Supports Chapter 26: Diet and the brain
and Chapter 19: Prevention is better
Medical News Today has just reported a study conducted by a Dutch researcher, Annemie Ploeger, in which she hypothesises that "Schizophrenia and autism probably share a common origin".
There is already research which links these conditions to our 'healthy' diet in infancy, but what is new is that Ploeger also indicts "disruptions" to the fetus during the early growth period - between 20 and 40 days after fertilisation - when the embryo is highly susceptible to such disruptions. Such 'disruptions' she puts down to the mother taking a morning sickess drug called softenon. However, morning sickness is less likely if the pregnant mother is eating a natural diet.
If Ploeger is right, and I have every reason to suspect that she is, an expectant mother's diet as well as the diet her baby eats during its postnatal formative period, may both play an important role in the growing incidences of both autism and schizophrenia.
http://www.medicalnewstoday.com/articles/133293.php
27 December 2008
17 December 2008
Low cholesterol increases risk of bone fracture
Supports Chapter 22: The dangers of low cholesterol
A new study shows that low levels of cholesterol, LDL and triglycerides are associated with fractures of the vertebrae in postmenopausal women.
“Many factors other than low bone mineral density (BMD) have been suggested as predictors of risk for osteoporosis-related fractures,” comment Ebru Alemdaroglu and colleagues from Ankara Numune Training and Research Hospital, Turkey.
They add that growing evidence suggests bone and fat metabolism are related, but data are limited and contradictory.
To investigate the effect of the serum lipid levels on BMD and vertebral fractures, Alemdaroglu and team examined lumbar spine, hip and radius bone mineral density (BMD) measurements, lateral dorsal and lumbar spine radiographs, and serum lipid levels in 107 postmenopausal women aged 45–79 years.
The researchers were able to score 89 radiographs with good technical properties using the Kleerekoper method. Vertebrae fractures were observed in 71% of the women.
Analysis showed that patients with vertebrae fractures had significantly lower levels of total cholesterol, triglycerides and LDL cholesterol than the patients without vertebrae fractures.
Total cholesterol level was most strongly associated with vertebral fracture. An increase of 1 mg/dl (0.03 mmol/l) total cholesterol was associated with a 2.2% decreased risk for vertebrae fracture.
The researchers reason that estrogen is synthesized by cholesterol and esterified forms of estrogen are stored and transported by lipoproteins. Thus, decreased LDL levels would be associated with decreased stored estrogen and may explain the relationship between vertebrate fracture and reduced serum lipids.
According to the T-scores obtained by BMD measurement, 36 (33.6%) of the 107 women examined were suffering from osteoporosis. Alemdaroglu and co-researchers report that the lipid profiles of women with osteoporosis did not differ significantly from those without osteoporosis.
There was no correlation between serum lipid levels and BMD at the lumbar spine, right hip and radius in any of the study participants. Only total cholesterol and LDL cholesterol were weakly associated with BMD at the forearm after the adjustment for possible confounders.
Sivas F, et al. Serum lipid profile: its relationship with osteoporotic vertebrae fractures and bone mineral density in Turkish postmenopausal women. Rheumatol Int 2008. [Online publication ahead of print]
DOI 10.1007/s00296-008-0784-4
COMMENT
The bottom line is: This is yet another indication that low cholesterol levels are not desirable.
A new study shows that low levels of cholesterol, LDL and triglycerides are associated with fractures of the vertebrae in postmenopausal women.
“Many factors other than low bone mineral density (BMD) have been suggested as predictors of risk for osteoporosis-related fractures,” comment Ebru Alemdaroglu and colleagues from Ankara Numune Training and Research Hospital, Turkey.
They add that growing evidence suggests bone and fat metabolism are related, but data are limited and contradictory.
To investigate the effect of the serum lipid levels on BMD and vertebral fractures, Alemdaroglu and team examined lumbar spine, hip and radius bone mineral density (BMD) measurements, lateral dorsal and lumbar spine radiographs, and serum lipid levels in 107 postmenopausal women aged 45–79 years.
The researchers were able to score 89 radiographs with good technical properties using the Kleerekoper method. Vertebrae fractures were observed in 71% of the women.
Analysis showed that patients with vertebrae fractures had significantly lower levels of total cholesterol, triglycerides and LDL cholesterol than the patients without vertebrae fractures.
Total cholesterol level was most strongly associated with vertebral fracture. An increase of 1 mg/dl (0.03 mmol/l) total cholesterol was associated with a 2.2% decreased risk for vertebrae fracture.
The researchers reason that estrogen is synthesized by cholesterol and esterified forms of estrogen are stored and transported by lipoproteins. Thus, decreased LDL levels would be associated with decreased stored estrogen and may explain the relationship between vertebrate fracture and reduced serum lipids.
According to the T-scores obtained by BMD measurement, 36 (33.6%) of the 107 women examined were suffering from osteoporosis. Alemdaroglu and co-researchers report that the lipid profiles of women with osteoporosis did not differ significantly from those without osteoporosis.
There was no correlation between serum lipid levels and BMD at the lumbar spine, right hip and radius in any of the study participants. Only total cholesterol and LDL cholesterol were weakly associated with BMD at the forearm after the adjustment for possible confounders.
Sivas F, et al. Serum lipid profile: its relationship with osteoporotic vertebrae fractures and bone mineral density in Turkish postmenopausal women. Rheumatol Int 2008. [Online publication ahead of print]
DOI 10.1007/s00296-008-0784-4
COMMENT
The bottom line is: This is yet another indication that low cholesterol levels are not desirable.
12 December 2008
Yet more vitamin D deficiency diseases
Supports Chapter 11: Our irrational fear of sunlight
I really should have delayed Trick and Treat; there is so much more evidence coming out in support of its various chapters and subjects since it went to print in September.
Two studies just published show even more dangers of ill-health caused by the current ‘keep out of the sun’ advice. These concern low levels of vitamin and Parkinson’s disease, and the inflammatory bowel diseases, Crohn’s disease and ulcerative colitis.
Parkinson’s disease
A team of doctors at the Department of Neurology, Emory University School of Medicine, Atlanta, GA, compared the prevalence of vitamin D deficiency in mainly white patients with Parkinson’s disease, with the prevalence in age-matched healthy controls and patients with Alzheimer disease, between 1992 and 2007.
They found significantly lower levels of vitamin D levels at a mean of 31.9 nmol/l in the Parkinson’s patients compared to the other two groups.
(Alzheimer’s patients levels were also lower than the levels in the healthy cohort, although the study was not set up to measure the effects of this.)
Evatt ML, et al Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol 2008; 65: 1348-52.
Inflammatory bowel disease
A causal connection between vitamin D deficiency and inflammatory bowel disease was reported at the Annual Scientific Meeting of the American College of Gastroenterology in Orlando, Florida, during October.
Lead researcher Dr Alex Ulitsky from the Medical College of Wisconsin in Milwaukee, USA, and his team found that Vitamin D deficiency was common among people with inflammatory bowel disease and is associated with increased disease activity and worse quality of life.
They found that nearly 50% of the patients were Vitamin D deficient at some point, with 11% being severely deficient. Vitamin D deficiency was also associated with reduced quality of life in patients with Crohn’s disease, but not in those with ulcerative colitis.
Although concerned mainly with Crohn’s disease and ulcerative colitis, Dr Ulitsky concluded: “All inflammatory bowel disease patients, irrespective of their disease, disease location or nature should have their Vitamin D levels checked regularly and corrected aggressively when insufficiency is found.”
Meeting website: http://www.acg.gi.org/acgmeetings/
COMMENT
There may be some excuse for people living at higher latitudes to have some vitamin D deficiency, particularly if they have darker skins, but for residents of Florida, with its almost year-long sunshine also to suffer must be a reflection on the appalling health advice they are given. We need to get out in the sun more, not less.
I really should have delayed Trick and Treat; there is so much more evidence coming out in support of its various chapters and subjects since it went to print in September.
Two studies just published show even more dangers of ill-health caused by the current ‘keep out of the sun’ advice. These concern low levels of vitamin and Parkinson’s disease, and the inflammatory bowel diseases, Crohn’s disease and ulcerative colitis.
Parkinson’s disease
A team of doctors at the Department of Neurology, Emory University School of Medicine, Atlanta, GA, compared the prevalence of vitamin D deficiency in mainly white patients with Parkinson’s disease, with the prevalence in age-matched healthy controls and patients with Alzheimer disease, between 1992 and 2007.
They found significantly lower levels of vitamin D levels at a mean of 31.9 nmol/l in the Parkinson’s patients compared to the other two groups.
(Alzheimer’s patients levels were also lower than the levels in the healthy cohort, although the study was not set up to measure the effects of this.)
Evatt ML, et al Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol 2008; 65: 1348-52.
Inflammatory bowel disease
A causal connection between vitamin D deficiency and inflammatory bowel disease was reported at the Annual Scientific Meeting of the American College of Gastroenterology in Orlando, Florida, during October.
Lead researcher Dr Alex Ulitsky from the Medical College of Wisconsin in Milwaukee, USA, and his team found that Vitamin D deficiency was common among people with inflammatory bowel disease and is associated with increased disease activity and worse quality of life.
They found that nearly 50% of the patients were Vitamin D deficient at some point, with 11% being severely deficient. Vitamin D deficiency was also associated with reduced quality of life in patients with Crohn’s disease, but not in those with ulcerative colitis.
Although concerned mainly with Crohn’s disease and ulcerative colitis, Dr Ulitsky concluded: “All inflammatory bowel disease patients, irrespective of their disease, disease location or nature should have their Vitamin D levels checked regularly and corrected aggressively when insufficiency is found.”
Meeting website: http://www.acg.gi.org/acgmeetings/
COMMENT
There may be some excuse for people living at higher latitudes to have some vitamin D deficiency, particularly if they have darker skins, but for residents of Florida, with its almost year-long sunshine also to suffer must be a reflection on the appalling health advice they are given. We need to get out in the sun more, not less.
