If the economy isn't grim enough for you, just check out the February issue of the Journal of HortScience, which contains a report on the sorry state of American fruits and veggies. Apparently produce in the U.S. not only tastes worse than it did in your grandparents' days, it also contains fewer nutrients — at least according to Donald R. Davis, a former research associate with the Biochemical Institute at the University of Texas, Austin. Davis claims the average vegetable found in today's supermarket is anywhere from 5% to 40% lower in minerals (including magnesium, iron, calcium and zinc) than those harvested just 50 years ago.
Highlight Reel:
1. On the Difficulty of Comparing "Then" and "Now:" Davis is quick to note that historical data can sometimes be misleading, if not altogether inaccurate. Take early measurements of iron in foods: because scientists failed to sufficiently remove clinging soil, iron levels appeared unusually high in certain vegetables like spinach, (which gave rise to the myth that it contained exorbitant amounts of the mineral — a myth further propagated by the popular cartoon character, Popeye). Then again, good historical data provides the only real-world evidence of changes in foods over time, and such data does exist — one farm in Hertfordshire, England, for example, has archived its wheat samples since 1843.
2. On the So-Called "Dilution Effect:" Today's vegetables might be larger, but if you think that means they contain more nutrients, you'd be wrong. Davis writes that jumbo-sized produce contains more "dry matter" than anything else, which dilutes mineral concentrations. In other words, when it comes to growing food, less is more. Scientific papers have cited one of the first reports of this effect, a 1981 study by W.M. Jarrell and R.B. Beverly in Advances in Agronomy, more than 180 times since its publication, "suggesting that the effect is widely regarded as common knowledge." (See pictures of fruit.)
Less studied, though, is the "genetic dillution effect," in which selective breeding to increase crop yield has led to declines in protein, amino acids, and as many as six minerals in one study of commercial broccoli grown in 1996 and '97 in South Carolina. Because nearly 90% of dry matter is carbohydrates, "when breeders select for high yield, they are, in effect, selecting mostly for high carbohydrate with no assurance that dozens of other nutrients and thousands of phytochemicals will all increase in proportion to yield."
2. On the "Industrialization" of Agriculture: Thanks to the growing rise of chemical fertilizers and pesticides, modern crops are being harvested faster than ever before. But quick and early harvests mean the produce has less time to absorb nutrients either from synthesis or the soil, and minerals like potassium (the "K" in N-P-K fertilizers) often interfere with a plant's ability to take up nutrients. Monoculture farming practices — another hallmark of the Big Ag industry — have also led to soil-mineral depletion, which, in turn, affects the nutrient content of crops.
The Lowdown:
If you're still not buying the whole "organic-is-better" argument, this study might convince you otherwise. As Davis points out, more than three billion people around the world suffer from malnourishment and yet, ironically, efforts to increase food production have actually produced food that is less nourishing. Fruits seem to be less affected by genetic and environmental dilution, but one can't help but wonder how nutritionally bankrupt veggies can be avoided. Supplementing them is problematic, too: don't look to vitamin pills, as recent research indicates that those aren't very helpful either.
25 February 2009
Vitamin Deficiency Underlies Tooth Decay
Malnutrition Causes Much More than Dental Disease
(OMNS, February 19, 2009) Cavities and gum diseases are not often regarded as serious diseases, yet they are epidemic throughout our society, from the youngest of children to the oldest of senior citizens. Research more than suggests that the same good nutrition that prevents cavities and gum diseases may also prevent other illnesses.
Dental caries and gum pathology are frequently associated with serious chronic health problems. Multiple independent studies published after 1990 document this. Cavities are associated with poor mental health [1-4]. Elderly individuals with dementia or Alzheimer's disease had an average of 7.8 teeth with fillings vs. an average of only 2.7 fillings for elderly individuals without dementia [1]. It is likely that the toxic heavy metal mercury, which makes up half of every amalgam filling, is a contributing factor.
