Myth 1: Lung Cancer Is A Disease Of The Elderly
Around 6% of lung cancer cases occur in people aged under 50 and 20% in people under 60. In the United States alone, 44,000 people aged under 60 develop the disease each year, the majority of them smokers. A smoker has around a 4% chance of developing lung cancer by the age of 60. Lung cancer is second only to heart disease as the leading cause of death in smokers aged 40 to 60.

Myth 2: Lung Cancer Is Exceedingly Rare In Non-Smokers
Around 30,000 cases of lung cancer are diagnosed in non-smokers in the United States each year, about 15% of total cases. Even among non-smokers, lung cancer is still one of the 10 most common forms of cancer. There are several risk factors for lung cancer unrelated to smoking including radon gas exposure, air pollution, asbestos exposure, and genetic factors.

Myth 3: Smoking Is More Prevalent In Japan Than The USA However Lung Cancer Rates In Japan Are Lower Than The USA, Therefore Smoking Is Not As Strong A Risk Factor For Lung Cancer As Commonly Believed
While it is true that lung cancer rates in Japan are low, despite a relatively high smoking rate, this appears to be the result of naturally low cancer rates in the country overall. Studies of Japanese men typically find that smokers have around a 10-fold increased risk of developing lung cancer compared to non-smokers, a similar figure to the United States. In both countries, smoking is by far the most important risk factor for lung cancer.

Myth 4: Due To Recent Advances In Medical Care, Lung Cancer Will Probably Be Curable In The Next Few Decades
Lung cancer is actually one of the few forms of cancer that has seen very little improvement in survival statistics over the last few decades. 5-year survival for lung cancer increased from 12% to 17% from 1978 to 2008 – a very modest improvement. There are no guarantees that lung cancer survival over the next 30 years won’t continue to remain low. Because early lung cancer is typically asymptomatic, the majority of cases are quite advanced at time of diagnosis and are very difficult to treat. Most lung cancer cases are considered terminal at diagnosis. Only Stage I and II non-small-cell lung cancers, which make up less than a quarter of all cases, have a realistic chance of cure.

Myth 5: The Effects Of Smoking Are Over-Estimated Because All Lung Cancer Deaths In Smokers Are Wrongly Assumed To Be A Result Of Their Smoking Habit
Statisticians estimate the risks associated with lung cancer by comparing lung cancer rates in non-smokers with smokers. For example, if lung cancer rates in smokers are estimated at 200 per 100,000 per year and rates in non smokers at 10 per 100,000 per year then smoking is associated with a 20-fold increase in the risk of lung cancer. This doesn’t mean that ever case of lung cancer in smokers is assumed to be a result of their habit, only the difference between the smoking and non-smoking rate is assumed to be the result of smoking. In the above example, 95% (190/200) of lung cancer cases in smokers would be directly attributable to smoking.

Myth 6: Light Smoking Of A Few Cigarettes A Day Has A Negligible Impact On Lung Cancer Risk
There hasn’t been a threshold established under which smoking has no impact on lung cancer risk. Studies of light and intermittent smokers typically find increased risk of lung cancer relative to non-smokers. For example, a Norwegian study, published in the journal Tobacco Control in 2005, found that the relative risk of lung cancer in smokers of 1-4 cigarettes a day compared to non-smokers was 2.79 and 5.03 for men and women respectively.

Myth 7: None Of My Relatives Died Of Lung Cancer Despite Many Of Them Smoking Heavily, Therefore I’m Not Overly Concerned About The Effects Of Smoking On My Health
While genetics play a role in determining an individuals risk of developing lung cancer, a lack of family history of the disease in no way guarantees an individual won’t develop lung cancer. The majority of people who develop lung cancer have no 1st or 2nd degree relatives who suffered the disease.

Myth 8: I’m A Smoker But Because I Exercise Regularly, Don’t Drink Heavily And Eat A Healthy Diet, My Chances Of Getting Lung Cancer Are Low
Neither alcohol consumption or physical fitness have an effect on lung cancer risk. There is some evidence that diets rich in fruits and vegetables have a protective effect on lung cancer however a heavy smoker with a healthy diet is still at a much greater risk of lung cancer than a non-smoker with a poor diet.