10 December 2008
Leading nutritionist shows how little she knows
Supports pretty well all of Trick and Treat
The UK's Daily Express published an article on Tuesday 9 December 2008 entitled "Did scientists get it wrong on the dangers of saturated fat?" It was written to publicise Trick and Treat: How 'healthy eating' is making us ill, but was in the form of a debate.
On the "Yes" side was me and my book, Trick and Treat. On the "No"side was an argument by a senior member of the British Nutrition Foundation, Dr Joanne Lunn. Her comments illustrate well why I felt it necessary to write Trick and Treat as she said that:
"The government, doctors and nutritionists don't base recommendations for reducing the amount of saturated fat in our diets on old research but on a growing body of evidence linking a diet high in saturated fat with a higher level of blood cholesterol and high blood cholesterol levels with a risk of cardiovascular disease."
The evidence I quoted in support of Trick and Treat is not 'old' evidence, but is right up-to-date; it includes studies published as recently as September this year. And that evidence shows over and over again that saturated fat does not cause cardiovascular diseases
Indeed, there has been so much evidence against 'healthy eating' since its inception in the 1980s that Professor Sylvan Lee Weinberg, a past President of the American College of Cardiology and a fervent supporter and advocate of 'healthy eating', finally wrote in the 4 March 2004 edition of the Journal of the American College of Cardiology, that:
Dr Lunn also said that "people will always ignore the evidence". But it is not I who am ignoring the evidence, it is people like Dr Lunn, and until those in authority stop ignoring the growing evidence that 'healthy eating' isn't healthy, our health can only deteriorate still further.
But, of course, if we didn't get ill, they wouldn't have a job, would they?
The UK's Daily Express published an article on Tuesday 9 December 2008 entitled "Did scientists get it wrong on the dangers of saturated fat?" It was written to publicise Trick and Treat: How 'healthy eating' is making us ill, but was in the form of a debate.
On the "Yes" side was me and my book, Trick and Treat. On the "No"side was an argument by a senior member of the British Nutrition Foundation, Dr Joanne Lunn. Her comments illustrate well why I felt it necessary to write Trick and Treat as she said that:
"The government, doctors and nutritionists don't base recommendations for reducing the amount of saturated fat in our diets on old research but on a growing body of evidence linking a diet high in saturated fat with a higher level of blood cholesterol and high blood cholesterol levels with a risk of cardiovascular disease."
The evidence I quoted in support of Trick and Treat is not 'old' evidence, but is right up-to-date; it includes studies published as recently as September this year. And that evidence shows over and over again that saturated fat does not cause cardiovascular diseases
Indeed, there has been so much evidence against 'healthy eating' since its inception in the 1980s that Professor Sylvan Lee Weinberg, a past President of the American College of Cardiology and a fervent supporter and advocate of 'healthy eating', finally wrote in the 4 March 2004 edition of the Journal of the American College of Cardiology, that:
"The low-fat, high-carbohydrate diet, promulgated vigorously . . . may well have played an unintended role in the current epidemics of obesity, lipid [blood fat] abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate, high-protein diet may have a salutary effect on the epidemics in question."Professor Weinberg is not alone; there is a growing number of doctors speaking out about the falsity of the current 'healthy' recommendations.
Dr Lunn also said that "people will always ignore the evidence". But it is not I who am ignoring the evidence, it is people like Dr Lunn, and until those in authority stop ignoring the growing evidence that 'healthy eating' isn't healthy, our health can only deteriorate still further.
But, of course, if we didn't get ill, they wouldn't have a job, would they?
03 December 2008
Study finds vegetarians have smaller brains
Supports Chapter 13: Homo carnivorous
Scientists at the Department of Physiology, Anatomy and Genetics, University of Oxford, have discovered that going veggie could be bad for your brain – with those on a meat-free diet six times more likely to suffer brain shrinkage.
The study involved tests and brain scans on community-dwelling volunteers aged 61 to 87 years without cognitive impairment at enrolment, over a period of five years. When the volunteers were retested five years later the medics found those with the lowest levels of vitamin B12 were also the most likely to have brain shrinkage. It confirms earlier research showing a link between brain atrophy and low levels of B12.
Vegans are the most likely to be deficient because the best sources of the vitamin are meat, particularly liver, milk and fish.
This study confirms other findings, covered in Trick and Treat, which shows that overall human brain sizes have reduced by an average 11% since we adopted an agricultural diet based on cereal grains rather than the meat-based diet of our Palaeolithic ancestors.
Vogiatzoglou A, et al. Vitamin B12 status and rate of brain volume loss in community-dwelling elderly. Neurology 2008; 71(11): 826-32.
30 November 2008
Low cholesterol increases suicide in bipolar patients
Supports Chapter 22: The dangers of low cholesterol
and Chapter 26: Diet and the brain
Several studies have been conducted looking at levels of blood cholesterol and its effect on the brain. Most have found that people with one or more of many mental illnesses from Alzheimer’s disease to depression tend to have lower blood cholesterol than healthy people, a few studies have been equivocal.
In a new study, to be published soon, scientists at the University Hospital Centre Zagreb, Croatia, investigated whether there were differences in the serum cholesterol levels in hospitalized bipolar disorder male patients with history of suicide attempts and without suicide attempts.
They found there was a significant difference. Men who attempted suicide had significantly lower levels of total cholesterol (median 3.9 mmol/L vs 4.8 mmol/L); they also had lower LDL (median 2.3 mmol/L vs 3.0 mmol/L).
This adds to the weight of evidence both in Trick and Treat, and to my earlier post, that low cholesterol levels can play havoc with the brain.
Vuksan-Cusa B, et al. Differences in cholesterol and metabolic syndrome between bipolar disorder men with and without suicide attempts. To appear in: Progress in Neuropsychopharmacology & Biological Psychiatry (2008)
doi: 10.1016/j.pnpbp.2008.10.017
and Chapter 26: Diet and the brain
Several studies have been conducted looking at levels of blood cholesterol and its effect on the brain. Most have found that people with one or more of many mental illnesses from Alzheimer’s disease to depression tend to have lower blood cholesterol than healthy people, a few studies have been equivocal.
In a new study, to be published soon, scientists at the University Hospital Centre Zagreb, Croatia, investigated whether there were differences in the serum cholesterol levels in hospitalized bipolar disorder male patients with history of suicide attempts and without suicide attempts.
They found there was a significant difference. Men who attempted suicide had significantly lower levels of total cholesterol (median 3.9 mmol/L vs 4.8 mmol/L); they also had lower LDL (median 2.3 mmol/L vs 3.0 mmol/L).
This adds to the weight of evidence both in Trick and Treat, and to my earlier post, that low cholesterol levels can play havoc with the brain.
Vuksan-Cusa B, et al. Differences in cholesterol and metabolic syndrome between bipolar disorder men with and without suicide attempts. To appear in: Progress in Neuropsychopharmacology & Biological Psychiatry (2008)
doi: 10.1016/j.pnpbp.2008.10.017
27 November 2008
High Protein Meals Help Keep The Fat Away
Supports Chapter 19: 'Healthy eating' is fattening
A low-calorie diet made up of higher protein meals improves the ability to burn fat among overweight and obese people and may be the key to shedding excess kilos, according to new Australian research.
The study found higher protein meals may have a subtle fat-burning effect in overweight or obese people. And the study showed the glycaemic index (GI) of a meal has no additional effect on fat breakdown.
Study co-author Dr. Marijka Batterman said: 'We know from past research that overweight or obese people are not as efficient at burning fat. This new study shows that fat oxidation, or the body's ability to 'burn' fat, improves in obese people when they eat a higher protein diet.'
Study participants were put on two protein-enriched meals and one standard meal, which all contained the same number of calories. The two protein-enriched meals differed in the type of carbohydrate they contained - either high- or low-GI. The amount of calories subjects burnt was then measured.
The high-protein meals led to the greatest level of fat oxidation. This plan included a cheese and tomato omelette for breakfast.
"We found a clear relationship between body composition and the effect of dietary protein on fat oxidation. Our bodies burn energy and use fat differently, and we need to take this into account when planning our diets,' said Dr. Batterman who works at the Smart Foods Centre, University of Wollongong.
Batterham M, et al. High-protein meals may benefit fat oxidation and energy expenditure in individuals with higher body fat. Nutrition & Dietetics 2008; 65(4):
http://www3.interscience.wiley.com/journal/121501657/abstract
A low-calorie diet made up of higher protein meals improves the ability to burn fat among overweight and obese people and may be the key to shedding excess kilos, according to new Australian research.
The study found higher protein meals may have a subtle fat-burning effect in overweight or obese people. And the study showed the glycaemic index (GI) of a meal has no additional effect on fat breakdown.
Study co-author Dr. Marijka Batterman said: 'We know from past research that overweight or obese people are not as efficient at burning fat. This new study shows that fat oxidation, or the body's ability to 'burn' fat, improves in obese people when they eat a higher protein diet.'
Study participants were put on two protein-enriched meals and one standard meal, which all contained the same number of calories. The two protein-enriched meals differed in the type of carbohydrate they contained - either high- or low-GI. The amount of calories subjects burnt was then measured.
The high-protein meals led to the greatest level of fat oxidation. This plan included a cheese and tomato omelette for breakfast.
"We found a clear relationship between body composition and the effect of dietary protein on fat oxidation. Our bodies burn energy and use fat differently, and we need to take this into account when planning our diets,' said Dr. Batterman who works at the Smart Foods Centre, University of Wollongong.
Batterham M, et al. High-protein meals may benefit fat oxidation and energy expenditure in individuals with higher body fat. Nutrition & Dietetics 2008; 65(4):
http://www3.interscience.wiley.com/journal/121501657/abstract
Sunshine Deficit May Diminish Vitamin D Levels And Harm Cardiovascular Health
Supports Chapter 11: Our irrational fear of sunlight
The temperature might not be the only thing plummeting this winter. Many people also will experience a decrease in their vitamin D levels, which can play a role in heart disease, according to a new review article in Circulation.