A recent authoritative review showed a clear association between cavities and heart diseases [5]. More importantly, this same study showed that people with poor oral health, on average, lead shorter lives. The association between cavities and diabetes is also a subject of active, ongoing research [6-8]. Connections between heart disease, diabetes, and dental decay have been suspected for decades. Many of the scientists who called attention to this have proposed that diets high in sugar and refined carbohydrates were the common cause of these diseases [9-15].
Dental diseases, mental diseases, heart disease, infectious respiratory diseases, and heart disease are all at least partially caused by common failures in metabolism. Such failures are inevitable when there is a deficiency of essential nutrients, particularly vitamins D, C, and niacin.
There is especially strong evidence for a relationship between vitamin D deficiency and cavities. Dozens of studies were conducted in the 1930's and 1940's [16-27]. More than 90% of the studies concluded that supplementing children with vitamin D prevents cavities. Particularly impressive was a study published in 1941 demonstrated the preventative affect of "massive" doses of vitamin D [28]. And yet no subsequent studies in the scientific literature suggested a need to follow up and repeat this work.
Vitamin D deficiency is linked to respiratory infections, cancer, heart disease, diabetes and other ailments [29]. The evidence for vitamin C was reviewed by Linus Pauling [15], and the evidence for niacin was reviewed by Abram Hoffer [30].
Obtaining vitamins in sufficient doses to help prevent dental disease is safe and easily accomplished. Between 5,000 and 15,000 IU of vitamin D may be obtained from modest exposure to sunshine in the middle of the day. Recommending that people regularly use the capacity of their skin to make vitamin D is common sense. Certainly 1,000 to 2,000 IU per day of vitamin D in supplemental form is safe. 2,000 milligrams per day of vitamin C, and hundreds of milligrams per day of niacin, help prevent tooth and mouth troubles. Sick individuals, and those who are prone to cavities, will typically benefit by starting with higher doses of vitamin D, vitamin C, and niacin under the supervision of an orthomolecular physician.
We believe that individuals taking these nutrients, along with good dental care, will have dramatically fewer cavities and gum operations than individuals just getting good dental care. This idea is easily tested, and the time has come to do so.
References:
[1] B Ellefsen; P Holm-Pedersen; D E Morse; M. Schroll; B. Andersen; G. Waldemar. Caries Prevalence in Older Persons with and without Dementia. Journal of the American Geriatrics Society, Volume 56, Number 1, January 2008, 59-67(9).
[2] J M Chalmers, K D Carter, A J Spencer. Caries incidence and increments in community-living older adults with and without dementia. Australian Research Center for Population Oral Health, Dental School, The University of Adelaide, Adelaide 5005, Australia. Gerodontology Volume 19 Issue 2, 80 - 94.
[3] Friedlander, A.H.; Mahler, M.E. Major depressive disorder psychopathology, medical management and dental implications. Graduate Medical Education, Veterans Affairs Greater Los Angeles Healthcare System (14), Los Angeles, CA, USA. Journal of the American Dental Association (2001), 132(5), 629-638.
[4] Stewart, R.; et. al. Oral Health and Cognitive Function in the Third National Health and Nutrition Examination Survey (NHANES III), Psychosomatic Medicine 70:936-941 (2008).
[5] Meurman, J.H.; Sanz, M.;Janket, S. Oral infection and vascular disease. Institute of Dentistry, University of Helsinki, Finland. Vascular Disease Prevention (2007), 4(4), 260-267.
[6] Touger-Decker R, Sirois D A, Vernillo A T. Diabetes mellitus: Nutrition and oral health relationships. Department of Primary Care, School of Health-Related Professions, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA. Editor(s): Touger-Decker, Riva. Nutrition and Oral Medicine (2005), 185-204.
[7] Diaz-Romero, R.; Casanova-Roman, R.; Beltran-Zuniga, M; Belmont-Padilla, J.; Mendez, J.; Avila-Rosas, H.. Oral Infections and Glycemic Control in Pregnant Type 2 Diabetics. Instituto Nacional de Perinatologia, Mexico City, Mex. Archives of Medical Research (2005), 36(1), 42-48.