Myth 9: There is No Evidence Or Conflicting Evidence That Passive Smoking Causes Lung Cancer
Most studies with a sufficiently large sample size find that passive smoking is a risk factor for lung cancer however the risks are actually quite small. A review of second hand smoking, published by the International Agency for Research on Cancer (IARC) in 2004, estimated that lung cancer risk was about 20-30% higher in non-smokers who were exposed to second hand smoke from their spouses.

Occupational exposure to passive cigarette smoke throughout a typical 40 year working life, for example in bar workers where smoking bans are not in place, has been estimated to increase an individuals lifetime risk of developing lung cancer by 0.1-0.4%. Low-level exposure to cigarette smoke outside of the above scenarios (for example occasional sharing of a car with a smoker), probably has a negligible effect on lung cancer risk.

Myth 10: Marijuana Smoking Causes Lung cancer
Interestingly, no link between marijuana smoking and lung cancer risk has been established however it is difficult to get a definitive idea of the health risks of marijuana smoke relative to cigarette smoke because very few people smoke marijuana heavily.

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The study, conducted by researchers at the Gillings School of Global Public Health, University of North Carolina (Chapel Hill), involved 3,664 boys and 3,412 girls who were 3.5 years of age. The researchers evaluated the childrens PSAI scores, which is a measure of the type of gender-linked activities a child participates in (higher scores indicate more masculine play while lower scores indicate more feminine play).

The researchers found that neither early soy exposure (exposure to soy milk or formula at <4 months age and/or sustained use at 6 months), or late soy exposure (soy milk or formula use between 4-15 months of age), were associated with PSAI scores in males. Interestingly, early soy exposure was associated with slightly higher (more masculine) PSAI scores in girls although scores were still in the normal range. Late soy exposure did no significantly influence PSAI scores in girls.

Other factors associated with higher PSAI scores in both boys and girls included: smoking during pregnancy, presence of an older brother, and advanced maternal age. Higher levels of maternal education were associated with lower PSAI scores in boys and higher PSAI scores in girls. Children, particularly boys, who had been primarily breast fed during infancy tended to have sightly lower PSAI scores than formula fed children.

The research comes on the back of several other studies published in the last few years that have looked at the effect of soy foods on males. One well known study, published in 2008 by researchers at the Harvard School for Public Health, found that those who consumed soy based foods on a regular basis had lower sperm concentrations than those who consumed little or no soy. The findings were controversial however in that the relationship was only significant in overweight and obese men, and only for those at the highest end for soy food consumption.

Other studies have found no relationship between soy intake and sperm quality. In 2008, Canadian researchers looked at the effects of soy protein isolate and milk protein isolate on sperm quality in 32 healthy males. No significant differences were found in sperm count, motility, or morphology, between the soy and milk protein groups. The researchers concluded that “Consumption of soy protein of low or high isoflavone content does not adversely affect semen quality in a sample of healthy adult men.”

Further evidence against a relationship between soy intake and male fertility can be found by the observation that Asian males tend to have similar levels of fertility to Caucasian men, despite consuming much more soy, although any differences in fertility due to soy consumption may be masked by the fact that Asian men are less likely to be overweight or obese than their Caucasian counterparts (obesity is a fairly strong risk factor for low fertility).

In any event, scientific evidence to date does not support a strong link between soy intake and either femininity, or lower levels of fertility in males and parents should not be unduly concerned about introducing soy products to their children for these reasons.

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After a steady increase since the 1960s, age adjusted cancer rates peaked in 1992 at 510.4 per 100,000 per year while the latest data from SEER, puts the current cancer rate at 463.4 per 100,000. Most of the reductions have come in the elderly, while cancer rates in the young and middle aged has increased slightly over the period – the cancer rate for those aged under 50 has increased from 98.2 per 100,000 to 101.1 per 100,000.