Vitamin D deficiency results in part from reduced exposure to sunlight, which is common during cold weather months when days are shorter and more time is spent indoors.
"Chronic vitamin D deficiency may be a culprit in heart disease, high blood pressure and metabolic syndrome," said Professor Sue Penckofer at Marcella Niehoff School of Nursing, Loyola University Chicago.
The review article cited a number of studies that linked vitamin D deficiency to heart disease. These studies found rates of severe disease or death may be 30 to 50 percent higher among sun-deprived individuals with heart disease.
Penckofer and colleagues concluded that diet alone is not sufficient to manage vitamin D levels. Treatment options to correct this level, such as vitamin D2 or D3, may decrease the risk of severe disease or death from cardiovascular disorders. The preferred range in the body is 30 - 60 ng/mL of 25(OH) vitamin D.
"Most physicians do not routinely test for vitamin D deficiency," said Penckofer. "However, most experts would agree that adults at risk for heart disease and others who experience fatigue joint pain or depression should have their vitamin D levels measured."
Wallis DE, Penckofer S, Sizemore GW. The "sunshine deficit" and cardiovascular disease.
Circulation 2008;118(14):1476-85. PMID: 18824654
The temperature might not be the only thing plummeting this winter. Many people also will experience a decrease in their vitamin D levels, which can play a role in heart disease, according to a new review article in Circulation.
Vitamin D deficiency results in part from reduced exposure to sunlight, which is common during cold weather months when days are shorter and more time is spent indoors.
"Chronic vitamin D deficiency may be a culprit in heart disease, high blood pressure and metabolic syndrome," said Professor Sue Penckofer at Marcella Niehoff School of Nursing, Loyola University Chicago.
The review article cited a number of studies that linked vitamin D deficiency to heart disease. These studies found rates of severe disease or death may be 30 to 50 percent higher among sun-deprived individuals with heart disease.
Penckofer and colleagues concluded that diet alone is not sufficient to manage vitamin D levels. Treatment options to correct this level, such as vitamin D2 or D3, may decrease the risk of severe disease or death from cardiovascular disorders. The preferred range in the body is 30 - 60 ng/mL of 25(OH) vitamin D.
"Most physicians do not routinely test for vitamin D deficiency," said Penckofer. "However, most experts would agree that adults at risk for heart disease and others who experience fatigue joint pain or depression should have their vitamin D levels measured."
Wallis DE, Penckofer S, Sizemore GW. The "sunshine deficit" and cardiovascular disease.
Circulation 2008;118(14):1476-85. PMID: 18824654
Role Of Vitamin D In Colon Cancer Therapy
Supports Chapter 11: Our irrational fear of sunlight
Vitamin D can tame the rogue colon cancer cell by adjusting everything from its gene expression to its cytoskeleton. In the Nov. 17 issue of the Journal of Cell Biology, Ordóñez-Morán and colleagues show that one pathway governs the vitamin's diverse effects. The results help clarify the actions of a molecule that is undergoing clinical trials as a cancer therapy.
Vitamin D stymies colon cancer cells in two ways. It switches on genes such as the one that encodes E-cadherin, a component of the adherens junctions that anchor cells in epithelial layers. The vitamin also induces effects on the cytoskeleton that are required for gene regulation and short-circuiting the Wnt/b-catenin pathway, which is overactive in most colon tumors. The net result is to curb division and prod colon cancer cells to differentiate into epithelial cells that settle down instead of spreading.
To delve into the mechanism, the team dosed colon cancer cells with calcitriol, the metabolically active version of vitamin D. Calcitriol triggered a surge of calcium into the cells and the subsequent switching on of RhoA-RhoGTPases, which have been implicated in the cytoskeletal changes induced by vitamin D. The activated RhoA in turn switched on one of its targets, the rho-associated coiled kinase (ROCK), which then roused two other kinases. Each step in this nongenomic pathway was necessary to spur the genomic responses, the researchers showed. The team also nailed down the contribution of the vitamin D receptor (VDR). The receptor was crucial at the beginning of the pathway, where it permitted the calcium influx, and at the end, where it activated and repressed genes.
The study is the first to show that vitamin D's genomic and nongenomic effects integrate to regulate cell physiology. One question the researchers now want to pursue is whether VDR from different locations - the nucleus, the cytosol, and possibly the cell membrane - has different functions in the pathway.
Ordóñez-Morán P, et al. RhoA-ROCK and p38MAPK-MSK1 mediate vitamin D effects on gene expression, phenotype, and Wnt pathway in colon cancer cells. 2008. J Cell Biol doi:10.1083/jcb.200803020.
Vitamin D can tame the rogue colon cancer cell by adjusting everything from its gene expression to its cytoskeleton. In the Nov. 17 issue of the Journal of Cell Biology, Ordóñez-Morán and colleagues show that one pathway governs the vitamin's diverse effects. The results help clarify the actions of a molecule that is undergoing clinical trials as a cancer therapy.
Vitamin D stymies colon cancer cells in two ways. It switches on genes such as the one that encodes E-cadherin, a component of the adherens junctions that anchor cells in epithelial layers. The vitamin also induces effects on the cytoskeleton that are required for gene regulation and short-circuiting the Wnt/b-catenin pathway, which is overactive in most colon tumors. The net result is to curb division and prod colon cancer cells to differentiate into epithelial cells that settle down instead of spreading.
To delve into the mechanism, the team dosed colon cancer cells with calcitriol, the metabolically active version of vitamin D. Calcitriol triggered a surge of calcium into the cells and the subsequent switching on of RhoA-RhoGTPases, which have been implicated in the cytoskeletal changes induced by vitamin D. The activated RhoA in turn switched on one of its targets, the rho-associated coiled kinase (ROCK), which then roused two other kinases. Each step in this nongenomic pathway was necessary to spur the genomic responses, the researchers showed. The team also nailed down the contribution of the vitamin D receptor (VDR). The receptor was crucial at the beginning of the pathway, where it permitted the calcium influx, and at the end, where it activated and repressed genes.
The study is the first to show that vitamin D's genomic and nongenomic effects integrate to regulate cell physiology. One question the researchers now want to pursue is whether VDR from different locations - the nucleus, the cytosol, and possibly the cell membrane - has different functions in the pathway.
Ordóñez-Morán P, et al. RhoA-ROCK and p38MAPK-MSK1 mediate vitamin D effects on gene expression, phenotype, and Wnt pathway in colon cancer cells. 2008. J Cell Biol doi:10.1083/jcb.200803020.
Tumours Fuelled By Lactic Acid
Supports Chapter 8: Why 'five portions'?
and Chapter 23: Cancer: disease of civilization
Researchers at Duke University Medical Center and the Université catholique de Louvain (UCL) have found that lactic acid is an important energy source for cancer cells. In further experiments, they discovered a new way to destroy the most hard-to-kill, dangerous cancer cells by preventing them from delivering lactic acid. The study was published in the Nov. 20 online edition of the Journal of Clinical Investigation.
Mark Dewhirst, DVM, Ph.D., professor of radiation oncology and pathology at Duke, and a co-author of the study said:"We have known for more than 50 years that low-oxygen, or hypoxic, cells cause resistance to radiation therapy . . . Over the past 10 years, scientists have found that hypoxic cells are also more aggressive and hard to treat with chemotherapy. The work we have done presents an entirely new way for us to go after them."
Many cancers have cells that burn fuel for activities in different ways. Cancer cells near blood vessels have adequate oxygen sources and can either burn glucose like normal cells, or lactic acid (lactate). Cancer cells further from vessels are hypoxic and need to burn a lot of glucose to keep going. Thei si very inefficient but they produce lactate as a waste product.
Cancer cells with good oxygen supply actually prefer to burn lactate, which frees up glucose to be used by the less-oxygenated cells. But when the researchers cut off the cells' ability to use lactate, the hypoxic cells didn't get as much glucose.
For the dangerous hypoxic cells, "it is glucose or death," said Pierre Sonveaux, the lead author and professor in the UCL Unit of Pharmacology & Therapeutics.
The next challenge was to discover how lactate moved into cancer cells. Because lactate recycling exists in exercising muscle to prevent cramps, the researchers imagined that the same molecular machinery could be used by cancer cells.
"We discovered that a transporter protein of muscle origin, MCT1, was also present in respiring tumor cells," said Dewhirst. The team used chemical inhibitors of MCT1 and cell models in which MCT1 had been deleted to learn its role in delivering lactate.
"We not only proved that MCT1 was important, we formally demonstrated that MCT1 was unique for mediating lactate uptake," said Professor Olivier Feron of the UCL Unit of Pharmacology & Therapeutics.
Blocking MCT1 did not kill the oxygenated cells, but it nudged their metabolism toward inefficiently burning glucose. Because the glucose was used more abundantly by the better-oxygenated cells, they used up most of the glucose before it could reach the hypoxic cells, which starved while waiting in vain for glucose to arrive.
"This finding is really exciting," Dewhirst said. "The idea of starving hypoxic cells to death is completely novel."
Even though hypoxic cancer cells have been identified as a cause of treatment resistance for decades, there has not been a reliable method to kill them. "They are the population of cells that can cause tumor relapse," said Professor Feron.
A significant advantage of the new strategy is that a new drug does not need to reach hypoxic cells far from blood vessels and it does not need to enter into cells at all - it merely needs to block the transporter molecule that moves the lactose, which is outside of the cells. "This finding will be really important for drug development," said Sonveaux.
----------------------------
Article adapted from original press release.
The point is that, as is explained in Trick and Treat, cancers thrive on glucose and its byproduct, lactic acid. But if you eat a low-carb, high-fat diet, this cannot happen and cancers are much less likely to survive.
and Chapter 23: Cancer: disease of civilization
Researchers at Duke University Medical Center and the Université catholique de Louvain (UCL) have found that lactic acid is an important energy source for cancer cells. In further experiments, they discovered a new way to destroy the most hard-to-kill, dangerous cancer cells by preventing them from delivering lactic acid. The study was published in the Nov. 20 online edition of the Journal of Clinical Investigation.