[8] Twetman, S.; Johansson, I.; Birkhed, D.; Nederfors, T. Caries incidence in young type 1 diabetes mellitus patients in relation to metabolic control and caries-associated risk factors. Caries Research (2002), 36(1), 31-35.
[9] Bommer, S. Diseases of civilization and nutrition. Ernaehrungsforschung (1963), 7 598-612.
[10] Miler-Sosnkowska, M. Role of dietary carbohydrates in relation to their metabolism. Inst. Zywienia Czlowieka, Akad. Roln., Warsaw, Pol. Postepy Higieny i Medycyny Doswiadczalnej (1975), 29(4), 537-55.
[11] Cremer, H.D.; Eyer, H. Carbohydrates. Inst. Ernaehrungswiss. I, Univ. Giessen, Giessen, Fed. Rep. Ger. Ernaehrungs-Umschau (1975), 22(10), 291-3.
[12] Newberne, P.M.. Nutrition: summary of evidence. Sweeteners: Issues, uncertainties. Acad. Forum, 4th (1975), 76-85, 252-3.
[13] Heraud, G. Sucrose and nutritional pathology. Sucrerie Francaise (1979), 120(24), 21-6.
[14] Nuttall, F.Q.; Gannon, M.C.. Sucrose and disease. Diabetes Care (1981), 4(2), 305-10.
[15] Pauling, L. "How to Live Longer and Feel Better." W.H. Freeman and Company, 1986. Revised 2006, Oregon State University Press. http://oregonstate.edu/dept/press/g-h/LiveLonger.html
[16] Tisdall, F.F. The effect of nutrition on the primary teeth. Child Development (1937) 8(1), 102-4.
[17] McBeath, E.C. Nutrition and diet in relation to preventive dentistry. NY J. Dentistry (1938) 8; 17-21.
[17] McBeath, E.C.; Zucker, T.F. Role of vitamin D in the control of dental caries in children. Journal of Nutrition (1938) 15; 547-64.
[19] East, B. R. Nutrition and dental caries. American Journal of Public Health 1938. 28; 72-6.
[20] Mellanby, M. The role of nutrition as a factor in resistance to dental caries. British Dental Journal (1937), 62; 241-52.
[21] His Majesty's Stationery Office, London. The influence of diet on caries in children's teeth. Report of the Committee for the Investigation of Dental Disease (1936).
[22] McBeath, F.C. Vitamin D studies, 1933-1934. American Journal of Public Health (1934), 24 1028-30.
[23] Anderson, P. G.; Williams, C. H. M.; Halderson, H.; Summerfeldt, C.; Agnew, R. Influence of vitamin D in the prevention of dental caries. Journal of the American Dental Association (1934) 21; 1349-66.
[24] Day, C. D.; Sedwick, H. J. Fat-soluble vitamins and dental caries in children. Journal of Nutrition (1934) 8; 309-28.
[25] Agnew, M. C.; Agnew, R. G.; Tisdall, F. F. The production and prevention of dental caries. Journal of the American Dental Association, JADA (1933) 20; 193-212.
[26] Bennett, N. G.; et al. The influence of diet on caries in children's teeth. Special Report Series - Medical Research Council, UK (1931) No. 159, 19.
[27] Mellanby, M.; Pattison, C. L. The influence of a cereal-free diet rich in vitamin D and calcium on dental caries in children. British Medical Journal (1932) I 507-10.
[28] Brodsky, R. H.; Schick, B.; Vollmer, H.. Prevention of dental caries by massive doses of vitamin D. American Journal of Diseases of Children (1941) 62; 1183-7.
[29] http://www.vitamindcouncil.org/
[30] Hoffer A, Saul AW. Orthomolecular Medicine for Everyone. Laguna Beach, California, Basic Health Pub, 2008. http://www.doctoryourself.com/orthomolecular.html
(OMNS, February 19, 2009) Cavities and gum diseases are not often regarded as serious diseases, yet they are epidemic throughout our society, from the youngest of children to the oldest of senior citizens. Research more than suggests that the same good nutrition that prevents cavities and gum diseases may also prevent other illnesses.