Men have seen the largest reductions in cancer rates with the male cancer rate declining by an impressive 19% since 1992. The female rate on the other hand has actually increased by 0.5%, partly as a result of improved screening for breast and cervical cancers and partly because the smoking rate hasn’t declined to the same extent in women as it has in men.

The graph below shows how incidence rates for the most common cancer types have changed over the last 20 years in the United States.

As can be seen from the graph, reductions in cancer rates have come primarily from smoking related cancers including lung cancer, which declined by 14%, stomach cancer (-30%), oral & pharynx cancer (-11%), and colorectal cancer (-28%). Over the same period, smoking rates in the USA have declined from 28% to 20%. Interestingly, pancreatic and breast cancer, for which smoking is also a risk factor, didn’t enjoy the same declines. In the case of breast cancer, reductions in smoking were offset by improved detection of smaller tumours, an increase in alcohol consumption, and a rise in obesity rates. The slight lift in the pancreatic cancer rate was likely due to poor diet, and increased rates of diabetes and obesity.

Thyroid cancer showed the most dramatic rise over the 20 year period with a massive 163% increase in incidence. Scientists are largely at a loss to explain why thyroid cancer rates have sky-rocketed. While improved detection of the disease can explain some of the increase, a 2009 study conducted by the American University’s Investigative Reporting Workshop found that there had been a rise in the rates of both small (2cm) thyroid cancer tumours over the period from 1980 to 2005. This is important because if higher thyroid cancer rates were the result of improved detection only, one would expect only the rate of the smaller, asymptomatic tumours to increase. Other potential reasons for the upward trend in thyroid cancer include higher rates of obesity and more exposure to radiation in the environment (for example, through increased CT scanner use). Fortunately thyroid cancer is highly treatable with a 5 year survival rate in excess of 99%.

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Several studies have been carried out to determine fibre levels in buildings containing asbestos. A 1991 study of 71 school buildings known to contain asbestos found average asbestos levels of 0.00023 fibres/ml for fibres greater than 5μm in length (fibres shorter than this have relatively low carcinogenic potential). An EPA study of 49 buildings conducted in 1989 found an average asbestos concentration of 0.00007 fibres/ml for fibres >5μm. That study also found no statistically significant difference between asbestos levels in buildings containing asbestos, buildings without asbestos, and outdoor air.

Finally, a more recent study, published in 2007 in the journal Regulatory Toxicology and Pharmacology looked at asbestos levels in 752 buildings from around the United States. The buildings all contained asbestos and were the subject of lawsuits by occupants claiming the asbestos exposure represented a significant health risk. The researchers found an average asbestos concentration of just 0.00012 for fibres >5μm. By comparison, outdoor air concentrations for asbestos are typically between 0.0001 and 0.0005 fibres/ml depending on how densely populated the area is.

To put these levels in perspective, the current permissible exposure limit for asbestos under OHSA regulations is 0.1 fibres/ml for fibres >5μm. Asbestos workers in the 1960s and 70s were typically exposed to levels in excess of 10 fibres/ml. Current asbestos exposure levels in buildings, even at the highest levels, are less than 1/1,000 times the OHSA limit and less than 1/1,000,000 of the level asbestos workers were exposed to in the past.

Another indication that environmental exposure to low levels of asbestos carries a negligible health risk can be seen by looking at mesothelioma rates of women in the United States over the last century. The mesothelioma rate has only marginally increased from about 0.2 cases per 100,000 in the early 20th century to its current rate of 0.33 cases per 100,000. The female mesothelioma rate can be considered a good indicator of the non-occupational risks of asbestos because very few women were employed in jobs that were considered a high risk of asbestos exposure. The male mesothelioma rate on the other hand has increased from about 0.3 per 100,000 in the early 20th century to a peak of 2.48 per 100,000 in 1992. The rate has since decreased gradually to 1.68 per 100,000 in 2008.

Finally, there has been recent publicity about an increase in mesothelioma rates among younger people due to significant exposure at schools where asbestos was commonly used for thermal and noise insulation. This is incorrect and as the graph to the right shows, the rate of mesothelioma for those aged under 50 has fallen substantially since 1975 to just 0.9 per million per year.

