Sunscreens

Most of the chemicals contained in sunscreens have minimal toxicological effects when first applied to the skin. However, when exposed to sunlight, the chemicals are heated and reactions occur between the sunscreen’s active and inactive ingredients and the epidermis. Most of the risks associated with sunscreens lie in the method used to stop the UV radiation harming our skins. Sunscreens use organic compounds to either reflect or absorb different parts of the UV spectrum. When the absorption method is used to protect us from UV radiation, the particles absorbing the UV are energised, or elevated to a higher energy level. This energy is re-emitted when the particles drop back to their former, lower energy level. The released energy enters the epidermis. It is this process that causes the skin damage.

Many of the chemicals in sunscreens have been found to cause phototoxic, photoallergic or photogenotoxic (DNA altering) effects. PABA (Paramino benzoic acid) has been found to increase the development of a particular DNA defect in human cells. When this occurs in people who lack the mechanism to repair the defect, they are more susceptible to skin cancer. When exposed to sunlight, PABA also readily generates oxygen radicals which harm DNA strands . An ester of PABA, amyl paradimethylarninobenzoate (Padimate A) was found to cause phototoxic reactions. Padimate A reacts with UVA to produce symptoms widely resembling sunburn. The similarity between sunburn and a phototoxic response has led people to mistakenly believe that the sunscreen causes sunburn. An ingredient commonly used in sunscreens, 2-phenylbenzimidazole-5-sulfonic acid (PBSA), strongly absorbs UVB radiation, thus becoming energised and capable of affecting adjacent skin tissue by damaging the guanine base sites of the cell’s genetic material. This may increase the risk of developing skin cancer.

Physical sunscreens contain inert materials such as titanium dioxide, zinc oxide and/or talc. They work on the basis of reflecting, scattering or blocking UVA and UVB radiation. The effectiveness of this type of sunscreen depends on the diameter or size of the particles or the thickness of the film (application) to reflect or scatter the visible light or UV radiation. No phototoxicity, contact sensitisation or photoallergy have been produced by these agents, although they may be so occlusive (that is, block so effectively) that they may cause blockage of the sweat glands, a condition known as miliaria.

Octyl Methoxycinnamate appears to be the most common chemical used in Australian sunscreens. This forms part of the group of photon absorbing chemicals, the cinnimates. Photoallergy has been reported as well as contact allergy.

Benzophenones, a constituent in sunscreens, have been found to cause contact allergy and photoallergy. Benzophenones, oxybenzone and mexenone have the potential to mimic and exacerbate a disease. One example is chronic actinic dermatitis, found predominantly in elderly men.

Dibenzoylmethanes have been incorporated into sunscreens since 1980 as UVA absorbers. Cases of photoallergy and contact allergy have been reported as well as cross reactions from prior exposure to dibenzoylemethanes. Instances of contact and photocontact allergy with dibenzoylmethane derivatives such as 5-methoxypsolaren (5-MOP) and isopropyl dibenzoyl methane (Eusolex 8020) have been found with sunscreen usage and it is often used in conjunction with Eusolex 6300.

There are instances of people using sunscreens who have reacted to the excipients (base materials/carriers) included in the formulation, such as the preservatives, fragrances and emulsifiers, which have caused contact allergies. So there is cause for concern not only about the active ingredients in sunscreens, but about the inert ingredients as well.

The question of whether sunscreens prevent skin cancer is an ambiguous one. A review of studies on skin cancer and sunscreens by Science News, found that people who use sunscreen are more likely to develop basal cell cancer than people who do not. Science News also examined ten studies of melanoma. Five of them concluded that people who used sunscreen were more likely than non-users to develop melanoma. Three of the studies found no association between melanoma and sunscreen use, and two studies found that people who used sunscreen were the most protected. Science News 65, found that epidemiological data was not conclusive. This may be because people involved in the studies were not wearing effective sunscreen, or were staying in the sun longer because they thought they were protected.

Other PABA derivatives that have caused sensitisation or photocontact sensitisation include octyl dimethyl PABA (padimate 0) and amyl dimethyl PABA (padimate A). Padimate A causes redness of the skin. The frequency of padimate 0 causing adverse reaction is less in comparison to PABA and monoglyceryl PABA because padimate 0 is not a true PABA ester.

In general, elderly people are more susceptible to chemically induced photosensitivity, be it photoallergic or phototoxic. This is due to several factors: their skin is thinner and more easily penetrated, they may be on medication that can enhance photosensitivity and their body’s capacity to excrete such substances once penetration has occurred is much slower.

In 1994, researchers at the Harvard Medical School found that the ingredient psolaren in sunscreens is an extremely efficient carcinogen. Experiments on rodents exposed to UVA also produced the same result - psolaren was found to be carcinogenic. It is worrying that psolaren is known to be a free radical generator when activated by UV radiation, and yet it is used in sunscreen ingredients. People with psoriasis are at greater risk, as their squamous cell carcinoma rate was found to be 83 times higher than that of the general population.

3-(4-Methyl-benzylldene) camphor (known as Eusolex 6300) is a sunscreening agent used widely in Europe. However, the United States Food and Drug Administration (FDA) disapproves of this ingredient due to the high incidence of allergic and photoallergic reactions reported.

Titanium dioxide has also been found to absorb 70% of UV, and in aqueous environments this leads to the formation of hydroxyl radicals which can initiate oxidation. This is known to cause breaks in DNA strands, leading to an increased risk of cancer. In response to titanium dioxide’s potency, manufacturers coat the particles to make them less active. Although this treatment has been found to reduce the chemical’s activity, it does not eliminate DNA damage altogether. Particles of titanium dioxide have been made smaller to stop the white paste effect on the skin, but this enables them to enter cells more easily and block sweat glands. Titanium dioxide does not itself cause photoallergic reactions on the skin, but it can create the skin condition miliaria, mentioned earlier, causing inflamed sweat glands and heat rash. Titanium dioxide is used in PABA sunscreens because it is not a sensitiser and blocks the appearance of photoallergic reactions.

Salicylates are known to cause photocontact allergy. Toxic effects from Octyl salicylate, a major derivative used in many sunscreens, has yet to be reported.

Cinnamates are chemically related to or can be found in coca leaves, cinnamic acid, cinnamic aldehyde and cinnamon oil. They are included in perfumes, topical medication, flavourings and sunscreens. The cinnamate derivative, p-methoxymethylcinnamate has been found to be cytotoxic, while 2 Ethoxyethyl-p-cinnamate (cinoxate), a major derivative of cinnamate, and used in sunscreen, causes the majority of the allergic and photoallergic reactions in humans. Cross reactions with other cinnamate derivatives have also been reported.

