approximately 15 to 30 percent of men already have some cancer cells present within the prostate gland. Keeping DHT levels in check is considered an important step in preventing these cancer cells from dividing and spreading, en masse, throughout the prostate gland, and metastasizing to other parts of the body. Thus, the ingestion of flaxseed on a daily basis provides important bioactive agents that indirectly slow the rate of prostate cell replication, reducing the chances of prostate enlargement (benign prostatic hyperplasia) and may also hinder the promotion of cancer development. These same phytoestrogens also bind to receptors on the prostate gland helping to block the influence of other hormones, which may stimulate rapid prostate cell division. Other herbal compounds such as saw palmetto, pygeum africanum, soy isoflavonoids and beta-sitosterol can also block the build up of DHT and have been shown to improve prostate health in a number of well designed clinical studies. I will discuss these herbal agents in Step 5. In my view, the daily ingestion of 50 gm of ground flaxseed each day should be included as a primary anti-aging, disease prevention strategy used by every adult male; as prostate cancer is the most common cancer in men and prostate enlargement problems will affect 80 percent of men if they live to old age.

Flaxseed and Cholesterol

Studies reveal that the same amount of flaxseed required to help maintain male and female reproductive tissue health (approximately 40-50 gm ground flaxseed) can also lower blood cholesterol by up to 10 percent in people with high cholesterol levels. More importantly, it lowers the bad cholesterol (LDL-cholesterol) by approximately 15 percent and concentrations of lipoprotein (a) [Lp(a)] by 7 percent. Lp(a) is now recognized as a significant risk factor for heart disease and flaxseed supplementation is the only known dietary intervention that can lower Lp(a) into a safer range, if it is elevated. As it turns out, flaxseed contains soluble dietary fiber, which has proven cholesterol-lowering effects. Soluble fiber binds to cholesterol in the intestinal tract and drags it out of the body in fecal matter. It also binds to bile acids, preventing their re-absorption back into the bloodstream and their subsequent conversion into cholesterol in the liver (bile acids are a precursor of cholesterol in the liver). All in all, daily flaxseed supplementation factors into a heart-healthy lifestyle program as well.

Flaxseed and Bowel Function

Flaxseed also contains insoluble dietary fiber, which acts as a bulking agent, or roughage, in the promotion of more regular bowel movements. Studies indicate that flaxseed supplementation provides a natural and gentle laxation effect, which is associated with relieving constipation, and promoting the health of the large bowel. Most people ingest less than half of the recommended amount of dietary fiber per day. By providing both soluble and insoluble dietary fiber, flaxseed is one of the few natural nutrition products that can help to keep cholesterol levels in check and maintain more optimal bowel function at the same time. Note that beans and peas, as well as psyllium husk fiber, also contain appreciable amounts of both cholesterol cruncher and colon cleaner fiber.

Flaxseed and Liver & Gallbladder Support

The daily ingestion of ground flaxseed has been shown to improve the flow of bile from the liver to the gallbladder, and ultimately into the intestinal tract. This effect helps to reduce the chances of gallstone formation and related gallbladder disease. Essentially, flaxseed supplementation induces a type of liver flushing effect, preventing the stagnation of bile, which can harden into stones if not eliminated in a timely fashion. Flaxseed supplementation also helps to prevent the conversion of bile into cholesterol, further facilitating a cholesterol-lowering effect by this action in the liver.

Flaxseed and Skin Texture

Although the mechanism of action remains a mystery, virtually everyone who begins using flaxseed supplementation on a daily basis comments on the improved texture and smoothness of their skin, all over their body. This is an effect that is usually noticed within the first month of using flaxseed on a daily basis. For those of us who use it, this is a wonderful additional benefit to its other premiere health-enhancing attributes.

Don’t Confuse Flaxseed Powder with Flaxseed Oil

Flaxseed oil, on the other hand, is a rich source of the omega-3 fat known as alpha-linolenic acid, which can be converted into prostaglandin series-3 (PG-3). PG-3 helps to reduce inflammation, produces vasodilation of arteries improving blood flow, reduces platelet stickiness, and improves the texture and smoothness of the skin. Omega-3 fats (including alpha-linolenic acid) have also been shown to slow the cell replication rate of breast, prostate and colon cells, an effect linked to decreased cancer risk. Taken together, the evidence suggests that the concurrent use of both flaxseed powder and flaxseed oil provide synergistic and important anti-aging and disease prevention properties. Flaxseed oil is not a rich source of phytoestrogens or dietary fiber, whereas flaxseed powder is not a rich source of alpha-linolenic acid. I personally ingest two heaping tablespoons of flaxseed powder each day, which I mix into a morning whey protein shake.

How to Use Flaxseed

You can purchase ground flaxseeds (often marketed as flaxseed powder) or you can grind whole flaxseeds in a coffee grinder on a daily basis to maximize freshness of the product. Make sure your flaxseeds or powder are from organic sources, as this form is easily attainable.

Studies reveal that ingesting 40-50 gm of ground flaxseed per day provides the health-promoting benefits reviewed in this section.

This is the equivalent of two heaping tablespoons of ground flaxseed (flaxseed powder).