Dental caries and gum pathology are frequently associated with serious chronic health problems. Multiple independent studies published after 1990 document this. Cavities are associated with poor mental health [1-4]. Elderly individuals with dementia or Alzheimer's disease had an average of 7.8 teeth with fillings vs. an average of only 2.7 fillings for elderly individuals without dementia [1]. It is likely that the toxic heavy metal mercury, which makes up half of every amalgam filling, is a contributing factor.
A recent authoritative review showed a clear association between cavities and heart diseases [5]. More importantly, this same study showed that people with poor oral health, on average, lead shorter lives. The association between cavities and diabetes is also a subject of active, ongoing research [6-8]. Connections between heart disease, diabetes, and dental decay have been suspected for decades. Many of the scientists who called attention to this have proposed that diets high in sugar and refined carbohydrates were the common cause of these diseases [9-15].
Dental diseases, mental diseases, heart disease, infectious respiratory diseases, and heart disease are all at least partially caused by common failures in metabolism. Such failures are inevitable when there is a deficiency of essential nutrients, particularly vitamins D, C, and niacin.
There is especially strong evidence for a relationship between vitamin D deficiency and cavities. Dozens of studies were conducted in the 1930's and 1940's [16-27]. More than 90% of the studies concluded that supplementing children with vitamin D prevents cavities. Particularly impressive was a study published in 1941 demonstrated the preventative affect of "massive" doses of vitamin D [28]. And yet no subsequent studies in the scientific literature suggested a need to follow up and repeat this work.
Vitamin D deficiency is linked to respiratory infections, cancer, heart disease, diabetes and other ailments [29]. The evidence for vitamin C was reviewed by Linus Pauling [15], and the evidence for niacin was reviewed by Abram Hoffer [30].
Obtaining vitamins in sufficient doses to help prevent dental disease is safe and easily accomplished. Between 5,000 and 15,000 IU of vitamin D may be obtained from modest exposure to sunshine in the middle of the day. Recommending that people regularly use the capacity of their skin to make vitamin D is common sense. Certainly 1,000 to 2,000 IU per day of vitamin D in supplemental form is safe. 2,000 milligrams per day of vitamin C, and hundreds of milligrams per day of niacin, help prevent tooth and mouth troubles. Sick individuals, and those who are prone to cavities, will typically benefit by starting with higher doses of vitamin D, vitamin C, and niacin under the supervision of an orthomolecular physician.
We believe that individuals taking these nutrients, along with good dental care, will have dramatically fewer cavities and gum operations than individuals just getting good dental care. This idea is easily tested, and the time has come to do so.
References:
[1] B Ellefsen; P Holm-Pedersen; D E Morse; M. Schroll; B. Andersen; G. Waldemar. Caries Prevalence in Older Persons with and without Dementia. Journal of the American Geriatrics Society, Volume 56, Number 1, January 2008, 59-67(9).
[2] J M Chalmers, K D Carter, A J Spencer. Caries incidence and increments in community-living older adults with and without dementia. Australian Research Center for Population Oral Health, Dental School, The University of Adelaide, Adelaide 5005, Australia. Gerodontology Volume 19 Issue 2, 80 - 94.
[3] Friedlander, A.H.; Mahler, M.E. Major depressive disorder psychopathology, medical management and dental implications. Graduate Medical Education, Veterans Affairs Greater Los Angeles Healthcare System (14), Los Angeles, CA, USA. Journal of the American Dental Association (2001), 132(5), 629-638.
[4] Stewart, R.; et. al. Oral Health and Cognitive Function in the Third National Health and Nutrition Examination Survey (NHANES III), Psychosomatic Medicine 70:936-941 (2008).
[5] Meurman, J.H.; Sanz, M.;Janket, S. Oral infection and vascular disease. Institute of Dentistry, University of Helsinki, Finland. Vascular Disease Prevention (2007), 4(4), 260-267.