By comparison, you are 60 times more likely to die in a car crash and almost twice as likely to be killed by lightning than you are of being diagnosed with mesothelioma before the age of 50.

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Many girls pick up the smoking habit in their teenage years in the belief that smoking will keep them slim however this research suggests a link between smoking and weight loss, may in-fact be a myth.

The researcher team, based at the University of Montreal in Canada, looked at data from the Nicotine Dependence in Teens study which involved 1,293 teenagers, initially between the ages of 12 and 13. The study continued for five years with data on height, weight, and triceps skin fold thickness collected every 3 months for the duration of the study.

The researchers found that 14% of teenage girls and 7% of teenage boys in the study smoked at least 30 cigarettes a month during the first half of the study and this increased to 18% of girls and 9% of boys over the second half of the study.

Researchers found that a 3 cigarette per day increase in cigarette use over a 2.5 year period led to a small 0.4 point reduction in BMI and a 0.7cm reduction in height for males and that on average teenage boys who smoked were 2.54 centimeters shorter than non-smokers. In females however no correlation between cigarette use and height or weight was found.

It had been thought that nicotine in cigarettes acts as a stimulant, increasing the metabolism of smokers however it appears this effect is negligible or may be canceled out by other compounds in cigarettes that act to slow down the metabolism.

According to the latest data by the American Cancer Society (ACS) on cigarette use by teenagers, 23% of high school students are current smokers (smoking at least once over the last month) while 9.4% are frequent smokers (smoking at least 20 times over the last month). The frequency of teenage smoking is 11% amongst African Americans, 16% amongst Hispanics, and 26% amongst whites.

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The researchers, based in Denmark, analyzed the data from 67 clinical trials to determine the effects of five common antioxidant supplements on mortality. The supplements analyzed were vitamin A, vitamin C, vitamin E, selenium, and beta carotene.

In total, 232,550 individuals were analyzed across the studies. A total of 136,023 individuals took supplements while the remaining 96,527 a placebo. Overall 17,880 (13.1%) people taking the antioxidants died while 10,136 (10.5%) of those taking the placebo died. The study found no difference in the effects of the antioxidants in healthy individuals compared to those suffering various diseases.

When analyzing the studies that had the lowest risk of experimental bias, the researchers found that vitamin A appeared to increased the relative risk of death by 16%, vitamin E increased the relative risk of death by 4%, and beta carotene increased the relative risk of death by 7%. The researchers did not find a significant effect of vitamin C on mortality and found that selenium reduced the risk of mortality by 9% however this effect was only weakly significant.

On average, participants across the studies received high levels of the vitamins and minerals, in some cases more than ten times the recommended daily allowance (RDA). The average dose of Vitamin A across the studies was 20,219 IU (the RDA in America is just 2,500 IU). The average dose of Vitamin E was 570 IU (the RDA for Vitamin E is around 25 IU), Vitamin C average dose was 497mg (the RDA for vitamin C is 60mg). The average dose of Beta carotene was 18mg and the average dose of selenium was 99ug (compared to an RDA of 60ug).

The authors urge caution over taking doses of vitamins well in excess of the recommended daily intake, particularly if the person already consumes five or more servings of vegetables a day. Vitamins are essential to the functioning of a healthy body however this doesn’t mean more is necessarily better. Vitamin and mineral supplementation is generally only recommended by health professionals when an individuals diet is lacking in fresh fruit and vegetables and therefore they may not be getting sufficient vitamins and minerals through diet alone.

The researchers also believe that stricter controls are needed in the booming dietary supplements industry which is estimated to be worth more than $20 billion a year.

The research is backed up by a 2005 study on the effects of high dose vitamin E on mortality published in the journal Annals of Internal Medicine. That study found that while mortality decreased slightly for low dosage vitamin E (below 150 IU per day), mortality increased at dosages beyond this level.

Studies have also found that beta carotene can increase the risk of developing prostate cancer. One study also found that beta-carotene increases the probability of developing lung cancer, particularly in those already at high risk such as smokers and those exposed to asbestos.

