Water And Weight Loss

Water helps to lose weight.
The liver's job is to convert the stored fat into energy, this metabolism of fat is directly influenced by the amount of water you drink. It directly affects your body fat and weight loss.

The liver also acts as a backup for the kidney, which needs plenty of water to work properly.The kidneys cannot function properly without enough water. When kidneys do not work to full capacity, some of their load is shifted on the liver. But if the liver has to do some of the kidney's work, it cannot do its job. It then can't metabolize fat quickly or efficiently so weight loss slows down.

So drinking water is important for losing weight. Water suppresses the appetite naturally and helps the body metabolize stored fat. Decrease in water intake will cause fat deposits to increase and an increase in water intake can actually reduce fat deposits.

Saturated Fat and Health: a Brief Literature Review, Part II

I'm aware of twelve major controlled trials designed to evaluate the relationship between saturated fat and risk of death, without changing other variables at the same time (e.g., increased vegetable intake, omega-3 fats, exercise, etc.). Here is a summary of the results:

• Two trials found that replacing saturated animal fat with polyunsaturated vegetable fat decreased total mortality.
• Two trials found that replacing saturated animal fat with polyunsaturated vegetable fat increased total mortality.
• Eight trials found that reducing saturated fat had no effect on total mortality.

Of the two trials that found a benefit of saturated fat reduction, neither was properly controlled. The first was conducted in Sweden and published in 1965. The intervention group reduced saturated animal fat and increased polyunsaturated vegetable fat. The control group was significantly older than the intervention group, confounding the results. In addition, physicians regularly monitored the intervention group while the control group went off their radar, thus the intervention group was getting better care. This is the definition of an improperly controlled trial.

The second study to "support" the idea that saturated fat increases total mortality was the Finnish mental hospitals trial. In this trial, two mental hospitals in different towns fed their patients different diets and monitored their health. One diet was low in animal fat and high in polyunsaturated vegetable fat, while the other was higher in saturated fat. Patients eating the polyunsaturated diet had a greatly reduced death rate, mostly due to a reduction in heart attacks. The study design was pitiful. They included all patients in their analysis, even those who stayed at the hospital for only one month or who checked in and out repeatedly. Furthermore, they used a "crossover" design where the hospitals switched diets halfway through the study. This was designed to control for location, but it means we don't know whether the increase in deaths after switching to the control diet was due to the saturated fat or the vegetable oil diet that preceded it for 6 years! The only reason I included this poor study in my list is that it's commonly cited as evidence against saturated fat.

The first study to show an increase in deaths from replacing saturated animal fat with polyunsaturated vegetable fat was the tragically named Anti-Coronary Club study. After four years, despite lowering their cholesterol substantially, the intervention group saw more than twice the number of deaths as the control group. Amazingly, rather than emphasizing the increased mortality, the study authors instead focused on the cholesterol reduction. This study was not properly controlled, but if anything, that should have biased it in favor of the intervention group.

The second study to show an increase in deaths from replacing saturated animal fats with polyunsaturated vegetable fats was the Sydney Diet-Heart study. This was one of the larger, longer, better-conducted trials. After five years, the intervention group saw about 50% more deaths than the control group.

I should also mention that one of the studies in the "no effect" category actually saw more than a four-fold increase in deaths after replacing saturated fat with corn oil, but somehow the result didn't achieve statistical significance (the paper states that p= 0.05-0.1, whatever that means). It may have simply been due to the small size of the study.

Overall, the data from controlled trials are clear: replacing animal fat with vegetable oil does not reduce your risk of dying! The same is true of reducing total fat. The main counterpoint to this conclusion is that the trials may have been too short to pick up the effect of saturated fat. However, two years was enough time to detect the effect of fish oil on death in the DART trial, and the trials I'm writing about lasted up to 8 years (not including the Finnish mental hospital trial or the Swedish one). There's also the fact that the greatest consumers of saturated fat in the world eat it for their entire lives and don't seem to suffer from it. Proponents of the theory that saturated fat is unhealthy have the burden of proof on their shoulders, and the data have failed to deliver.

Most trials of this nature are designed with cardiovascular outcomes in mind. Out of the twelve studies mentioned above, nine measured coronary heart disease mortality.

• Two found it was reduced when saturated fat was replaced with polyunsaturated vegetable fat.
• One found that is was increased when saturated fat was replaced with polyunsaturated vegetable fat.
• Six found no effect.