[6] Touger-Decker R, Sirois D A, Vernillo A T. Diabetes mellitus: Nutrition and oral health relationships. Department of Primary Care, School of Health-Related Professions, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA. Editor(s): Touger-Decker, Riva. Nutrition and Oral Medicine (2005), 185-204.
[7] Diaz-Romero, R.; Casanova-Roman, R.; Beltran-Zuniga, M; Belmont-Padilla, J.; Mendez, J.; Avila-Rosas, H.. Oral Infections and Glycemic Control in Pregnant Type 2 Diabetics. Instituto Nacional de Perinatologia, Mexico City, Mex. Archives of Medical Research (2005), 36(1), 42-48.
[8] Twetman, S.; Johansson, I.; Birkhed, D.; Nederfors, T. Caries incidence in young type 1 diabetes mellitus patients in relation to metabolic control and caries-associated risk factors. Caries Research (2002), 36(1), 31-35.
[9] Bommer, S. Diseases of civilization and nutrition. Ernaehrungsforschung (1963), 7 598-612.
[10] Miler-Sosnkowska, M. Role of dietary carbohydrates in relation to their metabolism. Inst. Zywienia Czlowieka, Akad. Roln., Warsaw, Pol. Postepy Higieny i Medycyny Doswiadczalnej (1975), 29(4), 537-55.
[11] Cremer, H.D.; Eyer, H. Carbohydrates. Inst. Ernaehrungswiss. I, Univ. Giessen, Giessen, Fed. Rep. Ger. Ernaehrungs-Umschau (1975), 22(10), 291-3.
[12] Newberne, P.M.. Nutrition: summary of evidence. Sweeteners: Issues, uncertainties. Acad. Forum, 4th (1975), 76-85, 252-3.
[13] Heraud, G. Sucrose and nutritional pathology. Sucrerie Francaise (1979), 120(24), 21-6.
[14] Nuttall, F.Q.; Gannon, M.C.. Sucrose and disease. Diabetes Care (1981), 4(2), 305-10.
[15] Pauling, L. "How to Live Longer and Feel Better." W.H. Freeman and Company, 1986. Revised 2006, Oregon State University Press. http://oregonstate.edu/dept/press/g-h/LiveLonger.html
[16] Tisdall, F.F. The effect of nutrition on the primary teeth. Child Development (1937) 8(1), 102-4.
[17] McBeath, E.C. Nutrition and diet in relation to preventive dentistry. NY J. Dentistry (1938) 8; 17-21.
[17] McBeath, E.C.; Zucker, T.F. Role of vitamin D in the control of dental caries in children. Journal of Nutrition (1938) 15; 547-64.
[19] East, B. R. Nutrition and dental caries. American Journal of Public Health 1938. 28; 72-6.
[20] Mellanby, M. The role of nutrition as a factor in resistance to dental caries. British Dental Journal (1937), 62; 241-52.
[21] His Majesty's Stationery Office, London. The influence of diet on caries in children's teeth. Report of the Committee for the Investigation of Dental Disease (1936).
[22] McBeath, F.C. Vitamin D studies, 1933-1934. American Journal of Public Health (1934), 24 1028-30.
[23] Anderson, P. G.; Williams, C. H. M.; Halderson, H.; Summerfeldt, C.; Agnew, R. Influence of vitamin D in the prevention of dental caries. Journal of the American Dental Association (1934) 21; 1349-66.
[24] Day, C. D.; Sedwick, H. J. Fat-soluble vitamins and dental caries in children. Journal of Nutrition (1934) 8; 309-28.
[25] Agnew, M. C.; Agnew, R. G.; Tisdall, F. F. The production and prevention of dental caries. Journal of the American Dental Association, JADA (1933) 20; 193-212.
[26] Bennett, N. G.; et al. The influence of diet on caries in children's teeth. Special Report Series - Medical Research Council, UK (1931) No. 159, 19.
[27] Mellanby, M.; Pattison, C. L. The influence of a cereal-free diet rich in vitamin D and calcium on dental caries in children. British Medical Journal (1932) I 507-10.