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The majority of studies to date on this issue have found that sun-screen use is actually associated with a higher risk of developing melanoma. One study, published in the June 1995 issue of the International Journal of Cancer found that regular sunscreen users were 50% more likely to develop melanoma than non-users even after adjusting for other variables such as age, sex, hair color and holiday time spent in sunny climates.

Another study, published in the Annals of Epidemiology in December 2007, involved researchers analyzing the results 18 studies that dealt with the issue of sunscreen use and melanoma. After pooling the results from each study, the researchers found a 20% increased risk of melanoma for sunscreen users compared to non-users. The melanoma risk associated with sunscreen use increase to 60% when only data from latitudes greater than 40 degrees from the equator was used.

The problem with sunscreens is that until recently sunscreens only offered protection against UVB radiation. While both basal cell carcinoma and squamous cell carcinoma appear to be caused primarily by UVB radiation, melanoma appears to be triggered by exposure to both UVA and UBA radiation. A study on the effects of UVA and UVB in fish found that both forms of UV radiation led to the development of melanoma.

A second problem is that while recent sunscreens offer broad spectrum protection, meaning they protect against both UVA and UVB radiation, most of these sunscreens don’t indicate the degree of UVA protection they confer. A sunscreens SPF rating is a measure of how effective it is at preventing sunburn. A sunscreen with an SPF rating of 20 for example, means a person would take 20 times longer to burn than they would if they were not wearing any sunscreen. SPF is a measure of the amount of UVB protection a sunscreen offers because it is UVB radiation that causes sunburn. The SPF rating tells us nothing about the protection it offers against UVA radiation (which doesn’t cause sunburn).

Many sunscreens claim to offer “broad-spectrum” protection, this tells the consumer nothing about how effective the sunscreens UVA protection is, only that it offers some protection. A recent study of sunscreens found that the majority of sunscreens are quite ineffective at blocking UVA radiation, even those that claim to offer broad spectrum protection. This means an individual can still be exposed to high amounts of UVA light, even when using a broad spectrum sunscreen.

Finally, humans require UVB light in order to synthesize Vitamin D. Sun screens reduce the bodies ability to synthesize Vitamin D by blocking UVB radiation. A lack of vitamin D has been associated with a greater risk of breast, colon, prostate, and ironically skin cancers.

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As little as fifteen years ago, those diagnosed with HIV could expect to develop AIDS and die from the illness on average just five years after diagnosis. This was due to the late stage HIV was generally diagnosed at and the limited treatment options available.

These days, improvements in treatment and early diagnosis mean that people can on average expect to live for 24 years after being diagnosed with HIV. Younger people and those that take their HIV medication correctly can expect to live even longer that this with life expectancies close to those without HIV.

HIV is curable

HIV medication in the form of anti-retroviral drugs can only control the illness, it cannot cure it. Some people stop HIV medication when the levels of the virus circulating in their system becomes negligible however the virus is still there and levels of the virus circulating in the body will increase again in the absence of medication.

HIV and AIDS are the same illness

Human Immunodeficiency Virus (HIV) reduces the ability of the immune system to fight infection making it more susceptible to certain illnesses and diseases that do not normally develop in people with healthy immune systems. Acquired Immune Deficiency Syndrome (AIDS) is the name given to the collection of these illnesses and diseases that result from HIV. If an individual develops illnesses or diseases that are classified as an AIDS defining illness they are considered to have AIDS.

AIDS defining illnesses include candidiasis (a fungal infection), recurring penumonia, tuberculosis, wasting syndrome, lymphoma, cervical cancer and esophagitis (inflammation of the esophagus).

HIV can be transmitted by casual contact with a sufferer

While saliva, sweat and urine from an HIV positive individual contain small amounts of the virus, kissing or sharing a bathroom or drink bottle with an HIV infected person does not lead to transmission of the virus.