Mark Dewhirst, DVM, Ph.D., professor of radiation oncology and pathology at Duke, and a co-author of the study said:"We have known for more than 50 years that low-oxygen, or hypoxic, cells cause resistance to radiation therapy . . . Over the past 10 years, scientists have found that hypoxic cells are also more aggressive and hard to treat with chemotherapy. The work we have done presents an entirely new way for us to go after them."
Many cancers have cells that burn fuel for activities in different ways. Cancer cells near blood vessels have adequate oxygen sources and can either burn glucose like normal cells, or lactic acid (lactate). Cancer cells further from vessels are hypoxic and need to burn a lot of glucose to keep going. Thei si very inefficient but they produce lactate as a waste product.
Cancer cells with good oxygen supply actually prefer to burn lactate, which frees up glucose to be used by the less-oxygenated cells. But when the researchers cut off the cells' ability to use lactate, the hypoxic cells didn't get as much glucose.
For the dangerous hypoxic cells, "it is glucose or death," said Pierre Sonveaux, the lead author and professor in the UCL Unit of Pharmacology & Therapeutics.
The next challenge was to discover how lactate moved into cancer cells. Because lactate recycling exists in exercising muscle to prevent cramps, the researchers imagined that the same molecular machinery could be used by cancer cells.
"We discovered that a transporter protein of muscle origin, MCT1, was also present in respiring tumor cells," said Dewhirst. The team used chemical inhibitors of MCT1 and cell models in which MCT1 had been deleted to learn its role in delivering lactate.
"We not only proved that MCT1 was important, we formally demonstrated that MCT1 was unique for mediating lactate uptake," said Professor Olivier Feron of the UCL Unit of Pharmacology & Therapeutics.
Blocking MCT1 did not kill the oxygenated cells, but it nudged their metabolism toward inefficiently burning glucose. Because the glucose was used more abundantly by the better-oxygenated cells, they used up most of the glucose before it could reach the hypoxic cells, which starved while waiting in vain for glucose to arrive.
"This finding is really exciting," Dewhirst said. "The idea of starving hypoxic cells to death is completely novel."
Even though hypoxic cancer cells have been identified as a cause of treatment resistance for decades, there has not been a reliable method to kill them. "They are the population of cells that can cause tumor relapse," said Professor Feron.
A significant advantage of the new strategy is that a new drug does not need to reach hypoxic cells far from blood vessels and it does not need to enter into cells at all - it merely needs to block the transporter molecule that moves the lactose, which is outside of the cells. "This finding will be really important for drug development," said Sonveaux.
----------------------------
Article adapted from original press release.
The point is that, as is explained in Trick and Treat, cancers thrive on glucose and its byproduct, lactic acid. But if you eat a low-carb, high-fat diet, this cannot happen and cancers are much less likely to survive.
23 November 2008
Low cholesterol increases suicide risk
Supports Chapter 22: The dangers of low blood cholesterol;
and Chapter 26: Diet and the brain
There is already a lot of evidence in Trick and Treat which shows that people with low cholesterol levels are more likely both to attempt to commit suicide and to succeed in those attempts. This latest study, from the University of Madrid, adds yet more weight to this evidence.
In this study ‘low cholesterol’ was defined as less than 160mg/dL (4.16 mmol/L). This level has been noted several times in the medical literature as a level below which suicide is more likely. And you should note that this level is well within what is considered ‘healthy’ by a cholesterol-lowering, drug pushing health industry.
What makes it worse, to my mind, is that suicide attempters in this study were those one might consider least likely to want to take their own lives: they were generally younger than 35, and had a ‘healthy’ weight, with a Body Mass Index of 22 or lower.
Perez-Rodriguez MM, et al. Low cholesterol may be associated with suicide attempt history. J Clin Psychiatry 2008 e1-e8 (pii: ej07m3866). Published online ahead of print.
and Chapter 26: Diet and the brain
There is already a lot of evidence in Trick and Treat which shows that people with low cholesterol levels are more likely both to attempt to commit suicide and to succeed in those attempts. This latest study, from the University of Madrid, adds yet more weight to this evidence.
In this study ‘low cholesterol’ was defined as less than 160mg/dL (4.16 mmol/L). This level has been noted several times in the medical literature as a level below which suicide is more likely. And you should note that this level is well within what is considered ‘healthy’ by a cholesterol-lowering, drug pushing health industry.
What makes it worse, to my mind, is that suicide attempters in this study were those one might consider least likely to want to take their own lives: they were generally younger than 35, and had a ‘healthy’ weight, with a Body Mass Index of 22 or lower.
Perez-Rodriguez MM, et al. Low cholesterol may be associated with suicide attempt history. J Clin Psychiatry 2008 e1-e8 (pii: ej07m3866). Published online ahead of print.
22 November 2008
Get out in the sun to protect your heart
Supports Chapter 11: Our irrational fear of sunlight
All the 'healthy eating' hype is aimed at preventing heart attacks caused by 'ischaemic heart disease', where the coronary arteries become blocked, either by a build-up of plaque in the artery walls, or by a blood clot. But there are many diseases of the heart – and the one that is responsible for the most deaths is a condition called 'heart failure' or 'sudden cardiac death' (SCD).
We have been told for many years that we should not go out in the sun unless we cover up and/or wear a strong sunscreen. But this measure dramatically reduces the amount of vitamin D our bodies can make from UVB sunlight (our major source of vitamin D). As a consequence, there is now a widespread deficiency of vitamin D in all industrialised countries, particularly those furthest from the equator.
There are also increasing numbers of cases of SCD in those countries.
The classic role of vitamin D for maintaining bone health is well documented and recent reports have linked vitamin D deficiency to various other diseases, including arterial hypertension, diabetes mellitus and cancer which are already covered in Trick and Treat.
A combined German/Austrian study published in October 2008 looked to answer the question of whether vitamin D deficiency also increased the risk of SCD. They found clear evidence that it did, concluding that:
So, this is yet another reason to get out in the sun – without sunscreen - as often as you can.
Pilz S, et al. Association of Vitamin D Deficiency with Heart Failure and Sudden Cardiac Death in a Large Cross-Sectional Study of Patients Referred for Coronary Angiography. J Clin Endocrinol Metab 2008; 93: 3927-3935.
All the 'healthy eating' hype is aimed at preventing heart attacks caused by 'ischaemic heart disease', where the coronary arteries become blocked, either by a build-up of plaque in the artery walls, or by a blood clot. But there are many diseases of the heart – and the one that is responsible for the most deaths is a condition called 'heart failure' or 'sudden cardiac death' (SCD).
We have been told for many years that we should not go out in the sun unless we cover up and/or wear a strong sunscreen. But this measure dramatically reduces the amount of vitamin D our bodies can make from UVB sunlight (our major source of vitamin D). As a consequence, there is now a widespread deficiency of vitamin D in all industrialised countries, particularly those furthest from the equator.
There are also increasing numbers of cases of SCD in those countries.
The classic role of vitamin D for maintaining bone health is well documented and recent reports have linked vitamin D deficiency to various other diseases, including arterial hypertension, diabetes mellitus and cancer which are already covered in Trick and Treat.
A combined German/Austrian study published in October 2008 looked to answer the question of whether vitamin D deficiency also increased the risk of SCD. They found clear evidence that it did, concluding that:
"Low levels of 25(OH)D and 1,25-dihydroxyvitamin D are associated with prevalent myocardial dysfunction, deaths due to heart failure, and SCD."
So, this is yet another reason to get out in the sun – without sunscreen - as often as you can.
Pilz S, et al. Association of Vitamin D Deficiency with Heart Failure and Sudden Cardiac Death in a Large Cross-Sectional Study of Patients Referred for Coronary Angiography. J Clin Endocrinol Metab 2008; 93: 3927-3935.
12 November 2008
If you are diabetic, beware of statins
Supports Chapter 1: Trick to treat, Chapter 2: What’s behind the screens? and Chapter 20: Diabetes deceit.
As diabetics are about eight times more likely to suffer a heart attack than the healthy population, not only are they told to eat an unhealthy 'healthy' diet, they are also routinely prescribed the cholesterol-lowering drugs called statins.
Disease of the blood vessels caused by diabetes mellitus represents a significant medical problem that has been firmly established in large clinical trials to be directly related to high glucose levels. At a cellular level, high glucose exposure damages endothelial cells (the cells that line the blood vessels) and inhibits their repair. Needless to say, this is highly undesirable and could account for many of the complications of diabetes.
Glucose does this by inhibiting the 'mevalonate pathway', a series of chemical processes that produce a number of compounds needed for endothelial cell repair.
Cholesterol is also a compound which is manufactured via the mevalonate pathway; it is this pathway that is inhibited by statins.
A brand new study from the University of Sydney, Australia, finds that statins, not surprisingly, which work by blocking not only cholesterol but also the other vital compounds that the body needs, have a similar effect to high levels of glucose.
It would seem foolhardy, therefore, to continue the practice of putting all (or indeed any) diabetics on statins.
Mather A, et al. High glucose induced endothelial cell growth inhibition is associated with an increase in TGFβ1 secretion and inhibition of Ras prenylation via suppression of the mevalonate pathway. Int J Biochem Cell Biol (2008),
doi:10.1016/j.biocel.2008.07.007
As diabetics are about eight times more likely to suffer a heart attack than the healthy population, not only are they told to eat an unhealthy 'healthy' diet, they are also routinely prescribed the cholesterol-lowering drugs called statins.
Disease of the blood vessels caused by diabetes mellitus represents a significant medical problem that has been firmly established in large clinical trials to be directly related to high glucose levels. At a cellular level, high glucose exposure damages endothelial cells (the cells that line the blood vessels) and inhibits their repair. Needless to say, this is highly undesirable and could account for many of the complications of diabetes.
