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
30 November 2008
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
Subscribe to:
Posts (Atom)