Some recorded cases of transmission from kissing where both individuals have bleeding from the mouth through gum disease for example, have been recorded but the risk is negligible. In theory, being bitten by an HIV positive individual could result in HIV transmission but again the risk is extremely small. The overwhelming transmission route for HIV is through sexual contact.

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One study, conducted by researchers at Harvard Univeristy, followed around 120,000 individuals over a 14 year period. The study found absolutely no correlation between egg consumption and the risk of heart disease. Those who consumed two or more eggs each day were found to have almost exactly the same risk of heart disease as those who never consumed eggs at all.

While eggs are one of the most concentrated sources of dietary cholesterol, the link between dietary cholesterol and serum (blood) cholesterol appears to be minimal since only a very small amount of the dietary cholesterol is absorbed into the blood. According to Cr. Meir Stampfer, one of the researchers involved in the study: “Eggs will raise blood levels of cholesterol, but the increase is actually very small and appears to be compensated for by other nutrients, beneficial nutrients, that are present in eggs.”

Another study published in 2007 in the Medical Science Monitor which involved 9,5000 people found that eating one or more eggs a day did not increase heart disease risk and may even cause a slight decrease in blood pressure levels.

The high levels of the vitamins B6, B9 and B12 contained in eggs may in fact help protect the heart as these vitamins help reduce homocysteine levels in the blood. High homocysteine levels may damage blood vessels, and degrade the main structural elements of arteries: collagen, elastin, and proteoglycans. Several studies have linked high homocysteine levels to an increased risk of cardiovascular disease.

Many also avoid eggs because they believe eggs to have high levels of fat, particularly saturated and trans fats, the so called “bad fats”. Eggs consist of only 10 percent fat however, and only a small amount of that fat (less than a third) is in the form of saturated fat. Eggs in fact have almost the exact ratio of saturated, monounsaturated, and polyunsaturated fats recommended by most dietitians.

Egss are also an extremely healthy, nutrient dense, food. Eggs consist of about 15 percent protein. Egg protein is extremely high quality protein, it has a biological value of 94 percent. The biological value is a measure of how efficient a particular protein source can be used by the body. Egg has one of the highest protein values, it is higher than soy milk (91%), cows milk (90%), chicken (80%), fish (76%) and beef (74%). One egg provides over 10 percent of the bodies daily protein requirements.

Eggs are extremely good sources of most vitamins and minerals. They have high levels of Vitamin A, Vitamin E, Thiamine (Vitamin B1), Riboflavin (Vitamin B2), Vitamin B6, Folate (Vitamin B9), Vitamin B12, Iron, Magnesium, Phosphorous, Zinc, Tryptophan, Iodine and Selenium. Eggs are also an excellent source of choline, a nutrient important for brain health.

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Aspartame critics claim that the sweetener causes everything from brain tumors and seizures to leukemia. Fortunately aspartame has been the subject of numerous studies of both humans and animals and has been shown to be safe at levels far beyond the acceptable daily intake (ADI).

The ADI for a product is determined by dividing the highest daily intake of aspartame that has no observable toxicological effects. This amount is determined through animal toxicology studies and is then divided by 100 to determine the ADI.

The ADI for aspartame is 50mg per kg of body weight. This amount of aspartame represents about 15 cans of diet soft drink a day for a 120 pound individual or about 70 table-top packets of sweetener. Studies have found that the average daily consumption of aspartame is just 3-5 percent of the ADI with around 9 in 10 individuals consuming less than ten percent of the ADI.

A few studies have shown a link between aspartame and certain cancers, however this is at aspartame levels equivalent of over 1000 cans of diet soft drink a day. One such study, which is often cited by aspartame critics as evidence of aspartame’s carcinogenic effects is called “First Experimental Demonstration of the Multipotential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague-Dawley Rats.” and is published in the journal Environmental Health Perspectives.

This study involved adding aspartame to the daily feed of mice from the age of 8 weeks for the remainder of the rats lifetimes. The rats received either 4, 20, 100, 500, 2500 or 5,000mg of aspartame per kg of body weight.