[28] Brodsky, R. H.; Schick, B.; Vollmer, H.. Prevention of dental caries by massive doses of vitamin D. American Journal of Diseases of Children (1941) 62; 1183-7.
[29] http://www.vitamindcouncil.org/
[30] Hoffer A, Saul AW. Orthomolecular Medicine for Everyone. Laguna Beach, California, Basic Health Pub, 2008. http://www.doctoryourself.com/orthomolecular.html
$8 Million Award in First Solo Tobacco Trial
FORT LAUDERDALE, Fla. (AP) — A jury ordered Philip Morris to pay $8 million in damages to the widow of a smoker who died of lung cancer in a case that could set a standard for roughly 8,000 similar lawsuits in Florida.
The six jurors deliberated over two days before returning the award for Elaine Hess, 63, whose husband, Stuart Hess, died in 1997 at age 55 after decades as a chain smoker.
The award amounts to $3 million in compensatory damages and $5 million in punitive damages against Philip Morris USA, based in Richmond, Va., and a unit of the Altria Group.
“It wasn’t about the money from the beginning,” Mrs. Hess said after the verdict. “It was about doing the right thing. I just really hope this can help all the thousands of families who have also suffered.”
The Hess case was the first to go to trial since the Florida Supreme Court in 2006 voided a $145 billion jury award in another class-action case, the highest punitive damage award in American history. The court said each smoker’s case had to be decided individually, but let stand that jury’s findings that tobacco companies knowingly sold dangerous products and hid their risks.
“We plan to challenge the verdict in the trial court and, if necessary, on appeal,” said Murray Garnick, an Altria Client Services vice president and associate general counsel. “We do not believe today’s verdict is predictive of the outcome of future cases.”
The Hess case has been closely watched by the tobacco industry and by thousands of other Florida smokers and survivors who have sued.
The original class-action lawsuit was filed in 1994 by a Miami Beach pediatrician, Dr. Howard Engle, who had smoked for decades and could not quit. The class of smokers was estimated at up to 700,000 when the giant $145 billion award was issued in 2000.
The six jurors deliberated over two days before returning the award for Elaine Hess, 63, whose husband, Stuart Hess, died in 1997 at age 55 after decades as a chain smoker.
The award amounts to $3 million in compensatory damages and $5 million in punitive damages against Philip Morris USA, based in Richmond, Va., and a unit of the Altria Group.
“It wasn’t about the money from the beginning,” Mrs. Hess said after the verdict. “It was about doing the right thing. I just really hope this can help all the thousands of families who have also suffered.”
The Hess case was the first to go to trial since the Florida Supreme Court in 2006 voided a $145 billion jury award in another class-action case, the highest punitive damage award in American history. The court said each smoker’s case had to be decided individually, but let stand that jury’s findings that tobacco companies knowingly sold dangerous products and hid their risks.
“We plan to challenge the verdict in the trial court and, if necessary, on appeal,” said Murray Garnick, an Altria Client Services vice president and associate general counsel. “We do not believe today’s verdict is predictive of the outcome of future cases.”
The Hess case has been closely watched by the tobacco industry and by thousands of other Florida smokers and survivors who have sued.
The original class-action lawsuit was filed in 1994 by a Miami Beach pediatrician, Dr. Howard Engle, who had smoked for decades and could not quit. The class of smokers was estimated at up to 700,000 when the giant $145 billion award was issued in 2000.
Diet Could Reduce Onset Of Eye Disease By 20%, Expert Says
ScienceDaily (Feb. 18, 2009) — University of Liverpool scientists claim that the degeneration of sight, caused by a common eye disease, could be reduced by up to 20% by increasing the amount of fruit, vegetables and nuts in the diet.
Age-related Macular Degeneration (AMD) is the leading cause of blindness in the UK, with 45% of those registered as blind suffering from the disease. The condition results in a gradual loss of central vision, due to the failure of cells in the macular – the light sensitive membrane at the centre of the retina. There is currently no cure for the more common ‘dry’ form of the disease, which is suffered by 90% of AMD patients.