Excipients act as the carriers or base materials of a product and ‘receive’ and carry the other ingredients. These chemicals include mineral oil, petrolatum, isopropyl esters, lanolin derivatives, aliphatic alcohols, emulsifiers, fragrances, thickeners and preservatives. Sunscreen toxicity can be caused by excipients in the formulations.

In studies, sensitive subjects tended to be older and often had a history of long-standing dermatitis. In a study of 603 people aged 40 and over, 114 people were tested and found to be allergic to ingredients in sunscreens. Fragrances, used extensively in sunscreens, produced the most common reaction: allergic contact dermatitis.

The FDA expressed their concerns about cancer when it was discovered that a combination of the 21 allowable sunscreen ingredients caused lesions that were not previously seen when the individual ingredients were tested separately.

How to prevent and reverse a heart attack and stroke.

Dr Dingle’s simple steps to lower your risk of heart attack and stroke without drugs.

Cardiovascular disease including heart attack and stroke, as well as cancer, alzheimer's and other chronic illnesses are primarily a result of oxidation and inflammation. To dramatically reduce your risk of chronic illnesses reduce your inflammation and oxidation in your body.

2g+ of Omega 3 oils/day

2g+ of vitamin C/day

lower your stress

drink more water (2-5 liters/day)

remove sugar and high GI foods from you diet, particularly soft drinks (no artificial sweeteners)

eat more fruit and vegetables, particularly raw vegetables (salad)

walk more

don’t smoke

Vitamin D

Vitamin D is one of the essential nutrients required by the human body. Unlike most vitamins, it is one that we can manufacture on our own, given the right conditions. Despite this, vitamin D is showing up increasingly in populations as the most widespread and critical nutrient deficiency; this deficiency is linked to many diseases and disorders, costing billions of dollars each year. Our changing lifestyles, including increased indoor living and campaigns warning people to stay out of the sun have meant that most people don’t get enough vitamin D. The resulting deficiency is compounded by the consumption of modern and processed foods devoid of any vitamin D.

Vitamin D refers to two biologically inactive precursors: D3, also known as cholecalciferol (made from cholesterol), and D2, also known as ergocalciferol. Vitamin D is the only nutrient that can actually be synthesized by the human body, which technically means that it is not a vitamin. The synthesizing of vitamin D in the body can be achieved through contact with solar ultraviolet B radiation emitted by the sun. Without the presence of this solar radiation the only way to get vitamin D is through diet—hence, it is still classified as a “vitamin.”

It is becoming increasingly common to find low levels of vitamin D in Western populations. Vitamin D uptake from the sun is not affected so much by seasonal changes but by how much time people spend in the sun. People require between 70nmol/L to 100nmol/L of vitamin D and in winter, when people spend less time outdoors, it is difficult to achieve these levels. Furthermore, current sun avoidance advice combined with the dietary habits of the general populous make the situation much worse—the average level in adults is around 25nmol/L - not even half the recommended level. Populations particularly at risk are seniors and infants but also any person spending too much time inside.

In addition to vitamin D obtained through UVB exposure to the sun, this vitamin can be found in foods such as eggs, butter and fortified milk, with the highest levels found in fish. Remember, we evolved as fisher- hunter gatherers and fish used to be an essential part of our nutrition. Vitamin D can also be provided by supplements. Numerous studies have concluded that sensible sun exposure and supplementation are the most effective ways of increasing vitamin D levels.

Once in the body, vitamin D is either stored in the body’s fat adipocytes or enters the liver. The vitamin D gets broken down in the kidneys for the regulation of calcium and dozens of metabolic functions. The broken-down vitamin D then interacts with vitamin D receptors in the small intestine and on osteoblasts to regulate calcium and phosphorous metabolism. It not only assists calcium uptake in the bones but also works as an immunity modulator. It continues to be metabolised in various tissues and cells for regulating cellular proliferation and differentiation as well as in the functioning of the immune system and macrophages. In addition, circulating concentrations of the broken-down vitamin D may help increase insulin production and alter fat metabolism.
Deficiencies in vitamin D have been linked with a range of problems with the musculoskeletal system including low bone and muscle problems, as well as cardiovascular disease, diabetes and metabolic syndrome, cancer and impacts on the immune system, Parkinson’s Disease, asthma, pain, and pre eclampsia.

Low levels of vitamin D can reduce the amount of calcium uptake in the bones which, over time, can lead to a loss in bone density. Pregnant women with vitamin D deficiency have been found to give birth to children who are at greater risk of being unable to store calcium in their bones, reducing their bone density and increasing the risk of bone fractures. In addition, these children experience higher level of dental caries. Low vitamin D in children will prevent them from reaching their bone mineral density and therefore increase their risk of osteoporosis and fracture later in life. In a study of 206 pregnant women during their second trimester, researchers reported that only 10.5% of the women had adequate levels of vitamin D.

In a study of 23,423 would-be first time mothers, the risk of pre-eclampsia was 27% lower in women who consumed vitamin D supplements with daily doses of 10 to 15 micrograms, compared to women who did not take supplements. Pre-eclampsia, affecting 2% to 3% of all pregnancies is estimated to be responsible for about 60,000 deaths each year worldwide.

Vitamin D deficiency is inversely related to a range of diseases, including respiratory infections such as influenza. In support of these findings, clinical trials have shown that vitamin D supplementation can reduce the risk of reactivation of latent tuberculosis infection. Vitamin D (in particular, D3) stimulates neutrophils, monocytes (natural killer cells) and the epithelial cells lining the lungs and protecting them from infection. So come winter-time and flu season get out and get a bit more sun along with some cod liver oil.

Studies have indicated that vitamin D supplementation may reduce the risk and difficulties associated with autoimmune disorders. In particular, there is strong evidence that vitamin D reduces the risk of multiple sclerosis and type 1 diabetes mellitus, and weaker evidence for rheumatoid arthritis, osteoarthritis, systematic lupus and erythematosusstar. There is no doubt about the link between vitamin D shortage and multiple sclerosis. There is a 41% decrease in MS risk for every 50 nanomoles per liter increase in 1,25-hydroxyvitamin in the blood. Vitamin D deficiency also predisposes to insulin resistance and pancreatic beta cell dysfunction. In a study of 10,366 Finnish children those given 2,000 IU of vitamin D3 per day throughout the first year of life experienced a 78% reduced risk of type 1 diabetes.

