Archive for December, 2010

MEDICAL NUTRITION THERAPY FOR TYPE I DIABETES

For patients with type I diabetes, medical nutrition therapy should emphasize the interrelationships among food, exercise, and insulin. Those receiving conventional insulin therapy must maintain consistency in the timing and amount of their food intake. Ideally, the insulin plan should be designed to match the patient’s preferred eating pattern. Earlier, the nutrition recommendations were for total calories and carbohydrates to be ‘fractionated’ between meals and snacks based on the insulin regimen. This is no longer recommended because it does not promote individualization. However, the timing of food intake should be synchronized with the administration of insulin. Because of the limitations of a conventional insulin regimen (i.e., 1 to 2 insulin injections per day), patients on such a regimen may need to alter their usual eating habits by incorporating consistency with timing and amounts of food.
Patients receiving intensive insulin therapy, i.e., multiple daily injections or pump infusion, have considerable flexibility in when and what to eat. Nevertheless, they too need to integrate their insulin regimen with their lifestyle and adjust the insulin doses when they deviate from their usual eating and exercise patterns. These patients can adjust their pre-meal insulin dose to compensate for deviation from their meal plan and exercise programme. Even with the increase in flexibility, the more consistent they are with their eating and physical activity, the easier is the overall management.
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MEDICAL NUTRITION THERAPY FOR TYPE I DIABETESFor patients with type I diabetes, medical nutrition therapy should emphasize the interrelationships among food, exercise, and insulin. Those receiving conventional insulin therapy must maintain consistency in the timing and amount of their food intake. Ideally, the insulin plan should be designed to match the patient’s preferred eating pattern. Earlier, the nutrition recommendations were for total calories and carbohydrates to be ‘fractionated’ between meals and snacks based on the insulin regimen. This is no longer recommended because it does not promote individualization. However, the timing of food intake should be synchronized with the administration of insulin. Because of the limitations of a conventional insulin regimen (i.e., 1 to 2 insulin injections per day), patients on such a regimen may need to alter their usual eating habits by incorporating consistency with timing and amounts of food.Patients receiving intensive insulin therapy, i.e., multiple daily injections or pump infusion, have considerable flexibility in when and what to eat. Nevertheless, they too need to integrate their insulin regimen with their lifestyle and adjust the insulin doses when they deviate from their usual eating and exercise patterns. These patients can adjust their pre-meal insulin dose to compensate for deviation from their meal plan and exercise programme. Even with the increase in flexibility, the more consistent they are with their eating and physical activity, the easier is the overall management.*3/356/5*

Posted on December 28th, 2010 by admin  |  No Comments »

REDUCING YOUR RISK OF CORONARY ARTERY DISEASE: ELEVATED CHOLESTEROL – THE NATURE OF CHOLESTEROL

The main types of lipoproteins are low-density  lipoprotein  (LDL)  and high-density lipoprotein (HDL). They are often referred to as LDL cholesterol and HDL cholesterol. HDL contains almost 50 percent protein and 20 percent cholesterol; LDL contains about 25 percent protein and 45 percent cholesterol. Another type of lipoprotein,   very low-density  lipoprotein (VLDL), contains mostly triglyceride and small amounts of protein and cholesterol.
The function of LDL is to transport cholesterol to sites throughout the body where it is used to repair the membranes of cells is deposited. Thus, LDL tends to promote accumulation of cholesterol in the walls of your arteries, somewhat in the manner that hard water promotes a buildup of lime inside the plumbing of your house. However, cholesterol deposits are spotty, rather than an even coating throughout the “pipes.”
HDL, however, mainly has the task of carrying cholesterol to the liver, where it is alerted and removed from the body. In a sense, HDL is like a “clean-up” crew that sops up excess cholesterol in the system and disposes of it before it can do any damage by accumulating where it is not needed.
LDL cholesterol is mainly to blame for the risk that is associated with cholesterol. The opposite is true for HDL cholesterol: because it works to eliminate excess cholesterol, the more HDL you have, the less cholesterol will deposit in atherosclerotic plaques. Therefore, a relatively low ratio of LDL to HDL is desirable for lowering your risk for development of coronary artery disease.
The role of very low-density lipoprotein (VLDL) cholesterol predetermining the risk of coronary artery disease is not well defined. A high level of VLDL seems to be an independent risk factor in women, but not in men._A high level of tryglicerides responds to a high level of VLDL cholesterol.
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REDUCING YOUR RISK OF CORONARY ARTERY DISEASE: ELEVATED CHOLESTEROL – THE NATURE OF CHOLESTEROLThe main types of lipoproteins are low-density  lipoprotein  (LDL)  and high-density lipoprotein (HDL). They are often referred to as LDL cholesterol and HDL cholesterol. HDL contains almost 50 percent protein and 20 percent cholesterol; LDL contains about 25 percent protein and 45 percent cholesterol. Another type of lipoprotein,   very low-density  lipoprotein (VLDL), contains mostly triglyceride and small amounts of protein and cholesterol.The function of LDL is to transport cholesterol to sites throughout the body where it is used to repair the membranes of cells is deposited. Thus, LDL tends to promote accumulation of cholesterol in the walls of your arteries, somewhat in the manner that hard water promotes a buildup of lime inside the plumbing of your house. However, cholesterol deposits are spotty, rather than an even coating throughout the “pipes.”HDL, however, mainly has the task of carrying cholesterol to the liver, where it is alerted and removed from the body. In a sense, HDL is like a “clean-up” crew that sops up excess cholesterol in the system and disposes of it before it can do any damage by accumulating where it is not needed.LDL cholesterol is mainly to blame for the risk that is associated with cholesterol. The opposite is true for HDL cholesterol: because it works to eliminate excess cholesterol, the more HDL you have, the less cholesterol will deposit in atherosclerotic plaques. Therefore, a relatively low ratio of LDL to HDL is desirable for lowering your risk for development of coronary artery disease.The role of very low-density lipoprotein (VLDL) cholesterol predetermining the risk of coronary artery disease is not well defined. A high level of VLDL seems to be an independent risk factor in women, but not in men._A high level of tryglicerides responds to a high level of VLDL cholesterol.*239\252\8*