It can be mixed into a protein shake or fruit juice (e.g., orange juice). Many people sprinkle it on to their cereal or mix it into a bowl of low-fat yogurt. It can also be baked into low-fat muffins or flax-bread. The important thing is that you consume at least 25 gm per day, but more ideally, 40-50 gm through whatever delivery system works for you. The best news is that it has a nutty, flavorful taste that is very palatable and enjoyable.

Flaxseed is truly one of nature’s gifts that you should incorporate into a proactive, anti-aging, disease prevention lifestyle. I personally recommend that you use it on a daily basis throughout your lifetime.

Flaxseed: Scientific References


Arjmandi BH, et al. Whole flaxseed consumption lowers serum LDL-cholesterol and lipoprotein (a) concentrations in postmenopausal women. Nutr Res 1998;18:1203-1214

Brzezinksi A, Debi A. Phytoestrogens: the natural selective estrogen receptor modulators? Eur J Obstet Gynecol Reprod Biol 1999;85(1):47-51
Chen, WJL, et al. Hypocholesterolemic effects of soluble fibers. In Kritchevsky D , Yahouny, GD, eds. Dietary Fiber: Basic and Clinical Aspects. New York:Plenum Press 1986:275-289
Clark WF, et al. A novel treatment for lupus nephritis: lignan precursor derived from flaxseed. Lupus 2000;9(6):429-436
Cunnane SC, et al. Nutritional attributes of traditional flaxseed in healthy young adults. Am J Clin Nutr 1995;61(1):62-68
Denis L, et al. Diet and its preventive role in prostate disease. Eur Urol 1999;35(5-6):377-387
Flaxseed Lowers Cholesterol. Nutr. Science News 1998;3(11):575
Gross PE, et al. Effect of dietary flaxseed in women with cyclical mastalgia. Program and abstract of the 23rd Annual San Antonio Breast Cancer Symposium. Dec 6-9, 2000; San Antonio Texas. Abstract 153. Breast Cancer Res Treat 2000;64:p49
Haggans CJ, et al. Effect of flaxseed consumption on urinary estrogen metabolites in postmenopausal women. Nutr Cancer 1999;33(2):188-195
Haggans CJ, et al. The effect of flaxseed and wheat bran consumption on urinary estrogen metabolites in premenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(7):719-725
Hutchins AM, et al. Flaxseed influences urinary lignan excretion in a dose-dependent manner in postmenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(10):1113-1118
Jenkins DJP, et al. Health aspects of partially defatted flaxseed, including effects on serum lipids, oxidative measures, and ex vivo androgen and progestin activity: a controlled crossover trial. Am J Clin Nutr 1999;69(3):395-402
Kitts DD, et al. Antioxidant activity of the flaxseed lignan secoisolariciresinol diglycoside and its mammalian lignan metabolites enterodiol and enterolactone. Mol Cell Biochem 1999;202(1-2):91-100
Kurzer MS, et al. Dietary Phytoestrogens. Annu Rev Nutr 1997;17:353-381
Li D, et al. Dietary supplementation with secolariciresinol diglycoside (SDG) reduces experimental metastasis of melanoma cells in mice. Cancer Lett 1999;142(1):91-96
Nesbitt PD, et al. Human metabolism of mammalian lignan precursors in raw and processed flaxseed. Am J Clin Nutr 1995;69(3):549-555
Prasad K, et al. Reduction in hypercholesterolemia atherosclerosis by CDC-flaxseed with very low alpha-linolenic acid. Atherosclerosis 1998;136(2):367-375
Richard SE, et al. Plasma insulin-like growth factor-1 levels in rats are reduced by dietary supplementation of flaxseed or lignan secoisolariciresinol diglycoside. Cancer Lett (Ireland) 2000;161(1):47-55
Sanghui A, et al. Inhibition of rat liver cholesterol 7-alpha hydroxylase and acyl C-A: cholesterol acyl transferase activities by enterodiol and enterolactone. In Kritchovsky D, ed. Proceedings of the Symposium on Drugs Affecting Lipid Metabolism. New York:Plenum Press, 1984:311-322
Tham DM, et al. Clinical Review 97: Potential health benefits of dietary phytoestrogens: a review of the clinical, epidemiological, and mechanistic evidence. J Clin Endocrinol Metab 1998;83(7):2223-2235
Thompson LU, et al. Anti-tumorigenic effect of mammalian lignan precursor from flaxseed. Nutr Cancer 1996;26:159-165
Tou JC, Thompson LU. Exposure to flaxseed as its lignan component during different developmental stages influences rat mammary gland structures. Carcinogenesis 1999;20(9):1831-1835
Velasquez M, et al. Dietary Phytoestrogens: a Possible role in renal disease protection. Am J Kidney Dis 2001;37(5):1056-1068
Zeigler J. Just the Flax, Ma’am: Researchers Testing Linseed. J Natl Cancer Instit 1994;86(23):1746-1748

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LIFELONG SUPPLEMENTS

Dr. James Meschino, 

DC, MS, ROHP

Global Integrative Medicine Academy

The Global Integrative Medicine Academy was created to satisfy a need, expressed by many health professionals, to establish credentials as experts in Nutritional Medicine. But, health professionals also needed to be able to complete the programme with a minimum impact on their career, family, and lifestyle. That is why the Advanced Nutritional Medicine and Sports Nutrition Certification Program was created.

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