Over time, vitamin D deficiency leads to osteopenia, precipitates and exacerbates osteoporosis, which causes the painful bone disease osteomalacia and leads to increased muscle weakness. Notably, vitamin D deficiency is also associated with an increased risk of falling and fractures. Frail older people confined to institutions may sustain fewer hip fractures if given vitamin D. A study of 302 women (average age 77.2) living in Perth, Australia found after 12 months of supplementation significantly more falls in the placebo group than in the vitamin D2 group (62.9% versus 53%, respectively). A study of 124 nursing home residents taking a daily vitamin D supplement of 800IU for five months reduced the number of falls among nursing home-dwelling elderly people by 70%. Lower blood concentrations of vitamin D increase the likelihood of hip fracture among menopausal women by up to 70%.

Numerous studies have shown that vitamin D deficiency is strongly associated with an increased risk in developing cardiovascular disease. Epidemiological studies report that the rates of coronary heart disease, higher rates of diabetes, hypertension and elevated LDL cholesterol, are strongly correlated with decreased vitamin D status. Vitamin D appears to be necessary to maintain adequate apolipoprotein A-I concentrations, the main component of HDL (good) cholesterol.
Vitamin D deficiency increases the risk of “all-cause mortality” and is associated with a 122% increase in the risk of “cardiovascular mortality” compared to the highest average Vitamin D levels. Researchers also found that low levels were linked to higher levels of inflammation markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6), which are important markers for chronic illnesses, including cardiovascular disease (These inflammation markers are a much better predictor of cardiovascular disease than cholesterol levels).

Deficient or insufficient vitamin D levels have been documented in patients with myocardial infarction, stroke, heart failure, and peripheral arterial disease. A study of 13,331 initially healthy men and women found that low levels of vitamin D may increase the risk of death from all causes by 26% when the lowest and highest average vitamin D levels were compared. In an examination of 1,739 participants in one study, low levels of vitamin D were associated with a 62% increased risk of cardiovascular events like heart attack, heart failure or stroke. The study also found that 28% of subjects had blood levels lower than 15 nanograms per millilitre (ng/mL). Only 10% of the participants had levels in the optimal range above 30 ng/mL.

Low vitamin D levels are linked with the formation of atherosclerosis. When researchers exposed macrophage cells (white blood cells) with and without vitamin D, they found that vitamin D inhibits the uptake of cholesterol by the macrophage cells. When people are deficient in vitamin D, the macrophage cells take in more cholesterol, and they can't get rid of it. The macrophages get clogged with cholesterol and become foam cells, which are one of the earliest markers of atherosclerosis. Macrophage activation is higher in people with diseases such as diabetes, and when found in combination with low vitamin D levels, the macrophages become loaded with cholesterol and eventually stiffen blood vessels and block blood flow.

A number of studies have also shown a link between low vitamin D and diabetes and metabolic syndrome. In a study of 15,088 subjects Vitamin D levels were inversely associated with hypertension, diabetes mellitus and hypertriglyceridemia. Other cross-sectional studies have confirmed the links between vitamin D deficiency and both hypertension and diabetes. One study reported that a daily intake of 800 IU of vitamin D compared with a daily intake of less than 400 IU of vitamin D reduced the risk of type 2 diabetes by one-third. A number of studies have shown a close link between vitamin D deficiency and metabolic syndrome. Vitamin D appears to be necessary to maintain adequate apolipoprotein A-I concentrations, the main component of HDL (good) cholesterol. One study found similar results with the lowest levels of vitamin D being associated with a 31% prevalence of metabolic syndrome, compared to only 10% for people with the highest average levels. The results also showed that vitamin D blood levels were associated with HDL cholesterol levels. Each increase of 10 ng/mL in 25(OH)D was associated with an increase of 3.8 to 4.2 mg/dL in HDL-C. An increase of just 1 mg/dL increment in HDL-C is associated with a 4% to 6% reduction in coronary heart disease risk.

There is now overwhelming evidence that supports increased vitamin D to lower the risk of developing and dying of prostate, breast, colon, ovarian, esophageal, non-Hodgkin's lymphoma and a variety of other lethal cancers. In a 10-year study of 1,179 healthy, postmenopausal women, researchers found that those taking large amounts of vitamin D3 had a 60% or higher chance of not getting cancer compared to their peers. In a review of data from 177 countries, extrapolation of results showed that as many as 50% of breast and colon cancer cases could be prevented by increasing vitamin D intake. According to the study, the median adult intake of vitamin D in the US is only 230 IU per day, versus the researchers' recommended 2000 IU per day. For every increase of 25 nmol/L in people’s blood, there was a 34% cancer risk reduction, with the most common cancers being those of the lung, colon and pancreas.

Vitamin D can protect women with pale skin from breast cancer and it can reduce the risk of pancreatic cancer especially in young men. In fact vitamin D appears to reduce the risk of other cancers as well such as colon-, prostate-, Hodgkin’s Lymphoma and lung cancer. A recent study of vitamin D intakes found increased intakes of the vitamin were associated with a 24% reduction in the risk of developing estrogen and progesterone positive breast tumours.

One explanation for cancers being reduced by vitamin D is vitamin D receptors (VDR). These are found in the tissues of the body and help maintain cellular growth and prevent cells from becoming malignant. Studies on both colon cancer cells and healthy prostate cells have demonstrated protective effects of vitamin D at a cellular level.

Vitamin D deficiency is widespread in developed countries such as the US, UK, Australia, New Zealand and Europe. US studies have found vitamin D deficiency is present in approximately 30% to 60% of the general population. Increasing vitamin D levels just a small amount would outweigh the benefits of most of the medication people take for chronic illness including medication taken for cardiovascular disease.

Considering the evidence, there is an overwhelming agreement between vitamin D researchers that current recommendations of 200 IU per day for children and adults up to 50 years of age for vitamin D need to be increased to 800 IU to 1000 IU vitamin D3. Numerous studies have shown supplementation to be effective in raising blood levels of Vitamin D levels with no evidence of intoxication reported in either the short- or long-term trial.