Professor Ian Grierson, Head of Ophthalmology at the University, has produced a comprehensive cooking guide called ‘Fruit for Vision’, designed to add fruit and vegetables into everyday meals. The recipes will help AMD sufferers slow down the degeneration process by increasing micronutrient, vitamin and antioxidant intake in the diet. Non-sufferers can also use the book to add fruit, nuts and vegetables into each meal to protect against the disease.
Professor Grierson said: “Poor eating habits have a huge impact on health in general and the health of your eyes is no exception. Eye problems such as AMD, cataract and even glaucoma can all be affected by what we eat. But a relatively minor change in diet - adding a little more fruit into our meals - can make a profound difference and can keep eye diseases like AMD at bay for up to 20% longer.
“There are of course other risk factors related to AMD such as age, light exposure, smoking and being overweight. But if we can improve the kind of food that we eat, we could dramatically reduce the number of people who may suffer from eye diseases in the future.”
Fruit for Vision is published by Indigo Creative Marketing and the Macular Disease Society.
About AMD
AMD occurs in two forms: - ‘Wet’ AMD, which is more severe, occurs when abnormal blood vessels grow within the eye. Bleeding and leaking from these vessels can cause rapid loss of vision. It is curable if caught soon enough, although treatment is extremely expensive. Dry AMD occurs as cells within the macular begin to die, leading to a build-up of waste products in a layer of cells below the retina. There is currently no cure for Dry AMD.
Age-related Macular Degeneration (AMD) is the leading cause of blindness in the UK, with 45% of those registered as blind suffering from the disease. The condition results in a gradual loss of central vision, due to the failure of cells in the macular – the light sensitive membrane at the centre of the retina. There is currently no cure for the more common ‘dry’ form of the disease, which is suffered by 90% of AMD patients.
Professor Ian Grierson, Head of Ophthalmology at the University, has produced a comprehensive cooking guide called ‘Fruit for Vision’, designed to add fruit and vegetables into everyday meals. The recipes will help AMD sufferers slow down the degeneration process by increasing micronutrient, vitamin and antioxidant intake in the diet. Non-sufferers can also use the book to add fruit, nuts and vegetables into each meal to protect against the disease.
Professor Grierson said: “Poor eating habits have a huge impact on health in general and the health of your eyes is no exception. Eye problems such as AMD, cataract and even glaucoma can all be affected by what we eat. But a relatively minor change in diet - adding a little more fruit into our meals - can make a profound difference and can keep eye diseases like AMD at bay for up to 20% longer.
“There are of course other risk factors related to AMD such as age, light exposure, smoking and being overweight. But if we can improve the kind of food that we eat, we could dramatically reduce the number of people who may suffer from eye diseases in the future.”
Fruit for Vision is published by Indigo Creative Marketing and the Macular Disease Society.
About AMD
AMD occurs in two forms: - ‘Wet’ AMD, which is more severe, occurs when abnormal blood vessels grow within the eye. Bleeding and leaking from these vessels can cause rapid loss of vision. It is curable if caught soon enough, although treatment is extremely expensive. Dry AMD occurs as cells within the macular begin to die, leading to a build-up of waste products in a layer of cells below the retina. There is currently no cure for Dry AMD.
Forget the antioxidants? Researchers cast doubt on role of free radicals in aging
For more than 40 years, the prevailing explanation of why we get old has been tied to what is called oxidative stress. This theory postulates that when molecules like free radicals, oxygen ions and peroxides build up in cells, they overwhelm the cells' ability to repair the damage they cause, and the cells age.
An industry of "alternative" antioxidant therapies -- such as Vitamin E or CoQ10 supplements in megadose format --has sprung up as the result of this theory. However, clinical trials have not shown that these treatments have statistically significant effects.
And now researchers at McGill University, in a study published in the February issue of the journal PLoS Genetics, are calling the entire oxidative stress theory into question. Their results show that some organisms actually live longer when their ability to clean themselves of this toxic molecule buildup is partially disabled. Collectively, these molecules are known as reactive oxygen species, or ROS for short.