Of the two that found an effect, the first was the Finnish mental hospital study. See above. The second was the L.A. Veterans Administration study, which was actually a good, eight-year study. However, it's worth noting three things about it: first, there were significantly more heavy smokers in the control group; second, overall mortality was the same in both groups, partly because of an increased cancer risk in the diet group; and third, it's the only well-conducted study of its kind to find such a result.

The study to find an increase in cardiovascular deaths was again the unfortunately-named Anti-Coronary Club trial. The Sydney Diet-Heart trial did not report cardiovascular mortality, which was almost certainly increased. Also, the study mentioned above that saw a "non-significant" four-fold increase in deaths on corn oil also saw a similar increase in cardiovascular deaths. I included it in the "no effect" category.

So not only do the best data not support the idea that saturated fat increases the overall risk of death, they don't even support the idea that it causes heart disease! In fact, the body seems to prefer saturated fat to unsaturated fats in the bloodstream. Guess what your liver does with carbohydrate when you eat a low-fat diet? It turns it into saturated fat (palmitic acid) and then pumps it into your bloodstream. We have the enzymes necessary to desaturate palmitic acid, so why does the liver choose to secrete it into the blood in its saturated form? Kitavan lipoproteins contain a lot of palmitic acid, which is not found in their diet. Are their livers trying to kill them? Apparently they aren't succeeding.

Eat the fat on your steaks folks. Just like your great-grandparents did, and everyone who came before.

Saturated Fat and Health: a Brief Literature Review, Part II

I'm aware of twelve major controlled trials designed to evaluate the relationship between saturated fat and risk of death, without changing other variables at the same time (e.g., increased vegetable intake, omega-3 fats, exercise, etc.). Here is a summary of the results:

• Two trials found that replacing saturated animal fat with polyunsaturated vegetable fat decreased total mortality.
• Two trials found that replacing saturated animal fat with polyunsaturated vegetable fat increased total mortality.
• Eight trials found that reducing saturated fat had no effect on total mortality.

Of the two trials that found a benefit of saturated fat reduction, neither was properly controlled. The first was conducted in Sweden and published in 1965. The intervention group reduced saturated animal fat and increased polyunsaturated vegetable fat. The control group was significantly older than the intervention group, confounding the results. In addition, physicians regularly monitored the intervention group while the control group went off their radar, thus the intervention group was getting better care. This is the definition of an improperly controlled trial.

The second study to "support" the idea that saturated fat increases total mortality was the Finnish mental hospitals trial. In this trial, two mental hospitals in different towns fed their patients different diets and monitored their health. One diet was low in animal fat and high in polyunsaturated vegetable fat, while the other was higher in saturated fat. Patients eating the polyunsaturated diet had a greatly reduced death rate, mostly due to a reduction in heart attacks. The study design was pitiful. They included all patients in their analysis, even those who stayed at the hospital for only one month or who checked in and out repeatedly. Furthermore, they used a "crossover" design where the hospitals switched diets halfway through the study. This was designed to control for location, but it means we don't know whether the increase in deaths after switching to the control diet was due to the saturated fat or the vegetable oil diet that preceded it for 6 years! The only reason I included this poor study in my list is that it's commonly cited as evidence against saturated fat.

The first study to show an increase in deaths from replacing saturated animal fat with polyunsaturated vegetable fat was the tragically named Anti-Coronary Club study. After four years, despite lowering their cholesterol substantially, the intervention group saw more than twice the number of deaths as the control group. Amazingly, rather than emphasizing the increased mortality, the study authors instead focused on the cholesterol reduction. This study was not properly controlled, but if anything, that should have biased it in favor of the intervention group.

The second study to show an increase in deaths from replacing saturated animal fats with polyunsaturated vegetable fats was the Sydney Diet-Heart study. This was one of the larger, longer, better-conducted trials. After five years, the intervention group saw about 50% more deaths than the control group.

I should also mention that one of the studies in the "no effect" category actually saw more than a four-fold increase in deaths after replacing saturated fat with corn oil, but somehow the result didn't achieve statistical significance (the paper states that p= 0.05-0.1, whatever that means). It may have simply been due to the small size of the study.

Overall, the data from controlled trials are clear: replacing animal fat with vegetable oil does not reduce your risk of dying! The same is true of reducing total fat. The main counterpoint to this conclusion is that the trials may have been too short to pick up the effect of saturated fat. However, two years was enough time to detect the effect of fish oil on death in the DART trial, and the trials I'm writing about lasted up to 8 years (not including the Finnish mental hospital trial or the Swedish one). There's also the fact that the greatest consumers of saturated fat in the world eat it for their entire lives and don't seem to suffer from it. Proponents of the theory that saturated fat is unhealthy have the burden of proof on their shoulders, and the data have failed to deliver.