Sensible sun exposure (or UVB irradiation) along with supplements are required to satisfy the body's vitamin D requirement. To achieve adequate levels of vitamin D we need to get one to two hours of sensible sun exposure a day. This should be during the morning or late afternoon. While it is prudent to avoid too much sun it is important to remember that the costs of vitamin D deficiency far outweigh the cost of skin cancer and some sun may also be necessary to reduce skin cancers. Remember, we did evolve in the sun but maybe not the hot midday sun, especially for those with fair skin.

milk and calcium myths

Milk Myths

I grew up in the 1960s, when every kid in Australia was given a free bottle of milk just before morning tea at school. I thought it was great. Now, 50 years on, maybe it was a big mistake. Today I see many people with allergies and reactions to milk; chronic illness related to milk is skyrocketing. Even the smallest amount of milk now causes me to have lots of mucus. Despite advertising claims, cow’s milk, as we know it, is not a healthy drink. Not only is it not a great source of calcium for bones but also there is mounting scientific evidence that consuming processed dairy has negative health consequences from colic in kids to breast cancer.

Milk is not the food it used to be. It is so highly processed that it no longer resembles the milk our ancestors consumed thousands of years ago. Today a cow (a Friesian cow) gives 25 litres per day compared to just a few litres daily that cows produced centuries ago. Modern farming practices have extended the milking period to 305 days per year (1). Pasteurization was necessary 100 years ago due to poor hygiene but today it destroys the enzymes that make milk easy to digest, particularly for infants. All milk, including human milk, comes with a rich array of nutrients, including 20 or more enzymes to help digest itself—such as lactase to digest lactose. Homogenisation forces the particles of fat through a series of sieves to mix it with water, just so cream does not settle on top. It then becomes difficult for the body to determine whether it is fat or water. Normally the two don’t go together.

Modern milk has been sold to millions of people around the world based on its supposed benefits in building healthy bones. The research shows that milk has, at best, questionable benefits for preventing osteoporosis and bone fractures and is in fact linked with many forms of chronic illness including cancer, cardiovascular disease, multiple sclerosis, diabetes type 1, Parkinson’s disease, gut disorders and allergies.

Calcium for bones?

Findings from long-term studies have cast doubt on the value of consuming the large amounts of dairy and calcium currently recommended. In particular, high calcium intake does not actually appear to lower a person’s risk for osteoporosis (2). There is evidence that the recommended levels in the West are too high, with countries such as India, Japan and Peru having an average daily calcium intake around 300 milligrams (mg) per day, less than half that in the Western world, and no increase in the incidence of bone fractures (3). If increased dairy consumption leads to reduced osteoporosis and fracture rates, then multi-country epidemiologic studies would show that countries with the highest dairy consumption, such as Australia, New Zealand, the U.S. and U.K., would have the lowest osteoporosis and fracture rates yet this is not the case. Although the consumption of dairy products in the United States is among the highest in the world, osteoporosis and fracture rates are simultaneously high (4,5).

Other areas of research also support this finding. A comprehensive literature review found that of 57 evidence-based scientific studies of dairy foods’ effects on bone health, “53% were not significant, 42% were favourable and 5% were unfavourable. Of 21 stronger-evidence studies, 57% were not significant, 29% were favourable and 14% were unfavourable” (6). In other words, despite the huge amount of money the dairy industry invests in research, there are many studies showing that milk has no benefit and that it has potentially negative effects.

In one study, a low intake of calcium (less than one glass of milk daily) was not associated with a significantly increased risk of any fracture, osteoporotic fracture or hip fracture and no significant relationship was observed by age for low milk intake and hip fracture risk (7). There was also no difference in risk of fracture or osteoporosis between men and women. In the Harvard Nurses’ Study of 77,761 mostly white women aged 34-59 who were followed over a 12-year period, those who drank little or no milk compared to the high milk drinkers (three glasses or more) had no reduction in risk of hip or arm fracture (8). The bottom line is that the studies do not support what we are constantly told by the dairy industry, media, governments and dieticians. So why do we keep getting told this message? If it was so clear cut to warrant a health message from the government you would expect all the research to support it. Not only is this not the case but there is also plenty of research to show the complete opposite.

It is simplistic to think that the calcium in our diet goes straight to our bones. The “calcium balance” is where the calcium intake from food is compared to the amount of calcium lost through excretion and unabsorbed mineral in sweat, faeces and urine. The remaining amount, whether positive or negative, is the calcium balance (9). If a person’s calcium balance is positive, there is an excess of calcium in the body, a proportion of which goes directly to increasing bone mineral density (10). If, however, a person’s balance is negative, more calcium is lost than is consumed, and therefore calcium from bone mineral must be reabsorbed into the bloodstream to provide the difference (10). This causes a lowering of bone mineral density and therefore is a factor in the onset of osteoporosis and fracture risk in later life 10. The amount of calcium that is absorbed and retained in the body from dairy products is about 30% of the total calcium consumed (9).

A number of factors help explain this discrepancy. First, calcium absorption is inversely related to the amount of calcium consumed in the diet, with low levels of calcium intake resulting in the most efficient absorption rates (11). This phenomenon may be partly responsible for the fact that many non-dairy-consuming societies around the world have few adverse health effects (such as osteoporosis and fracture) even with relatively low calcium intake (12).

Dairy products contain significant levels of protein, fat (in cheese, cream, butter and full cream products), sugar (in flavoured milks and yoghurts), sodium and phosphorous, all of which reduce the bioavailability of the calcium it contains. The presence of proteins has been demonstrated to have a negative influence on calcium absorption. Protein in milk causes an increase in urinary calcium excretion (13). Some dairy products, especially processed cheeses, clearly increase the urinary excretion of calcium as a result of their increased sodium, sulfur-containing amino acid, and phosphorus content (14). Interestingly, high-fat dairy products such as cheese, butter, chocolate and ice cream have also been found to be acid-forming foods (like protein and alcohol) (15,16), and so the question is raised: how effective are dairy products at ensuring bone health and are there other, more effectual dietary alternatives?

What is good for the bone

While protein has a negative effect on calcium availability, magnesium and potassium, which are found in high concentrations in plants we eat as food, have been recognized as having a largely positive influence (17). These minerals appear to decrease the rate of bone attrition and urinary excretion of calcium from the body when present in moderate quantities. Milk has a poor calcium-to-magnesium ratio and contains low concentrations of potassium, while plant sources have a much higher concentration. Potassium appears to buffer the effects of acidic foods by protecting against calcium loss from the renal acid load of protein (6).

Vitamin D, derived primarily from sunlight, certain oils (including cod liver oil) and fortified foods (including dairy products), is the major nutritional factor affecting calcium absorption (4). Scientific studies have repeatedly shown that inadequate vitamin D levels result in impaired calcium absorption in the body (4,9). The role of vitamin D in milk is also found to significantly lower the risk of fracture (5). Many people in Western populations are now recognised as being deficient in vitamin D (see my earlier article on the topic).