Glucose does this by inhibiting the 'mevalonate pathway', a series of chemical processes that produce a number of compounds needed for endothelial cell repair.
Cholesterol is also a compound which is manufactured via the mevalonate pathway; it is this pathway that is inhibited by statins.
A brand new study from the University of Sydney, Australia, finds that statins, not surprisingly, which work by blocking not only cholesterol but also the other vital compounds that the body needs, have a similar effect to high levels of glucose.
It would seem foolhardy, therefore, to continue the practice of putting all (or indeed any) diabetics on statins.
Mather A, et al. High glucose induced endothelial cell growth inhibition is associated with an increase in TGFβ1 secretion and inhibition of Ras prenylation via suppression of the mevalonate pathway. Int J Biochem Cell Biol (2008),
doi:10.1016/j.biocel.2008.07.007
08 November 2008
High body fat linked to poor bone density
Supports Chapter 25: Deficiency diseases
New research suggests that body fat may have an impact on bone mineral density.
Results of a study by Kathryn Piehowski, RD, of Pennsylvania State University showed that bone mineral density in normal weight women was higher than in overweight women.
The report suggested that the reasons why fatter women should have a lower bone mineral density were unclear. Piehowski suggests that inflammation may well play a role, as high levels of body fat are associated with greater levels of inflammation, and some inflammatory mediators are known to promote bone loss.
Well, it might. But there may well be another reason. Fatter women tend to be those on calorie controlled, carbohydrate-based diets. These are inevitably low in fat and, as fat comes mainly with protein, low in protein as well. Although women are told that low bone density can be caused by eating a high-protein diet, in fact the opposite is true. The real reason for the low bone density in fatter women, therefore, could well be their reliance on a ‘healthy’ diet
Too Much Body Fat Bad for Bones? WebMD Health News. October 31st 2008.
New research suggests that body fat may have an impact on bone mineral density.
Results of a study by Kathryn Piehowski, RD, of Pennsylvania State University showed that bone mineral density in normal weight women was higher than in overweight women.
The report suggested that the reasons why fatter women should have a lower bone mineral density were unclear. Piehowski suggests that inflammation may well play a role, as high levels of body fat are associated with greater levels of inflammation, and some inflammatory mediators are known to promote bone loss.
Well, it might. But there may well be another reason. Fatter women tend to be those on calorie controlled, carbohydrate-based diets. These are inevitably low in fat and, as fat comes mainly with protein, low in protein as well. Although women are told that low bone density can be caused by eating a high-protein diet, in fact the opposite is true. The real reason for the low bone density in fatter women, therefore, could well be their reliance on a ‘healthy’ diet
Too Much Body Fat Bad for Bones? WebMD Health News. October 31st 2008.
More children being prescribed drugs for obesity-related health problems
Supports pretty much the whole of Trick and Treat!
A new study of chronic medication use in children aged 5 to 19 revealed that the number of prescriptions issued for type 2 diabetes medications more than doubled between 2002 and 2005. In the same period the number of prescriptions for type 2 diabetes medications issued to girls aged 10 to 14 rose by 166%. The use of cholesterol-lowering and anti-hypertensive medications rose by 15% and 1.8%, respectively.
Co-author of the study, Donna R. Halloran, an assistant professor at Saint Louis University School of Medicine, said that the increasing use of chronic medication is mainly due to the increasing prevalence of childhood obesity. She added that the study findings also showed that more children are being diagnosed with chronic conditions, and doctors are increasingly using medication to treat these conditions.
Comment
But these drugs only mitigate and mask the symptoms of these conditions; they do absolutely nothing to stop the causes. As\Trick and Treat shows very clearly, our ‘healthy’ diet is a major contributor to these conditions. That is why they are in creasing at such an alarming rate.
Cox ER, Halloran DR, Homan SM, Welliver S, Mager DE. Trends in the prevalence of chronic medication use in children: 2002-2005. Pediatrics. 2008;122(5):e1053.
A new study of chronic medication use in children aged 5 to 19 revealed that the number of prescriptions issued for type 2 diabetes medications more than doubled between 2002 and 2005. In the same period the number of prescriptions for type 2 diabetes medications issued to girls aged 10 to 14 rose by 166%. The use of cholesterol-lowering and anti-hypertensive medications rose by 15% and 1.8%, respectively.
Co-author of the study, Donna R. Halloran, an assistant professor at Saint Louis University School of Medicine, said that the increasing use of chronic medication is mainly due to the increasing prevalence of childhood obesity. She added that the study findings also showed that more children are being diagnosed with chronic conditions, and doctors are increasingly using medication to treat these conditions.
Comment
But these drugs only mitigate and mask the symptoms of these conditions; they do absolutely nothing to stop the causes. As\Trick and Treat shows very clearly, our ‘healthy’ diet is a major contributor to these conditions. That is why they are in creasing at such an alarming rate.
Cox ER, Halloran DR, Homan SM, Welliver S, Mager DE. Trends in the prevalence of chronic medication use in children: 2002-2005. Pediatrics. 2008;122(5):e1053.
Cases of type 2 diabetes rise by 90%
Supports Chapter 19: ‘Healthy eating’ is fattening, and Chapter 20: Diabetes deceit
The US Centers for Disease Control and Prevention (CDC) have revealed that the number of cases of type 2 diabetes in the US almost doubled within just ten years, from 4.8 people per 1,000 in 1995 -1997 to 9.1 people per thousand in 2005 - 2007.
But this may be a massive underestimation because many people are unaware that they have diabetes until one or more complications rears its ugly head.
The CDC puts the blame for this dramatic rise in type-2 diabetes on the epidemic. They say that type-2 diabetes: "can be prevented or delayed by moderate weight loss and increased physical activity."
This may be right; however, it’s too much carbohydrate in the diet that causes diabetes, just as it causes obesity. That’s things like 6 to 11 portions of starchy foods and five portions of fruit and veg. I wonder how the people who trot out this unhealthy advice will defend themselves when the s**t hits the fan and Trick and Treat gives those harmed by this unhealthy advice the ammunition they need to sue them.
State-Specific Incidence of Diabetes Among Adults -- Participating States, 1995-1997 and 2005-2007. CDC Morbidity and Mortality Weekly Report. 2008;57:1169-1173.
The US Centers for Disease Control and Prevention (CDC) have revealed that the number of cases of type 2 diabetes in the US almost doubled within just ten years, from 4.8 people per 1,000 in 1995 -1997 to 9.1 people per thousand in 2005 - 2007.
But this may be a massive underestimation because many people are unaware that they have diabetes until one or more complications rears its ugly head.
The CDC puts the blame for this dramatic rise in type-2 diabetes on the epidemic. They say that type-2 diabetes: "can be prevented or delayed by moderate weight loss and increased physical activity."
This may be right; however, it’s too much carbohydrate in the diet that causes diabetes, just as it causes obesity. That’s things like 6 to 11 portions of starchy foods and five portions of fruit and veg. I wonder how the people who trot out this unhealthy advice will defend themselves when the s**t hits the fan and Trick and Treat gives those harmed by this unhealthy advice the ammunition they need to sue them.
State-Specific Incidence of Diabetes Among Adults -- Participating States, 1995-1997 and 2005-2007. CDC Morbidity and Mortality Weekly Report. 2008;57:1169-1173.
03 November 2008
Dietary Committee's Industry Ties Ignored
Supports Chapter One: Trick to treat
The US Departments of Agriculture and Health and Human Services failed to tell the public about relevant conflicts of interest on the newly impaneled Dietary Guidelines advisory committee, which a year from now will recommend changes to the government's daily food intake advice.
A Center for Science in the Public Interest analysis reveals that nearly half the roster's 13 members have taken funding from the food and pharmaceutical industries.
None of those industry ties were disclosed by the government; and, according to Robert Post, director of the Center for Nutrition Policy and Promotion, none received waivers declaring that their expertise was needed to round out the committee, which the law requires before scientists with conflicts of interest can serve on federal advisory committees.
When it comes to it, it's pretty obvious that their wealth is much more important than your health.
http://takeaction.cspinet.org/
The US Departments of Agriculture and Health and Human Services failed to tell the public about relevant conflicts of interest on the newly impaneled Dietary Guidelines advisory committee, which a year from now will recommend changes to the government's daily food intake advice.
A Center for Science in the Public Interest analysis reveals that nearly half the roster's 13 members have taken funding from the food and pharmaceutical industries.
None of those industry ties were disclosed by the government; and, according to Robert Post, director of the Center for Nutrition Policy and Promotion, none received waivers declaring that their expertise was needed to round out the committee, which the law requires before scientists with conflicts of interest can serve on federal advisory committees.
When it comes to it, it's pretty obvious that their wealth is much more important than your health.
http://takeaction.cspinet.org/
'Healthy' carbs increase cancer risk
Supports Chapter 8: Why 'five portions'? and Chapter 23: Cancer: Disease of civilization.
Scientists at the German Cancer Research Center (DKFZ), Heidelberg, Germany have published a review of some key biological mechanisms that may provide important metabolic links between nutrition, physical activity and cancer.
These include insulin resistance and reduced glucose tolerance, which are caused by eating a 'healthy' carbohydrate-based diet.
Also included are increased activation of the growth hormone/IGF-I axis, alterations in sex-steroid synthesis and/or bioavailability, and low-grade chronic inflammation through the effects of adipokines and cytokines.
These, too, may be adversely affected by our so-called 'healthy' lifestyle. For example, cholesterol is a major building block in the production of the sex hormones; inflammation may be caused by any form of stress which raises levels of cortisol in the blood as well as high levels of glucose and insulin.
This latest study confirms several earlier studies which have found that a carb-based diet increaes the risk of several types of cancer – and significantly, the ones that are now on the increase.
Dossus L, Kaaks R. Nutrition, metabolic factors and cancer risk. Best Pract Res Clin Endocrinol Metab. 2008; 22: 551-71.