Posted on December 21st, 2010 by admin  |  No Comments »

WE REALLY ARE LIVING IN SEA OF CHEMICALS

In the last twenty years, the number of toxic chemicals sprayed on cereal crops has trebled in areas of intensive farming. Around 80 per cent of arable fields are regularly coated with up to thirty-six herbicides, fungicides and insecticides. While the total weight of chemicals has dropped, the overall number has risen. This is more sinister than it sounds because while the effects on health of individual compounds are measured, the cumulative effect of a number of chemicals is little understood. The combined effect is suspected of having a stronger carcinogenic impact than that of single chemicals, in the same way that the combined effect of pesticides and other chemicals is suspected to be a strong contributor to ‘Gulf War Syndrome’. Professor Ashford, health adviser to the United Nations, has said, ‘It is not a question of a single substance poisoning an organism, but rather a multi-stage process which interferes with the whole system.’ The rise in the number of chemicals sprayed has been synonymous with a sharp decline in many species of wild birds. This is partly due to their natural food not being available, the grubs and insects having been killed off, but they are also unable to tolerate the chemical load. And for some reason the authorities who license the use of these chemicals expect us to be able to cope with a chemical burden which is too much for wildlife.
There are many examples in the natural world of species which are being affected by mysterious sex hormone-mimicking chemicals, resulting in abnormal sexual development. On Lake Apopka in Florida, alligators are hatching which are predominantly female, or if they are male, they have abnormally small genitals. Male Texan turtles are being born with ovaries. Ranched minks fed on fish from the Great Lakes fail to reproduce, while those fed on fish from other areas breed as normal. And there is a mysterious rise in polar bears with dual-sex
organs – about 4 per cent in a population of 2,000 bears-much higher than can be accounted for by chance.
These suspicious events are not confined to animals living in polluted waters. There has been a steady increase in boys born with very small penises, undescended testicles or indeterminate sex organs, as well as a serious drop in adult male fertility since the 1950s. Because of these environmental and human issues the chemicals in question are being nicknamed ‘gender benders’. By stark contrast to what is happening to human fertility, it has been observed that organically reared animals have grown increasingly productive over three generations.
It is not just our external environment which is becoming contaminated, but our homes as well. Chemicals called nonylphenols, used in plastic products such as babies’ bottles and water jugs, and chlorine compounds and dioxin, which are used to bleach paper products, detergents, toiletries and even spermicides, are suspected to be contributors to the breast cancer problem. These chemicals, along with agrichemicals, mimic oestrogens and are called xenoestrogens. Concentrations of toxic compounds can be up to 500 times higher inside the home than outdoors as they are trapped by four walls.
The oestrogenic effect of these artificially manufactured compounds was discovered by accident by Ana Soto, MD, and Carlos Sonnenschein, PhD, at Tufts University in Boston, USA, who noticed that cells stored in plastic flasks had suddenly started to grow as if they were in the presence of oestrogens, whereas in previous experiments there had not been a problem. They identified the offending and mysterious substance as nonylphenol, used to stop plastic from cracking. The chemical was present in the plastic flasks. When they switched to using glass flasks the problem stopped. Not long afterwards, they showed that nonylphenols can also cause breast tissue growth. Other nonylphenols include atrazine, the most common pesticide in the USA, and PCBs (polychlorinated biphenyls).
Studies have measured DDE (the breakdown product of DDT) and PCB levels in serum samples of breast cancer patients and have found that a four-fold increase in the risk of breast cancer is associated with higher levels of these chemicals. The conclusions of one study stated, ‘organochlorine residues may be an important etiologic factor in breast cancer’, and ‘the implications are far-reaching for public health intervention world-wide’. One Danish study showed that Dieldrin and organochlorine were associated with a significant dose-related increase in breast cancer.
The pesticide Lindane is the major organochloride still in use in the UK, and it has come under criticism for a direct link with breast cancer. Interest has been stirred among researchers as to whether Lindane, along with similar chemicals such as DDT, could cause breast cancer. Lindane has been found in 30 per cent of all milk samples and, while the quantities are small, the chemical has the unfortunate habit of being stored in our fat cells, and building up over time. Lindane has also been found in breast tissue samples, and areas of high incidence of breast cancer seem to coincide with areas which boast the most extensive usage of Lindane. In the USA, Lindane has been listed as a probable/possible human carcinogen since the late 1970s, and many countries, including Holland, Sweden, Finland, Denmark, Singapore, Japan and Israel, have banned it. For some reason the UK continues to allow its use.