Interestingly the control group, which consisted of rats which received no aspartame actually died earlier than most of the groups receiving aspartame. In fact, in the female rats, the control group had the shortest survival time and the group of rats that received the 5,000mg per kg dose of aspartame (equivalent to 1,500 cans of diet soda a day) actually lived the longest of all the groups. At the age of 120 weeks around 29 percent of the rats on the highest aspartame diet were still alive compared to just 16 percent for the control group.

As each rat died, an autopsy was performed to determine the presence of tumors. While at high levels of aspartame, the rats did display a slightly greater likelihood of developing tumors, the researchers failed to take into account the fact that these rats lived significantly longer than the control group of rats and therefore naturally would expect to have a slightly greater rate of tumor development.

The researchers concluded that “Our research shows that [aspartame] is a multi-potential carcinogenic compound whose carcinogenic effects are evident even at a daily dose of 20mg/kg bw, much less than the current ADI for humans in Europe (40mg/kg bw) and in the United States (50mg/kg bw).” This however was not shown in the results, at lower levels of aspartame there was virtually no effect on tumor rates. For example amongst male rats, the number of rats that developed tumors was lower in the 4mg, 20mg and 500mg groups compared to the control group. The control group had a tumor rate of 35.3% compared to 29.3%, 32% and 34% in the 4mg, 20mg and 500mg groups respectively.

The largest study on humans to date was conducted by the National Cancer Institute and was published in April 2006. The study found absolutely no correlation between aspartame use and the rate of leukemias, lymphomas and brain tumors.

With no studies showing adverse effects from aspartame at levels relevant to humans and over 100 studies attesting to the safety of aspartame, even at levels far beyond what could possibly be consumed by humans, people should not be concerned by consuming some aspartame in their diet.

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The research study was carried out by Professor Brendan Stewart who is a cancer specialist at the University of New South Wales, Australia. Stewart analyzed numerous research reports and categorized various activities and chemical agents on their likelihood of causing cancer.

According to Stewart the research was carried out in order to give people some perspective on cancer risk, particularly in the case of low risk events that are often over-hyped in the media.

According to Stewart “[I am] not critical of the media or the investigators, but the very nature of the media in the community’s interest means that attention is often focused on these low levels of risk,”

“Our tool will help establish if the level of risk is high, say on a par with smoking, or unlikely such as using deodorants, artificial sweeteners, drinking coffee,” Stewart added.

Five risk bands were used to categorize each potential risk factor: proven carcinogens, likely carcinogens, inferred carcinogens, unknown carcinogens, and unlikely carcinogens.

Among the proven carcinogens were:
1) Tobacco smoking which was a proven cause of cancers of the mouth, throat, lungs, esophagus, stomach, and pancreas.
2) Alcohol consumption, which has been proven to increase the risk of cancers of the oral cavity, esophagus, liver and the breast.
3) Occupational exposure to various chemicals such as soot and tar, asbestos, radon, benzene and formaldehyde among others.
4) Deliberate exposure to the sun which increases skin cancer risk.
5) Passive smoking which increases lung cancer risk.
6) Drinking water contamination with arsenic.

Likely carcinogens included particles in air pollution, smoking marijuana, tanning beds and chemicals in processed meats.

Activities and chemicals unlikely to be carcinogenic, despite often being reported in the media as being so included:
1) Artificial sweetener consumption
2) Coffee consumption
3) Regular deodorant use
4) Drinking fluoridated water
5) Exposure to electromagnetic fields (such as cellphone towers, cellphones, wireless networks)
6) Breast implants
7) Amalgam dental fillings

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1) The incidence of diabetes is much lower among light and moderate alcohol drinkers compared to those that abstain from drinking or drink heavily.

2) Light to moderate alcohol consumption actually improves insulin resistance in most diabetics.

An Italian study found that in type-2 diabetes, the action of insulin was improved with alcohol consumption and the improvement was due to an increase in insulin sensitivity, not an increase in insulin secretion. The study involved performing intravenous glucose tolerance tests on 8 healthy individuals and 8 type-2 diabetics. The test was performed twice, once were the subjects sipped tapped water for an hour prior to, and during the test. The second time the subjects sipped up to 40 grams of alcohol in the form of vodka.