PMID: 18971118
Scientists at the German Cancer Research Center (DKFZ), Heidelberg, Germany have published a review of some key biological mechanisms that may provide important metabolic links between nutrition, physical activity and cancer.
These include insulin resistance and reduced glucose tolerance, which are caused by eating a 'healthy' carbohydrate-based diet.
Also included are increased activation of the growth hormone/IGF-I axis, alterations in sex-steroid synthesis and/or bioavailability, and low-grade chronic inflammation through the effects of adipokines and cytokines.
These, too, may be adversely affected by our so-called 'healthy' lifestyle. For example, cholesterol is a major building block in the production of the sex hormones; inflammation may be caused by any form of stress which raises levels of cortisol in the blood as well as high levels of glucose and insulin.
This latest study confirms several earlier studies which have found that a carb-based diet increaes the risk of several types of cancer – and significantly, the ones that are now on the increase.
Dossus L, Kaaks R. Nutrition, metabolic factors and cancer risk. Best Pract Res Clin Endocrinol Metab. 2008; 22: 551-71.
PMID: 18971118
01 November 2008
Patients With Parkinson's and Alzheimer's Diseases need vitamin D
Supports Chapter 11: Our irrational fear of sunlight, and Chapter 26: Diet and the brain
A study by researchers at Emory University School of Medicine published in October 2008 compared the amount of vitamin D, which we get from sunlight, and the prevalence of Parkinson's and Alzheimer's diseases with the amounts of vitamin D in healthy people. The study was over a 15-year period.
What it found was that people suffering these two distressing and debilitating diseases was that they had significantly lower levels of vitamin D than healthy people.
Although the researchers call for more research to be done, it has really been quite obvious for some years that one aspect of prevention of these diseases is to get out in the sun as much as possible. This is particularly important if you live in higher latitudes such as northern Europe, the northern states of the US or Canada. This new study adds weight to what I wrote in Trick and Treat.
Evatt ML, et al .Prevalence of Vitamin D Insufficiency in Patients With Parkinson Disease and Alzheimer Disease. Arch Neurol. 2008;65:1348-1352.
PMID: 18852350
A study by researchers at Emory University School of Medicine published in October 2008 compared the amount of vitamin D, which we get from sunlight, and the prevalence of Parkinson's and Alzheimer's diseases with the amounts of vitamin D in healthy people. The study was over a 15-year period.
What it found was that people suffering these two distressing and debilitating diseases was that they had significantly lower levels of vitamin D than healthy people.
Although the researchers call for more research to be done, it has really been quite obvious for some years that one aspect of prevention of these diseases is to get out in the sun as much as possible. This is particularly important if you live in higher latitudes such as northern Europe, the northern states of the US or Canada. This new study adds weight to what I wrote in Trick and Treat.
Evatt ML, et al .Prevalence of Vitamin D Insufficiency in Patients With Parkinson Disease and Alzheimer Disease. Arch Neurol. 2008;65:1348-1352.
PMID: 18852350
Low-carb, high-fat should be the preferred diet for diabetics
Supports Chapter 14: The Metabolic syndrome and the glycaemic index, and Chapter 20: Diabetes deceit
A new paper looking at diet in the treatment of diabetes and the metabolic syndrome points out that there is a better way to treat both conditions than the 'healthy' carbohydrate-based, low-fat diet currently recommended. It reverses current guidelines as it recommends reducing carbs and increasing fats, particularly animal fats.
The authors say:
This means that there should be no concern about dietary fat, and that carbohydrate restriction the preferred method for treating type 2 diabetes and metabolic syndrome.
The authors: "emphasize the ability of low carbohydrate diets to improve glycemic control, hemoglobin A1C and to reduce medication."
Which, of course, is what diabetics want. No doubt it will be strongly opposed by the diabetes and drugs industries.
Feinman RD, Volek JS. Carbohydrate restriction as the default treatment for type 2 diabetes and metabolic syndrome. Scandinavian Cardiovascular Journal 2008; 42: 256 - 263.
DOI: 10.1080/14017430802014838
A new paper looking at diet in the treatment of diabetes and the metabolic syndrome points out that there is a better way to treat both conditions than the 'healthy' carbohydrate-based, low-fat diet currently recommended. It reverses current guidelines as it recommends reducing carbs and increasing fats, particularly animal fats.
The authors say:
"Dietary carbohydrate restriction in the treatment of diabetes and metabolic syndrome is based on an underlying principle of control of insulin secretion and the theory that insulin resistance is a response to chronic hyperglycemia and hyperinsulinemia. As such, the theory is intuitive and has substantial experimental support.The paper then summarises the available evidence and shows that, in fact, substituting fat for carbohydrate actually improves cardiovascular risk factors.
"It has generally been opposed by health agencies because of concern that carbohydrate will be replaced by fat, particularly saturated fat, thereby increasing the risk of cardiovascular disease as dictated by the so-called diet-heart hypothesis."
This means that there should be no concern about dietary fat, and that carbohydrate restriction the preferred method for treating type 2 diabetes and metabolic syndrome.
The authors: "emphasize the ability of low carbohydrate diets to improve glycemic control, hemoglobin A1C and to reduce medication."
Which, of course, is what diabetics want. No doubt it will be strongly opposed by the diabetes and drugs industries.
Feinman RD, Volek JS. Carbohydrate restriction as the default treatment for type 2 diabetes and metabolic syndrome. Scandinavian Cardiovascular Journal 2008; 42: 256 - 263.
DOI: 10.1080/14017430802014838
30 October 2008
Arthritis patients face increased risk of mood disorders
Supports Chapter 25: Deficiency diseases and Chapter 26: Diet and the brain
The results of a world-wide study confirm that people with arthritis are more likely to suffer from mood disorders and other mental health conditions than other people.
Researchers from Shanghai Mental Health Center in China studied data from a health survey of more than 85,000 adults in 17 countries in the Americas, Europe, the Middle East, Africa, Asia and the South Pacific. They specifically assessed associations between arthritis and the prevalence of anxiety, mood and alcohol use disorders.
They found that people with arthritis were almost twice as likely to suffer from mood and anxiety disorders as those without arthritis. This was similar across all the countries studied.
It could be argued that people who suffer the pain and discomfort of arthritis are more likely to be depressed than people who aren't, but there is also a dietary component: This study adds weight to others that show that both conditions may be caused or exacerbated by eating the same 'healthy' diet. That is one which is based on cereal grains in foods such as bread, and is low in fat.
He Y, et al. Mental disorders among persons with arthritis: results from the World Mental Health Surveys. Psychol Med 2008; 38: 1639-1650. doi:10.1017/S0033291707002474
The results of a world-wide study confirm that people with arthritis are more likely to suffer from mood disorders and other mental health conditions than other people.
Researchers from Shanghai Mental Health Center in China studied data from a health survey of more than 85,000 adults in 17 countries in the Americas, Europe, the Middle East, Africa, Asia and the South Pacific. They specifically assessed associations between arthritis and the prevalence of anxiety, mood and alcohol use disorders.
They found that people with arthritis were almost twice as likely to suffer from mood and anxiety disorders as those without arthritis. This was similar across all the countries studied.
It could be argued that people who suffer the pain and discomfort of arthritis are more likely to be depressed than people who aren't, but there is also a dietary component: This study adds weight to others that show that both conditions may be caused or exacerbated by eating the same 'healthy' diet. That is one which is based on cereal grains in foods such as bread, and is low in fat.
He Y, et al. Mental disorders among persons with arthritis: results from the World Mental Health Surveys. Psychol Med 2008; 38: 1639-1650. doi:10.1017/S0033291707002474
Eating fruit may increase heart attack risk
Supports Chapters 8: Why 'five portions', and Chapter 21: Diseases of the heart and blood vessels
Dr Hans Selye first proposed that stress may be a cause of heart attacks back in 1950. There is now a considerable body of evidence to support this hypothesis, but the mechanism has been obscure.
There is also a hypothesis that a low pH in the blood (denoting acidity) increases cardiac risk. So we are told to avoid eating 'acid forming' foods such as meat, fats and dairy, and eat more 'alkaline foods' such as fruit and vegetables.
A recent hypothesis by Dr Carlos Monteiro in Brazil may have the answer - and it turns current acid/alkaline foods hypothesis advice on its head.
We have lived by eating meat and its 'saturated' fat for the whole of our existence as a species; ischaemic heart disease, against which 'healthy eating' is targeted, only 'took off' in the 20th century. The idea that our traditional diet should suddenly become the cause of this modern disease is a fraud and a delusion. Yet it is the sole basis for the current paradigm. It is also the basis for the 'acid/alkaline' theory.
But there is an acid that can lower pH in the blood and cause harm, and that is lactic acid. It’s not ingested lactic acid but produced by the body in response to stress. We live now in stressful times, where our 'fight-or-flight' reflex must be working overtime. A principal result of such stresses is increased levels of lactic acid in the blood.
A 'healthy' diet of glucose, fructose and other sugars from carbohydrates also raises blood lactic acid as a by-product of the metabolism of glucose for energy from dietary carbohydrates. The worst of these is the fruit sugar, fructose, which increases blood pressure and other heart attack risk factors.
If a low-carb, high-fat diet is adopted, that naturally reduces lactic acid production from anaerobic metabolism of glucose by increasing aerobic metabolism of fats for energy.
Carlos ETB Monteiro. Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project at http://www.infarctcombat.org/AcidityTheory.pdf
Dr Hans Selye first proposed that stress may be a cause of heart attacks back in 1950. There is now a considerable body of evidence to support this hypothesis, but the mechanism has been obscure.
There is also a hypothesis that a low pH in the blood (denoting acidity) increases cardiac risk. So we are told to avoid eating 'acid forming' foods such as meat, fats and dairy, and eat more 'alkaline foods' such as fruit and vegetables.