The adequacy of non-dairy centred diets to support bone health has been demonstrated by a recent study conducted in Spain among adolescent males. It reported that a Mediterranean-type intervention diet based on fresh fruits and vegetables, olive oil, fish and legumes provided the same amount of dietary calcium as the subject’s usual (baseline) diet, although the food sources of that calcium varied significantly. The intervention diet also resulted in a significant increase in calcium absorption and retention, while significantly reducing the amount of calcium excreted in urine. This may be partially attributed to the lowered potential renal acid load of the diet, particularly from a high intake of fruit and vegetables (19,20). Therefore, the study concludes, the adoption of a Mediterranean-style diet low in dairy can assist in maximising peak bone mass and preventing osteoporosis without milk or other dairy products (21).

Perhaps the most important part of the bone mass equation is a healthy mixture of minerals from unprocessed plant foods and physical activity, particularly weight-bearing exercises (22,6).
In response to learning these facts about milk, many people ask me, “But where can we get our calcium?” No other animal on the planet experiences bone problems at the rates humans do. Most other animals get calcium from their normal, often vegetarian diet. Our primate cousins, even those such as the gorilla which are much heavier and stronger than us, get all the calcium they need from unprocessed plant foods and cows get theirs from grass and have an excess of calcium.

So where should we be getting our calcium?

References

1. Maruyama et al. 2010
2. Papadimitropoulos et al. 2002
3. Babbar et al. 2006
4. Lanou et al. 2005
5. Feskanich et al. 2003
6. Weinsier and Krumdieck 2000
7. Kanis et al. 2005
8. Roba 2005
9. Allen 1982
10. Atkinson et al. 2008
11. Gallagher et al. 1979
12. Jackson et al. 2001
13. Beresteijn et al. 1990
14. Heaney et al. 1982
15. Alexy et al. 2008
16. Buclin et al. 2001
17. Tucker et al. 1999
18. Allen 1982
19. New 2003
20. Remer 2000
21. Seiquer et al. 2008
22. Black et al. 2002

Multiple Sclerosis (MS) a preventable disease

Just over a year ago a student of mine motivated me to look into multiple Sclerosis. Bruce put up a slide quoting the official authorities saying there was no link between MS and nutrition. He then presented a slide with more than 40 peer reviewed scientific papers on the link between MS and nutrition. Along with Bruce it continually confuses me as to why such supposed authorities continue to deny the existence of nutritional treatments and even worse the role of poor nutrition in the causes. Since inspiring me I have now seen dozens of people suffering from MS begin a new life through really simple changes in nutrition and one of the simplest changes follows on from one of my earlier articles on vitamin D. Many Australians just don’t get enough sun anymore. But more on that later. What is even more important is that this information can help prevent the development of MS in the beginning.

There is now overwhelming evidence of the risk of developing MS is linked to a number of environmental factors such as excessive dietary intake of saturated fats and deficiencies in polyunsaturated fatty acids, vitamin D and antioxidants (1,2). As a result of these findings good nutrition appears critical in limiting the development and ongoing effects of MS and enhance quality of life while limiting the risk of secondary conditions (3).

Over the past 200 years MS has significantly increased in incidence and prevalence. MS is a disease that effects an estimated 2.5 million people worldwide with over 18, 000 people in Australia with the disease, the incidence rate in Australia is increasing by 7% each year and financially costs approximately 2 billion dollars each year 4. It is twice as common in females (who have lower vitamin D than males) as in males and is the most frequent neurodegenerative disease in young adults 5,1. Geographically MS is common across northern Europe, Scandinavia and across the US and is much higher in incidence among whites then other racial groups (5).The disease is very rare in Japan, the Indian subcontinent and is unknown to black Africans however these groups are at significant risk to developing MS, when they go to other places to live, which supports the concept that an environmental factor is responsible for MS (5).

MS is a chronic, degenerative and autoimmune initiated inflammatory disease of the central nervous system, which may involve the brain, optic nerve or spinal cord and is characterized by demyelination (5,6). That is the myelin, that wraps around and insulates the nerve axons in the central nervous system, suffers self-destruction and degeneration (7). This means damaged myelin results in damaged nerve axons and causes the various disabilities of MS (7). It is worth noting here that myelin is around 80% lipids (fats) and cholesterol (which I have written on in past articles) makes up an indispensable component of myelin membranes (8). The inflammatory reactions are poorly controlled and result in substantial damage to the myelin (7). As a result of demyelination MS patients suffer functional impairments such as abnormal walking mechanics, poor balance, muscle weakness and fatigue which result in individuals reduced ability to perform activities of daily living (9).

The single most important factor linked to the development of MS is a reduced supply of vitamin D (7), which I have written on extensively in the past. Research has shown that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin is a natural immune system regulator with anti-inflammatory action (10). Vitamin D is received from two sources, diet and sunshine, however it is considered diet provides insignificant amounts and therefore sensible exposure to sunlight is considered the most effective source (11). Even Scandinavian diets (rich in oily fish) scarcely exceed a few hundred IU/d of vitamin D (12). Sunshine is therefore the principal natural source of vitamin D, providing approximately 90% of requirements. Sunbathing can provide 10,000–20,000 IU in 15–30 min, but this will only last a few weeks before it needs to be replenished (13,14). It is interesting to note that women generally have lower serum levels than men (15,16) and have significantly higher levels of MS.

There is a 41% decrease in MS risk for every 50 nanomoles per liter increase in vitamin D (1,25-hydroxyvitamin) in the blood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest (18). There is significant epidemiological data from Australia that shows a very strong correlation between vitamin D supply from ultraviolet (UV) radiation and MS prevalence (7). The correlation is indeed stronger than that of UV radiation exposure and melanoma development (7). Globally countries of high latitudes with insufficient UV radiation for most of the year report a higher incidence of MS 19,20. One case-control study has also shown that vitamin D status in individuals at the time of diagnosis of MS is significantly lower then healthy controls, indicating a further link (19).

It is theorized that vitamin D deficiencies may lead to an increase in T-helper cell autoimmune responses and therefore resulting in excessive damage to the myelin and MS symptoms (21).

Vitamin D supply through dietary intake also appears critical, as it has been reported that through vitamin D supplements there is an inverse relationship with MS (19). The role of vitamin D is supported by animal studies where mouse models have shown that vitamin D deficient mice succumb faster to MS but once administered with vitamin D the symptoms diminish (22).