Lindane is sometimes described on products aimed at agrochemical companies as
gamma-HCH. While 80 per cent of Lindane is used in agriculture, it is also used in medicines (for the treatment of scabies and headlice), in veterinary products and to treat timber for pest control. Its use has more than doubled since 1987. One aspect about the use of Lindane which certainly gives me pause for thought is that around a third of its use is for sugar beet, a crop which is grown for sugar production (and I do not consider sugar a necessary component of our food supply), and as a farm animal feed (and we probably eat a surfeit of meat and dairy produce in the UK). Surely the use of a toxic organochlorine cannot really be justified in these
circumstances?
It has been found that women with breast cancer have more pesticide residues in their body tissues than women who do not have breast cancer – up to 40 per cent more chlorinated pesticides in their breast tissue and much higher blood levels of DDE. While DDT has been banned in the UK and USA for quite some time, Third World countries from which we import our food still use it, and while levels are supposed to be checked, there have been notorious problems with certification procedures in those countries. Additionally, in the UK, over 50 per cent of wood pigeons tested in the mid-1990s contained DDT residues, in some cases by up to five times the maximum anticipated residue level, indicating that DDT was still being used illegally ten years after being banned.
As these oestrogenic chemicals are all fat-soluble, they concentrate in the fat cells and milk of animals and humans. By gravitating to fat in the body they also end up in high quantities in breast tissue where they probably do the most damage. This is one possible reason why research into diets high in animal fats has shown an increased risk of breast cancer. Interestingly, a paper published in 1990 which followed what happened after Israel banned a number of chemicals in 1978 which were determined to be correlated to breast cancer risk, recorded that incidence of the disease dropped by a massive 30 per cent in younger women under forty-four years of age (younger women’s breast tissue is more sensitive to carcinogenic agents), while at the same time incidence continued to rise worldwide.
The lacquers that coat the inside of many food cans pose yet another hazard. It has been found that they leach significant levels of biosphenol-A which exhibits an oestrogenic effect. The leaching is worse in foods which have been packed in oil, such as sardines and pilchards.
Xenoestrogens probably contribute to breast cancer risk in a number of ways:
- They bind with oestrogen receptors and then prompt the breast tissue to grow and multiply in the same way that oestradiol (E2) does.
- They trigger the release of a chemical called ‘tumour-growth factor’ (the name speaks for itself).
- They can even cause the number of oestrogen receptors to increase on the cell surface, making the cell even more susceptible to influence by oestrogens.
The research is far from conclusive on the issue of xenoestrogens, which begs the question: should we take these concerns seriously, until they are proven? The contribution of synthetic chemicals to oestrogen exposure may come from many different chemicals, some of them exceedingly persistent, such as PCBs, and others that are not persistent and leave no telltale evidence of exposure in blood or fat.’ They go on to say, ‘Also, studies have usually treated all 209 chemicals in the PCB family as one, even though various members of this chemical family have completely different and in some cases opposite biological effects.’ While human studies are the ideal, we may be beyond the point where they are viable as so many chemicals are now present in the human body, and one researcher at Tufts University in Boston, USA, concluded that in-vitro studies (in a test-tube, rather than animal or human experiments) were essential for ‘evolving dietary strategies and tactics against the adverse health effects of environmental
chemicals’ because ‘it is impossible to have a chemical-free environment (my emphasis).
With important questions being raised about the safety of these chemicals, it seems to be a dangerous policy for long-term health that governments have not exercised more caution on the use of the majority of them. But we live in a world governed by short-term economics, and it is interesting that much of the research into cancer is funded by the very companies that produce these xenoestrogen chemicals.
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Posted on December 14th, 2010 by admin  |  No Comments »