A recent hypothesis by Dr Carlos Monteiro in Brazil may have the answer - and it turns current acid/alkaline foods hypothesis advice on its head.
We have lived by eating meat and its 'saturated' fat for the whole of our existence as a species; ischaemic heart disease, against which 'healthy eating' is targeted, only 'took off' in the 20th century. The idea that our traditional diet should suddenly become the cause of this modern disease is a fraud and a delusion. Yet it is the sole basis for the current paradigm. It is also the basis for the 'acid/alkaline' theory.
But there is an acid that can lower pH in the blood and cause harm, and that is lactic acid. It’s not ingested lactic acid but produced by the body in response to stress. We live now in stressful times, where our 'fight-or-flight' reflex must be working overtime. A principal result of such stresses is increased levels of lactic acid in the blood.
A 'healthy' diet of glucose, fructose and other sugars from carbohydrates also raises blood lactic acid as a by-product of the metabolism of glucose for energy from dietary carbohydrates. The worst of these is the fruit sugar, fructose, which increases blood pressure and other heart attack risk factors.
If a low-carb, high-fat diet is adopted, that naturally reduces lactic acid production from anaerobic metabolism of glucose by increasing aerobic metabolism of fats for energy.
Carlos ETB Monteiro. Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project at http://www.infarctcombat.org/AcidityTheory.pdf
25 October 2008
Low carb diet found to lower insulin levels
Supports Chapter 14: The metabolic syndrome and the glycaemic index; and Chapter 20: Diabetes deceit
If you want a long and healthy life, without diseases such as diabetes with its wide range of complications, you need to ensure stability in blood sugar and insulin levels. This means that foods such as meat, fish, eggs and green vegetables, which don't disrupt blood sugar (and therefore insulin) levels, are the ones you should eat.
This concept of controlling carb intake is not considered 'healthy' by the establishment, who want to profit from diabetes. But its not just relevant for diabetics, but also for those who would prefer not to develop diabetes.
A recent study tested the effects of low-carb and low fat (and higher carb) diets in a group of obese adolescents aged 12-18.it showed that the high-fat, low carbohydrate diet out-performed the low fat one in critical areas: insulin levels were lower in those eating a lower carb diet; as was insulin resistance and beta-cell exhaustion.
In other words, those adolescents on a lower carb diet saw improvements in their biochemistry which would, generally speaking, put them at reduced risk of developing type 2 diabetes over time.
This evidence is in line with other research which has found that the consumption of blood sugar-disruptive 'healthy' carbohydrate-based diets arer associated with an increased risk of diabetes.
Demol S, et al. Low-carbohydrate (low & high-fat) versus high-carbohydrate low-fat diets in the treatment of obesity in adolescents. Acta Paediatr. 2008 Sep 29. [Epub ahead of print] [PMID: 1882649]
If you want a long and healthy life, without diseases such as diabetes with its wide range of complications, you need to ensure stability in blood sugar and insulin levels. This means that foods such as meat, fish, eggs and green vegetables, which don't disrupt blood sugar (and therefore insulin) levels, are the ones you should eat.
This concept of controlling carb intake is not considered 'healthy' by the establishment, who want to profit from diabetes. But its not just relevant for diabetics, but also for those who would prefer not to develop diabetes.
A recent study tested the effects of low-carb and low fat (and higher carb) diets in a group of obese adolescents aged 12-18.it showed that the high-fat, low carbohydrate diet out-performed the low fat one in critical areas: insulin levels were lower in those eating a lower carb diet; as was insulin resistance and beta-cell exhaustion.
In other words, those adolescents on a lower carb diet saw improvements in their biochemistry which would, generally speaking, put them at reduced risk of developing type 2 diabetes over time.
This evidence is in line with other research which has found that the consumption of blood sugar-disruptive 'healthy' carbohydrate-based diets arer associated with an increased risk of diabetes.
Demol S, et al. Low-carbohydrate (low & high-fat) versus high-carbohydrate low-fat diets in the treatment of obesity in adolescents. Acta Paediatr. 2008 Sep 29. [Epub ahead of print] [PMID: 1882649]
24 October 2008
Breakfast cereals can damage children and make them fat
Supports Chapter 18: Prevention is better; Chapter 19: 'Healthy eating' is fattening
It's not surprising that today's children are become so obese. On average, sugar accounts for more than one-third of the weight of children's cereals compared to less than one-quarter of adult cereals. Some breakfast cereals aimed children are two-thirds sugar. Even the rest is composed of starch, a carbohydrate which the digestion converts into sugar.[1]
Yet the 'health industry' labels these as 'healthy'!
Schwartz MB, Vartanian LR, Wharton CM, Brownell KD. Examining the nutritional quality of breakfast cereals marketed to children. J Am Diet Assoc 2008; 108:702-5. (PMID: 18375229)
It's not surprising that today's children are become so obese. On average, sugar accounts for more than one-third of the weight of children's cereals compared to less than one-quarter of adult cereals. Some breakfast cereals aimed children are two-thirds sugar. Even the rest is composed of starch, a carbohydrate which the digestion converts into sugar.[1]
Yet the 'health industry' labels these as 'healthy'!
Schwartz MB, Vartanian LR, Wharton CM, Brownell KD. Examining the nutritional quality of breakfast cereals marketed to children. J Am Diet Assoc 2008; 108:702-5. (PMID: 18375229)
23 October 2008
Trick and Treat goes to Number One on Amazon - over a week before publication
The official publication date for Trick and Treat: How 'healthy eating' is making us ill is 30 October 2008 in the UK.
Following the first article about Trick and Treat in the Telegraph on Monday, 20 October, Trick and Treat shot right up to Number One in Amazon.co.uk's Public Health and Preventive Medicine category, and 158 overall.
http://www.amazon.co.uk/Trick-Treat-Healthy-Eating-Making/dp/1905140223/ref=sr_1_1?ie=UTF8&s=books&qid=1224686093&sr=1-1
Following the first article about Trick and Treat in the Telegraph on Monday, 20 October, Trick and Treat shot right up to Number One in Amazon.co.uk's Public Health and Preventive Medicine category, and 158 overall.
http://www.amazon.co.uk/Trick-Treat-Healthy-Eating-Making/dp/1905140223/ref=sr_1_1?ie=UTF8&s=books&qid=1224686093&sr=1-1
22 October 2008
Lipitor advertising misleading over lack of benefits for women.
Supports Chapter One: Trick to Treat
Experts in epidemiology and law claim that in the advertising of the world’s best selling drug, Lipitor (atorvastatin), its manufacturer, Pfizer, failed to disclose the fact that there are no known benefits for women in taking the drug.
They argue that unqualified claims of protection against heart attacks made in advertisements for Lipitor may be misleading and that this advertising raises concerns about the way the US Food and Drug Administration regulates drugs.
The authors, Theodore Eisenberg, a professor of law at Cornell Law School, and Martin Wells, professor of clinical epidemiology at Cornell University Weill Medical College, claim that a substantial portion of the multibillion dollar market in statins may be made up of users for whom the drugs offer no benefit.
They say that women prescribed the Lipitor should be entitled to compensation to recoup the costs of treatment. The same should also apply to other statins, of course, as no study of cholesterol-lowering in women - by any drug - has shown a benefit.
Eisenberg T, Wells MT. Statins and Adverse Cardiovascular Events in Moderate-Risk Females: A Statistical and Legal Analysis with Implications for FDA Preemption Claims. Journal of Empirical Legal Studies 2008 Sep 5;5(3):507 - 550 (doi:10.1111/j.1740-1461.2008.00132.x)
Experts in epidemiology and law claim that in the advertising of the world’s best selling drug, Lipitor (atorvastatin), its manufacturer, Pfizer, failed to disclose the fact that there are no known benefits for women in taking the drug.
They argue that unqualified claims of protection against heart attacks made in advertisements for Lipitor may be misleading and that this advertising raises concerns about the way the US Food and Drug Administration regulates drugs.
The authors, Theodore Eisenberg, a professor of law at Cornell Law School, and Martin Wells, professor of clinical epidemiology at Cornell University Weill Medical College, claim that a substantial portion of the multibillion dollar market in statins may be made up of users for whom the drugs offer no benefit.
They say that women prescribed the Lipitor should be entitled to compensation to recoup the costs of treatment. The same should also apply to other statins, of course, as no study of cholesterol-lowering in women - by any drug - has shown a benefit.
Eisenberg T, Wells MT. Statins and Adverse Cardiovascular Events in Moderate-Risk Females: A Statistical and Legal Analysis with Implications for FDA Preemption Claims. Journal of Empirical Legal Studies 2008 Sep 5;5(3):507 - 550 (doi:10.1111/j.1740-1461.2008.00132.x)
Aspirin should not routinely be used to prevent heart attacks in diabetics
Supports Chapter 20: Diabetes deceit
Aspirin should not be routinely prescribed to diabetics for the prevention of heart attack and stroke, say researchers.
The Prevention of Progression of Arterial Disease and Diabetes (POPADAD) Trial involved 1,276 people with type 1 or type 2 diabetes who had no symptoms of coronary heart disease. Participants had either a daily 100 mg aspirin tablet plus antioxidant capsule, an aspirin tablet plus placebo capsule, a placebo tablet plus antioxidant capsule, or a placebo tablet plus placebo capsule.
Results showed that aspirin – whether taken alone or in combination with an antioxidant capsule – did not significantly reduce the risk of death from coronary heart disease or stroke, or non-fatal myocardial infarction or stroke.
The researchers conclude: “This trial does not provide evidence to support the use of aspirin or antioxidants in primary prevention of cardiovascular events and mortality.”
Let's face it, as Type-2 diabetes is so easily and quickly rectified merely by a change of diet, why take risks with any drugs?
Belch J, MacCuish A, Campbell I, et al. The prevention of progression of arterial disease and diabetes (POPADAD) trial: factorial randomised placebo controlled trial of aspirin and antioxidants in patients with diabetes and asymptomatic peripheral arterial disease. BMJ 2008;337:a1840. doi: 10.1136/bmj.a1840
Aspirin should not be routinely prescribed to diabetics for the prevention of heart attack and stroke, say researchers.