The idea that an increase in saturated fats in modern diets may result in increased risks for MS (and diabetes type 2) has been known since the early 1950’s and reinforced on several occasions (23). Epidemiological studies in Norway have shown inland farming communities with high intake of animal products had higher MS incidence rates then coastal communities where consumption of fish is high while subsequent studies have also shown a negative correlation between MS and the consumption of fish, fruits and vegetables (23). Any wonder the rates of MS are increasing so fast in Australia knowing the poor diet most kids are having. It has been shown that MS sufferers have deficiencies in essential polyunsaturated fatty acids (PUFA), primarily the omega 3 fats which is demonstrated in that the lipid and fatty acid composition in plaque tissue from the MS brain is altered compared to the normal brain white matter (1).

It is believed that humans evolved on a diet with a ratio of omega-6 to omega-3 of approximately 1:1 where as in western diets the ratio is varied between 15:1 – 20:1 24. We just have too much vegetable oil (omega 6) in our diet. It is literally added liberally to all processed foods.

A large study conducted over a 35 year period showed MS patients on a diet with low saturated fat and supplementation with cod liver oil provided long term benefits on mortality, relapse severity and disability, particularly if initiated during the earliest stages of MS (25). The results of this have shown that MS patients can expect to survive and be ambulant and otherwise normal to an advanced age if following an extreme low fat diet and omega-3 supplementation (26). The rarity of MS in the Japanese, whose diet consist of low saturated fat and high omega-3 fatty acids is another indication of the role of omega 3 oils in MS (27). There is now significant evidence to show it is a contributing factor to the development of the disease in conjunction with other environmental factors (7).

The development of MS is also believed to be linked to oxidant stress in the body from a lack of antioxidants (28). Along with other possible environmental factors the actual role of oxidative stress in patients with MS is poorly understood (29). The brain and nervous system are particularly susceptible to oxidative damage due to the low content of antioxidants in this area of the body due to them having to be imported (30).

Studies have shown that oxidative stress causes an activation where the production of pro-inflammatory chemical messengers called cytokines occurs which then contributes to the process of demyelination (31). Having sufficient antioxidants therefore ensures neuroprotection through suppression of inflammation, this limits the effects of MS (29,31,32).

Oligodendrocytes, a particular type of brain cell, that produce the extensive myelin sheaths are known to be particularly vulnerable to oxidative stress, this helps explain the lack of remyelination during remission stages 1. Oxidation (free radicals) literally stops the repair work on any damage to the myelin sheath.

In helping to prevent and restrict the development of MS there are a number of recommendations that can be applied as determined through scientific studies:
• Regular moderate sun exposure (15-30 min/day)
• Decreased intake of saturated fat and omega-6 PUFA accompanied with an increased consumption of omega-3 PUFA through consumption of fish and supplementation
• Daily supplement of vitamin D to ensure circulating level of vitamin D remains between 100 – 150 nanomoles per liter
• Consume at least 5-7 serves of antioxidant rich fruits and vegetables each day and supplement.

Acknowledgements. Bruce Greatwitch

References:
1. Meeteren et. al. 2005
2. Liuzzi et. al. 2007
3. Timmerman, Stuifbergin 1999
4. MS research Australia 2008
5. Undurti 2003
6. Kanwar, 2005
7. Embry 2004
8. Saher et al 2005
9. White et. al. 2004
10. Van Amerongen 2004
11. Cantorna, Mahon 2004
12. Mark and Carson, 2006
13. Hollis, 2005
14. Vieth, 2007
15. Yetley, 2008
16. Zadshir et al 2005
17. Anonymous 2007
18. VanAmerongen et. al. 2004
19. Barnes et. al. 2007
20. Kampman et. al. 2007
21. Toohey 2004
22. Mandavilli 2007
23. Nordvik et. al. 2000
24. Simopoulos 2002
25. Swank cited in Weinstock-Guttman et. al. 2005
26. Swank, Goodwin 2003
27. Undurti 2003
28. Lutskii, Esaulenko 2007
29. Koch et. al. 2006
30. Syburra, Passi, 1999
31. Gonsette 2008
32. Gilgun-Sherki et. al. 2004

Non-ionising Electromagnetic Radiation

There is so much confusion nowadays about the pros and cons of radiation I thought it best to try and clarify it as best I could. People are exposed to non-ionising radiation through natural sources such as the sun as well as human-generated sources: computers, microwaves ovens, mobile phones, radar systems and power lines. From the sun, UV radiation is a major concern related to sunburn, skin damage and skin cancer. Too much sun can have a negative effect on one’s immune system. On the other hand, without enough exposure to the sun, the body does not produce vitamin D. But more on that at a later date.

Microwave radiation or Microwaves are extremely high frequency radio waves on the electromagnetic radiation spectrum. While some microwaves and radiofrequency radiation occur naturally—the sun, the earth and the ionosphere create natural sources of low-level RF and MW radiation fields—the incidence of non-naturally occurring radiation has increased dramatically with the advance of technology. Microwaves can be used to carry satellite signals for communication in televisions, AM and FM radio, computers, global positioning systems and mobile phones. Microwaves can also be used to generate heat through the extremely rapid reversal in the polarity of electrons affected by magnetic and electric fields via a tube called a magnetron—this occurs in almost every kitchen and restaurant throughout the industrialised world, with the ubiquitous microwave oven.

Microwaves and radiofrequencies represent one of the most common and fastest growing environmental influences about which anxiety and speculation are spreading. Yet very little is known about the results of exposure to microwaves; even less is known about the relative dangers of different sources of microwaves. We do, however, know that microwaves can be reflected, transmitted or absorbed by matter in their path. Absorption occurs in matter that contains moisture, including human beings.

Living organisms absorb microwaves and radiofrequency energy at the molecular, cellular, tissue and whole-body levels. Heating of internal organs is a consequence of the absorption of energy. The energy is absorbed by water within the tissue; therefore, tissues with high water density and low blood density—such as the eyes and testes—are particularly vulnerable.