While both groups showed improved glucose tolerance after alcohol consumption, the improvement was more marked in the individuals with type-2 diabetes. The graph below shows the blood plasma glucose concentrations for tje type-2 diabetics during the test. The results with alcohol are in black while the results with water in white. The bar graph shows the area under the curve of the line graph.

The researchers concluded that “The present study shows that alcohol intake improves insulin sensitivity and glucose tolerance in type-2 diabetic subjects and this amelioration is proportionally greater compared with matched healthy volunteers.”

An analysis of 15 studies involving over 350,000 men in total on the effects of alcohol consumption on type-2 diabetes incidence found that moderate drinkers were 30% less likely to develop diabetes than heavy drinkers or those who didn’t drink at all. The findings are reported in issue 28, 2005, of the medical journal diabetes care.

While excessive long-term alcohol consumption can certainly impair insulin function both in diabetics and non-diabetics and is associated with high blood pressure, brain damage, liver damage and heart disease, light to moderate alcohol consumption has been shown to have health benefits such as a decreased risk of strokes and heart attacks. There is no reason why diabetics cannot enjoy moderate alcohol consumption in the same way non-diabetics can and in-fact moderate consumption does appear to have some benefits in terms of an improvement in insulin resistance.

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While it is true that high blood cholesterol (known as serum cholesterol) levels and a lower ratio of high density lipoprotein (HDL) to low density lipoprotein (LDL) are associated with a higher incidence of heart disease, many myths exist as to what actually increases cholesterol in the blood.

Myth 1: Eating high cholesterol foods increases blood cholesterol, therefore high cholesterol foods increase coronary heart disease risk.

There is actually little correlation between dietary cholesterol consumption and cholesterol levels in the blood.

One of the biggest studies into the effects of cholesterol intake on blood cholesterol levels was the Framingham heart study which began in 1948 and followed over 5,000 adults aged 30 to 62. The study found that dietary cholesterol had no correlation at all with blood cholesterol. Men both above and below the median cholesterol intake had the same average blood cholesterol level of 6.16 mmol/L. Women consuming below the median cholesterol amount had a blood cholesterol level of 6.37 which interestingly was higher than that for the group that consumed more than the median amount of cholesterol who had an average level of 6.26 mmol/L.

The researchers concluded that there was no evidence of a relationship between dietary cholesterol and the development of coronary heart disease.

These findings are backed up by other studies that suggest healthy individuals blood cholesterol levels are unlikely to be significantly effected by dietary cholesterol consumption. In a 2005 study, Yale researchers fed 49 adult participants two eggs a day for six weeks. Despite eggs being very high in cholesterol, neither “bad” LDL cholesterol, nor total cholesterol increased amongst the participants.

Myth 2: Eating food high in saturated fat increases both blood cholesterol levels and heart disease risk.

Again there is little evidence pointing to a direct link between high saturated fat intake and either heart disease or high blood cholesterol levels.

The Tecumseh study was a research study that attempted to find a correlation between fat and/or cholesterol consumption and the amount of cholesterol in the blood. The study involved over 2,000 adults in Tecumseh, Michigan – participants recorded all food consumed in the 24 hour period prior to a blood cholesterol test. The study found no correlation between total fat intake or saturated fat intake and blood cholesterol. Furthermore no correlation was found between dietary cholesterol intake and blood cholesterol.

In the last 100 years, despite a significant rise in coronary heart disease rates, there has been little change in total fat consumption and there has actually been a significant decrease in saturated fat consumption (which are generally animal fats) and an increase in polyunsaturated fat consumption (plant based fats in general).

So if dietary cholesterol and saturated fat intake don’t increase cholesterol what does? Exercise, weight loss, and not smoking are all associated with decreases in both blood cholesterol and increases in the ratio of “good” to “bad” cholesterol. It is interesting to note that over the last 100 years, obesity rates have increased dramatically and sedentary lifestyles have become much more common suggesting these are more likely to blame for increased coronary heart disease rates.

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