The Prevention of Progression of Arterial Disease and Diabetes (POPADAD) Trial involved 1,276 people with type 1 or type 2 diabetes who had no symptoms of coronary heart disease. Participants had either a daily 100 mg aspirin tablet plus antioxidant capsule, an aspirin tablet plus placebo capsule, a placebo tablet plus antioxidant capsule, or a placebo tablet plus placebo capsule.
Results showed that aspirin – whether taken alone or in combination with an antioxidant capsule – did not significantly reduce the risk of death from coronary heart disease or stroke, or non-fatal myocardial infarction or stroke.
The researchers conclude: “This trial does not provide evidence to support the use of aspirin or antioxidants in primary prevention of cardiovascular events and mortality.”
Let's face it, as Type-2 diabetes is so easily and quickly rectified merely by a change of diet, why take risks with any drugs?
Belch J, MacCuish A, Campbell I, et al. The prevention of progression of arterial disease and diabetes (POPADAD) trial: factorial randomised placebo controlled trial of aspirin and antioxidants in patients with diabetes and asymptomatic peripheral arterial disease. BMJ 2008;337:a1840. doi: 10.1136/bmj.a1840
We should get out in the sun more - in the middle of the day
Supports Chapter 11: Our irrational fear of sunshine
Health recommendations are that we should avoid sun exposure for three to five hours around noon because of the skin cancer risk. But a group of doctors at the Institute for Cancer Research, Montebello, Oslo, Norway, say this may be wrong and may even promote melanoma. They have determined that, to get an optimal vitamin D from the sun at a minimal risk of getting malignant melanoma, around noon the best time to go out in the sun exposure. This add weight to the studies in Trick and Treat (click above for the abstract)
This would give a maximal yield of vitamin D at a minimal CMM risk.
Moan J, Dahlback A, Porojnicu AC. At what time should one go out in the sun? Adv Exp Med Biol. 2008; 624: 86-8
12 October 2008
High cholesterol is better for memory
Supports Chapter 26: Diet and the brain
High cholesterol is better for memory and cognitive function in the elderly
A study assessed cognitive function and cholesterol levels in 185 participants between the ages of 85 and 101. These participants were recruited from the New York City area.
Bloods were drawn to assess total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol, as well as for APOE genotyping.
In contrast to the researchers' expectations, they found that "high total cholesterol and high LDL cholesterol were associated with higher memory scores for noncarriers of the APOE4 allele. No significant associations between cognitive performance and lipid profile were found for carriers of the APOE4 allele."
High cholesterol in individuals above the age of 79 has actually been found to be associated with reduced risk of dementia.
High total cholesterol has also been correlated with a lower risk of mortality in the elderly. It may be conjectured that high levels of cholesterol suggests better health than that of individuals with lower levels of cholesterol.
They concluded that "high cholesterol is associated with better memory function."
West R, Schnaider Beeri M, Schmeidler J, et al. Better Memory Functioning Associated With Higher Total and Low-Density Lipoprotein Cholesterol Levels in Very Elderly Subjects Without the Apolipoprotein e4 Allele. Am J Geriatr Psychiatry 2008;16:781–785
High cholesterol is better for memory and cognitive function in the elderly
A study assessed cognitive function and cholesterol levels in 185 participants between the ages of 85 and 101. These participants were recruited from the New York City area.
Bloods were drawn to assess total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol, as well as for APOE genotyping.
In contrast to the researchers' expectations, they found that "high total cholesterol and high LDL cholesterol were associated with higher memory scores for noncarriers of the APOE4 allele. No significant associations between cognitive performance and lipid profile were found for carriers of the APOE4 allele."
High cholesterol in individuals above the age of 79 has actually been found to be associated with reduced risk of dementia.
High total cholesterol has also been correlated with a lower risk of mortality in the elderly. It may be conjectured that high levels of cholesterol suggests better health than that of individuals with lower levels of cholesterol.
They concluded that "high cholesterol is associated with better memory function."
West R, Schnaider Beeri M, Schmeidler J, et al. Better Memory Functioning Associated With Higher Total and Low-Density Lipoprotein Cholesterol Levels in Very Elderly Subjects Without the Apolipoprotein e4 Allele. Am J Geriatr Psychiatry 2008;16:781–785
Carbs cause obesity
Supports Chapter 20: Healthy eating is fattening
Carbs may destroy appetite regulation over time
People who eat diets high in carbs and sugar may lose their natural ability to regulate their appetite, researchers warned today. The ability to regulate appetite may decline with age depending on what is eaten, new research suggests.
A team from Monash University in Victoria, Australia, say that appetite-suppressing cells are attacked by free radicals after eating. This degeneration is more significant after meals high in carbohydrates and sugars.
People who consume more carbohydrates and sugars experience more damage to their appetite-control cells, which could result in over-eating and weight gain, the researchers believe.
Dr Zane Andrews, the lead author, says that the damage to appetite suppressing cells creates a cellular imbalance between our need to eat and signals to the brain to stop eating. "People in the age group of 25 to 50 are most at risk," he said. "The neurons that tell people in this crucial age range not to over-eat are being killed-off.
"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMCs kick in. However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied."
It could therefore play an important role in adult-onset obesity. Dr Andrews said. "A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration."
These findings were published in the journal Nature. The team are now looking at whether carbohydrates and sugars affect the brain in other ways, including risk of neurological conditions such as Parkinson's disease.
Andrews ZB, et al. UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals. Nature 454, 846 - 851 (30 Jul 2008), doi: 10.1038/nature07181,
Carbs may destroy appetite regulation over time
People who eat diets high in carbs and sugar may lose their natural ability to regulate their appetite, researchers warned today. The ability to regulate appetite may decline with age depending on what is eaten, new research suggests.
A team from Monash University in Victoria, Australia, say that appetite-suppressing cells are attacked by free radicals after eating. This degeneration is more significant after meals high in carbohydrates and sugars.
People who consume more carbohydrates and sugars experience more damage to their appetite-control cells, which could result in over-eating and weight gain, the researchers believe.
Dr Zane Andrews, the lead author, says that the damage to appetite suppressing cells creates a cellular imbalance between our need to eat and signals to the brain to stop eating. "People in the age group of 25 to 50 are most at risk," he said. "The neurons that tell people in this crucial age range not to over-eat are being killed-off.
"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMCs kick in. However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied."
It could therefore play an important role in adult-onset obesity. Dr Andrews said. "A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration."
These findings were published in the journal Nature. The team are now looking at whether carbohydrates and sugars affect the brain in other ways, including risk of neurological conditions such as Parkinson's disease.
Andrews ZB, et al. UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals. Nature 454, 846 - 851 (30 Jul 2008), doi: 10.1038/nature07181,
11 October 2008
Welcome to Trick and Treat
The Second Opinions website started as a collection of articles. For about 10 years, I had been researching the role of foods in a number of 'diseases of civilisation' — mostly heart disease and obesity at that time — and it had become very obvious that what our governments, as well as doctors, dieticians and nutritionists were telling us had very little basis is any coherent body of evidence; in fact all the evidence tended to point the other way. This meant that the conditions the dietary recommendations were meant to benefit, would probably get worse rather than better. And that is what did happen and that is what is still happening as the numbers of cases of diseases such as obesity and diabetes have risen dramatically since 'healthy eating' was introduced in the 1980s.
It seemed that the only way to reach a lot of people and let them know what was going on, was either to write a book or to write a website. I have ended up doing both.
I started writing my latest book, Trick and Treat: How 'healthy eating is making us ill, in 1989. I called it Diet and be Damned. The publisher, Hodder Headline, told me they thought it was too important a book to publish as I was then an unknown author; they advised me to write a 'diet book'. I have written three since then, as well as other, more technical works.
Now, 19 years after I first conceived it, the health situation has become so bad in western countries, as 'Big-Pharma' and 'Big-Food' have assumed control of our health for their profit, that I decided I must finish what I had started almost two decades ago. 2008 also marks the 60th anniversary of the British National Health Service (NHS). What better time could there be for such a book as Trick and Treat.
Trick and Treat
This title is a play on words with the title of the American children's 'extortion with menaces' game, trick or treat. But where trick or treat gives its victims a choice, the modern 'health industry' does not. With them it is both Trick and Treat. The health industry needs us to be ill so that it can profit fby it. For this reason, they trick us into an unhealthy lifestyle so that they can treat the resultant illnesses.
Stop Press
The problem with a book like this is that it is finished quite some time before it is published. The purpose of this blog is to list some of the supportive studies and evidence published after Trick and Treat was finished.
It seemed that the only way to reach a lot of people and let them know what was going on, was either to write a book or to write a website. I have ended up doing both.
I started writing my latest book, Trick and Treat: How 'healthy eating is making us ill, in 1989. I called it Diet and be Damned. The publisher, Hodder Headline, told me they thought it was too important a book to publish as I was then an unknown author; they advised me to write a 'diet book'. I have written three since then, as well as other, more technical works.
Now, 19 years after I first conceived it, the health situation has become so bad in western countries, as 'Big-Pharma' and 'Big-Food' have assumed control of our health for their profit, that I decided I must finish what I had started almost two decades ago. 2008 also marks the 60th anniversary of the British National Health Service (NHS). What better time could there be for such a book as Trick and Treat.
Trick and Treat
This title is a play on words with the title of the American children's 'extortion with menaces' game, trick or treat. But where trick or treat gives its victims a choice, the modern 'health industry' does not. With them it is both Trick and Treat. The health industry needs us to be ill so that it can profit fby it. For this reason, they trick us into an unhealthy lifestyle so that they can treat the resultant illnesses.
Stop Press
The problem with a book like this is that it is finished quite some time before it is published. The purpose of this blog is to list some of the supportive studies and evidence published after Trick and Treat was finished.
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