Scientists have known for a long time about the capacity of RF radiation to cause this type of heating and have discovered that prolonged exposure to RF radiation can lead to health problems such as fatigue, reduced mental concentration and, in the case of very high levels, cataracts. These effects are similar to subjecting a person to an extremely warm environment. Other possible thermal effects include foetal abnormalities, decreased thyroid function, cardiovascular mortality, impaired ability to perform complex tasks and the suppression of behavioural responses, gonadal function and natural killer cell activity. Studies have shown that environmental levels of microwaves and radiofrequency energy routinely encountered by the general public are far below levels necessary to produce significant heating and increased body temperature. However, there is concern for whole body heating amongst the elderly and those on specific medications that affect thermoregulatory function. Also of concern are people with cardiac and circulatory problems, those with implanted medical electronic devices (e.g., heart pacemakers), fever sufferers, infants and pregnant women.

The majority of studies in this area are concerned with cataracts, arguably the major hazard associated with microwave radiation. A cataract is a clouding of the lens within the eye. Authorities concerned with producing safety standards agree that little is known with any real certainty about the effects of microwave radiation beyond its thermal effects. However, microwave studies contain too many shortcomings to rule out the possibility that microwaves cause adverse health effects.

The recognition of non-thermal effects has been highly controversial, due to conflicting and inconclusive studies. Studies are complex, investigating possible effects of microwave radiation—from cancer to effects on the operation of all systems and parts of the human body. Cancer studies have examined cancers of the breasts, lungs, testicles and brain, as well as ocular melanoma and leukaemia. Other studies have included assessments of the relationships between radiation and cardiovascular disease, birth defects and hormone secretion rates. Research has also shown the effect of microwaves on reducing a cell’s ability to perform apoptosis, that is when the cell terminates its own life as a part of the life cycle of the cell, increasing the risk of spontaneous mutations, including cancer.

An example of the controversy surrounding microwaves occurred with a 1990 leaked draft EPA report in the USA, recommending that radiofrequency microwave radiation be considered a “possible human carcinogen.” The White House moved quickly to suppress the draft and commissioned another report, which stated that there was no EMF cancer risk. Unfortunately, politics has its influence in too many places it should not.

Multiple Sclerosis (MS) a preventable disease

Just over a year ago a student of mine motivated me to look into multiple Sclerosis. Bruce put up a slide quoting the official authorities saying there was no link between MS and nutrition. He then presented a slide with more than 40 peer reviewed scientific papers on the link between MS and nutrition. Along with Bruce it continually confuses me as to why such supposed authorities continue to deny the existence of nutritional treatments and even worse the role of poor nutrition in the causes. Since inspiring me I have now seen dozens of people suffering from MS begin a new life through really simple changes in nutrition and one of the simplest changes follows on from one of my earlier articles on vitamin D. Many Australians just don’t get enough sun anymore. But more on that later. What is even more important is that this information can help prevent the development of MS in the beginning.

There is now overwhelming evidence of the risk of developing MS is linked to a number of environmental factors such as excessive dietary intake of saturated fats and deficiencies in polyunsaturated fatty acids, vitamin D and antioxidants 1,2. As a result of these findings good nutrition appears critical in limiting the development and ongoing effects of MS and enhance quality of life while limiting the risk of secondary conditions 3.

Over the past 200 years MS has significantly increased in incidence and prevalence. MS is a disease that effects an estimated 2.5 million people worldwide with over 18, 000 people in Australia with the disease, the incidence rate in Australia is increasing by 7% each year and financially costs approximately 2 billion dollars each year 4. It is twice as common in females (who have lower vitamin D than males) as in males and is the most frequent neurodegenerative disease in young adults 5,1. Geographically MS is common across northern Europe, Scandinavia and across the US and is much higher in incidence among whites then other racial groups 5.The disease is very rare in Japan, the Indian subcontinent and is unknown to black Africans however these groups are at significant risk to developing MS, when they go to other places to live, which supports the concept that an environmental factor is responsible for MS 5.

MS is a chronic, degenerative and autoimmune initiated inflammatory disease of the central nervous system, which may involve the brain, optic nerve or spinal cord and is characterized by demyelination 5,6. That is the myelin, that wraps around and insulates the nerve axons in the central nervous system, suffers self-destruction and degeneration 7. This means damaged myelin results in damaged nerve axons and causes the various disabilities of MS7. It is worth noting here that myelin is around 80% lipids (fats) and cholesterol (which I have written on in past articles) makes up an indispensable component of myelin membranes 8. The inflammatory reactions are poorly controlled and result in substantial damage to the myelin 7. As a result of demyelination MS patients suffer functional impairments such as abnormal walking mechanics, poor balance, muscle weakness and fatigue which result in individuals reduced ability to perform activities of daily living 9.

The single most important factor linked to the development of MS is a reduced supply of vitamin D 7, which I have written on extensively in the past. Research has shown that the active hormonal form of vitamin D, 1,25-dihydroxyvitamin is a natural immune system regulator with anti-inflammatory action 10. Vitamin D is received from two sources, diet and sunshine, however it is considered diet provides insignificant amounts and therefore sensible exposure to sunlight is considered the most effective source 11. Even Scandinavian diets (rich in oily fish) scarcely exceed a few hundred IU/d of vitamin D 12. Sunshine is therefore the principal natural source of vitamin D, providing approximately 90% of requirements. Sunbathing can provide 10,000–20,000 IU in 15–30 min, but this will only last a few weeks before it needs to be replenished 13,14. It is interesting to note that women generally have lower serum levels than men 15,16 and have significantly higher levels of MS.

There is a 41% decrease in MS risk for every 50 nanomoles per liter increase in vitamin D (1,25-hydroxyvitamin) in the blood. The prevalence of MS is highest where environmental supplies of vitamin D are lowest 18. There is significant epidemiological data from Australia that shows a very strong correlation between vitamin D supply from ultraviolet (UV) radiation and MS prevalence 7. The correlation is indeed stronger than that of UV radiation exposure and melanoma development 7. Globally countries of high latitudes with insufficient UV radiation for most of the year report a higher incidence of MS 19,20. One case-control study has also shown that vitamin D status in individuals at the time of diagnosis of MS is significantly lower then healthy controls, indicating a further link 19.

It is theorized that vitamin D deficiencies may lead to an increase in T-helper cell autoimmune responses and therefore resulting in excessive damage to the myelin and MS symptoms 21.

Vitamin D supply through dietary intake also appears critical, as it has been reported that through vitamin D supplements there is an inverse relationship with MS 19. The role of vitamin D is supported by animal studies where mouse models have shown that vitamin D deficient mice succumb faster to MS but once administered with vitamin D the symptoms diminish 22.