Dr. Siegfried Hekimi of McGill's Department of Biology, said most of the evidence for the oxidative stress theory is circumstantial, meaning oxidative stress could just as easily be a result of aging as its cause.
"The problem with the theory is that it's been based purely on correlative data, on the weight of evidence," explained Hekimi, McGill's Strathcona Chair of Zoology and Robert Archibald & Catherine Louise Campbell Chair in Developmental Biology. "It is true that the more an organism appears aged, whether in terms of disease, or appearance or anything you care to measure, the more it seems to be suffering from oxidative stress".
"This has really entrenched the theory," he continued, "because people think correlation is causation. But now this theory really is in the way of progress."
Hekimi and postdoctoral fellow Jeremy Van Raamsdonk studied mutant Caenorhabditis elegans worms. They progressively disabled five genes responsible for producing a group of proteins called superoxide dismutases (SODs), which detoxify one of the main ROS. Earlier studies seemed to show that decreased SOD production shortened an organism's lifespan, but Hekimi and Van Raamsdonk did not observe this. In fact, they found quite the opposite.
None of their mutant worms showed decreased lifespan compared to wild-type worms, even though oxidative stress was clearly raised. In fact, one variety actually displayed increased lifespan, the researchers said.
"The mutation that increases longevity affects the main SOD found in mitochondria inside the animals' cells," said Hekimi. "This is consistent with earlier findings that mitochondria are crucial to the aging process. It seems that reducing mitochondrial activity by damaging it with ROS will actually make worms live longer."
The researchers hasten to point out that they are not suggesting that oxidative stress is good for you.
"ROS undoubtedly cause damage to the body," Hekimi said. "However, they do not appear to be responsible for aging."
An industry of "alternative" antioxidant therapies -- such as Vitamin E or CoQ10 supplements in megadose format --has sprung up as the result of this theory. However, clinical trials have not shown that these treatments have statistically significant effects.
And now researchers at McGill University, in a study published in the February issue of the journal PLoS Genetics, are calling the entire oxidative stress theory into question. Their results show that some organisms actually live longer when their ability to clean themselves of this toxic molecule buildup is partially disabled. Collectively, these molecules are known as reactive oxygen species, or ROS for short.
Dr. Siegfried Hekimi of McGill's Department of Biology, said most of the evidence for the oxidative stress theory is circumstantial, meaning oxidative stress could just as easily be a result of aging as its cause.
"The problem with the theory is that it's been based purely on correlative data, on the weight of evidence," explained Hekimi, McGill's Strathcona Chair of Zoology and Robert Archibald & Catherine Louise Campbell Chair in Developmental Biology. "It is true that the more an organism appears aged, whether in terms of disease, or appearance or anything you care to measure, the more it seems to be suffering from oxidative stress".
"This has really entrenched the theory," he continued, "because people think correlation is causation. But now this theory really is in the way of progress."
Hekimi and postdoctoral fellow Jeremy Van Raamsdonk studied mutant Caenorhabditis elegans worms. They progressively disabled five genes responsible for producing a group of proteins called superoxide dismutases (SODs), which detoxify one of the main ROS. Earlier studies seemed to show that decreased SOD production shortened an organism's lifespan, but Hekimi and Van Raamsdonk did not observe this. In fact, they found quite the opposite.
None of their mutant worms showed decreased lifespan compared to wild-type worms, even though oxidative stress was clearly raised. In fact, one variety actually displayed increased lifespan, the researchers said.
"The mutation that increases longevity affects the main SOD found in mitochondria inside the animals' cells," said Hekimi. "This is consistent with earlier findings that mitochondria are crucial to the aging process. It seems that reducing mitochondrial activity by damaging it with ROS will actually make worms live longer."
The researchers hasten to point out that they are not suggesting that oxidative stress is good for you.
"ROS undoubtedly cause damage to the body," Hekimi said. "However, they do not appear to be responsible for aging."
Subscribe to:
Posts (Atom)