The idea that an increase in saturated fats in modern diets may result in increased risks for MS (and diabetes type 2) has been known since the early 1950’s and reinforced on several occasions 23. Epidemiological studies in Norway have shown inland farming communities with high intake of animal products had higher MS incidence rates then coastal communities where consumption of fish is high while subsequent studies have also shown a negative correlation between MS and the consumption of fish, fruits and vegetables 23. Any wonder the rates of MS are increasing so fast in Australia knowing the poor diet most kids are having. It has been shown that MS sufferers have deficiencies in essential polyunsaturated fatty acids (PUFA), primarily the omega 3 fats which is demonstrated in that the lipid and fatty acid composition in plaque tissue from the MS brain is altered compared to the normal brain white matter 1.

It is believed that humans evolved on a diet with a ratio of omega-6 to omega-3 of approximately 1:1 where as in western diets the ratio is varied between 15:1 – 20:1 24. We just have too much vegetable oil (omega 6) in our diet. It is literally added liberally to all processed foods.

A large study conducted over a 35 year period showed MS patients on a diet with low saturated fat and supplementation with cod liver oil provided long term benefits on mortality, relapse severity and disability, particularly if initiated during the earliest stages of MS 25. The results of this have shown that MS patients can expect to survive and be ambulant and otherwise normal to an advanced age if following an extreme low fat diet and omega-3 supplementation 26. The rarity of MS in the Japanese, whose diet consist of low saturated fat and high omega-3 fatty acids is another indication of the role of omega 3 oils in MS 27. There is now significant evidence to show it is a contributing factor to the development of the disease in conjunction with other environmental factors 7.

The development of MS is also believed to be linked to oxidant stress in the body from a lack of antioxidants 28. Along with other possible environmental factors the actual role of oxidative stress in patients with MS is poorly understood 29. The brain and nervous system are particularly susceptible to oxidative damage due to the low content of antioxidants in this area of the body due to them having to be imported 30.

Studies have shown that oxidative stress causes an activation where the production of pro-inflammatory chemical messengers called cytokines occurs which then contributes to the process of demyelination 31. Having sufficient antioxidants therefore ensures neuroprotection through suppression of inflammation, this limits the effects of MS 29,31,32.

Oligodendrocytes, a particular type of brain cell, that produce the extensive myelin sheaths are known to be particularly vulnerable to oxidative stress, this helps explain the lack of remyelination during remission stages 1. Oxidation (free radicals) literally stops the repair work on any damage to the myelin sheath.

In helping to prevent and restrict the development of MS there are a number of recommendations that can be applied as determined through scientific studies:
• Regular moderate sun exposure (15-30 min/day)
• Decreased intake of saturated fat and omega-6 PUFA accompanied with an increased consumption of omega-3 PUFA through consumption of fish and supplementation
• Daily supplement of vitamin D to ensure circulating level of vitamin D remains between 100 – 150 nanomoles per liter
• Consume at least 5-7 serves of antioxidant rich fruits and vegetables each day and supplement.

Acknowledgements. Bruce Greatwitch

References:
1. Meeteren et. al. 2005
2. Liuzzi et. al. 2007
3. Timmerman, Stuifbergin 1999
4. MS research Australia 2008
5. Undurti 2003
6. Kanwar, 2005
7. Embry 2004
8. Saher et al 2005
9. White et. al. 2004
10. Van Amerongen 2004
11. Cantorna, Mahon 2004
12. Mark and Carson, 2006
13. Hollis, 2005
14. Vieth, 2007
15. Yetley, 2008
16. Zadshir et al 2005
17. Anonymous 2007
18. VanAmerongen et. al. 2004
19. Barnes et. al. 2007
20. Kampman et. al. 2007
21. Toohey 2004
22. Mandavilli 2007
23. Nordvik et. al. 2000
24. Simopoulos 2002
25. Swank cited in Weinstock-Guttman et. al. 2005
26. Swank, Goodwin 2003
27. Undurti 2003
28. Lutskii, Esaulenko 2007
29. Koch et. al. 2006
30. Syburra, Passi, 1999
31. Gonsette 2008
32. Gilgun-Sherki et. al. 2004

VItamins D and Sunscreen Study

Dr Dingle recently took part in a few radio interviews that discussed the complications of sunscreen and vitamin D. Given the increase in interest on this topic I have place a link on the Dr Dingle web page to give everyone free access to the articles.

Enjoy

Dr Dingle Free Information Sheets

Cholesterol is good for you

Not only is cholesterol not the enemy, but also it is essential to good health and wellbeing. Every cell in the body needs cholesterol in its membrane, where cholesterol plays a critical role in cell communication. Without cholesterol, cell membranes are incomplete and, as a result, their functional role deteriorates. Cholesterol is also used in the mitochondria of the cell and plays a vital role in cell energy production—not to mention its essential role in the brain structure and function. Cholesterol is the starting material of many essential chemicals including vitamin D, steroid hormones and the bile acids necessary for digestion.

For major drug companies, convincing the public that lower cholesterol levels equal good health is a marketing scheme. The goal of these companies is not your good health; it’s their profits. This “marketing messaging” has gone too far, especially considering that recent studies show that cholesterol may have protective properties against cancer.

Cholesterol is the most abundant organic molecule in the brain which contains almost a quarter of the unesterified cholesterol present in the entire body. In 2001, in groundbreaking research and with media fanfare, cholesterol was identified as the synaptogenic factor that is responsible for the development of synapses, the connections in the brain. The glial cells of the central nervous system that perform the housekeeping functions in the brain produce their own cholesterol for the specific purpose of providing nerve cells with the vital component required for synapse function. Cholesterol is also required for the function of serotonin receptors in the brain. Serotonin is the chemical in our brain that makes us feel happy. Low cholesterol level has been associated with mortality due to suicides and accidental deaths.

A thirty-year study published in 1987 provides evidence that elevated cholesterol in people over the age of 50 does not increase the risk of heart attack. Cholesterol levels of people free of coronary heart disease (CHD) and cancer were measured; the study found that there was no increase in death rate in those with high cholesterol. Research on the effects of cholesterol levels and age shows that high cholesterol levels in people over the age of 75 are protective, not harmful. A separate study published in the European Heart Journal (1997) found that the risk of cardiac death was the same in groups of people with low or normal cholesterol levels as those with high cholesterol.

Maybe we need to rethink the billions of dollars we spend each year on drugs that lower cholesterol and spend the money on the real risk factors associated with cardiovascular disease: our lifestyles and choices, including nutritional and environmental factors that increase inflammation.

Stay tuned because there is more to come over the next weeks.