Most trials of this nature are designed with cardiovascular outcomes in mind. Out of the twelve studies mentioned above, nine measured coronary heart disease mortality.

• Two found it was reduced when saturated fat was replaced with polyunsaturated vegetable fat.
• One found that is was increased when saturated fat was replaced with polyunsaturated vegetable fat.
• Six found no effect.

Of the two that found an effect, the first was the Finnish mental hospital study. See above. The second was the L.A. Veterans Administration study, which was actually a good, eight-year study. However, it's worth noting three things about it: first, there were significantly more heavy smokers in the control group; second, overall mortality was the same in both groups, partly because of an increased cancer risk in the diet group; and third, it's the only well-conducted study of its kind to find such a result.

The study to find an increase in cardiovascular deaths was again the unfortunately-named Anti-Coronary Club trial. The Sydney Diet-Heart trial did not report cardiovascular mortality, which was almost certainly increased. Also, the study mentioned above that saw a "non-significant" four-fold increase in deaths on corn oil also saw a similar increase in cardiovascular deaths. I included it in the "no effect" category.

So not only do the best data not support the idea that saturated fat increases the overall risk of death, they don't even support the idea that it causes heart disease! In fact, the body seems to prefer saturated fat to unsaturated fats in the bloodstream. Guess what your liver does with carbohydrate when you eat a low-fat diet? It turns it into saturated fat (palmitic acid) and then pumps it into your bloodstream. We have the enzymes necessary to desaturate palmitic acid, so why does the liver choose to secrete it into the blood in its saturated form? Kitavan lipoproteins contain a lot of palmitic acid, which is not found in their diet. Are their livers trying to kill them? Apparently they aren't succeeding.

Eat the fat on your steaks folks. Just like your great-grandparents did, and everyone who came before.

Saturated Fat and Health: a Brief Literature Review, Part I

Even years ago, when I watched my saturated fat intake, I always had a certain level of cognitive dissonance about it. I knew that healthy non-industrial cultures often consumed large amounts of saturated fat. For example, the Masai of East Africa, who traditionally subsist on extremely fatty milk, blood and meat, do not appear to experience heart attacks. Their electrocardiogram readings are excellent and they have the lowest level of arterial plaque during the time of their lives when they are restricted (for cultural reasons) to their three traditional foods. They get an estimated 33% of their calories from saturated animal fat.

Then there are the Pacific islanders, who often eat large amounts of highly saturated coconut. Kitavans get 17% of their calories from saturated fat (Americans get about 10% on average), yet show no trace of heart disease, stroke or overweight. The inhabitants of the island of Tokelau, who I learned about recently, eat more saturated fat than any other culture I'm aware of. They get a whopping 55% of their calories from saturated fat! Are they keeling over from heart attacks or any of the other diseases that kill people in modern societies? Apparently not. So from the very beginning, the theory faces the problem that the cultures consuming the most saturated fat on Earth have an undetectable frequency of heart attacks and other modern non-communicable diseases.

Humans have eaten saturated animal fat since our species first evolved, and historical hunter-gatherers subsisted mostly on animal foods. Our closest recent relatives, neanderthals, were practically carnivores. Thus, the burden of proof is on proponents of the theory that saturated fat is unhealthy.

There have been countless studies on the relationship between saturated fat and health. The first studies were epidemiological. Epidemiological studies involve collecting data from one or more populations and seeing if any specific factors associate with the disease in question. For example, the Framingham Heart study collected data on diet, lifestyle and mortality from various diseases and attempted to connect diseases to lifestyle factors. This type of study is useful for creating hypotheses, but it can only determine associations. For example, it can establish that smokers tend to die more often from heart disease than non-smokers, but it can't determine that smoking is actually the cause of heart disease. This is because multiple factors often travel together. For example, maybe smokers also tend to take care of themselves less in other ways, sleeping less, eating more sugar, etc.

Epidemiological data are often incorrectly used to demonstrate causality. This is a big problem, and it irritates me to no end. There's only one way to show conclusively that a diet or lifestyle factor actually causes something else: a controlled trial. In a controlled trial, researchers break participants into two groups: an intervention group and a control group. If they want to know the effect of saturated fat on health, they will advise the participants in each group to eat different amounts of saturated fat, and keep everything else the same. At the end of the trial, they can determine the effect of saturated fat on health because it was the only factor that differed between groups. In practice, reducing saturated fat also involves either increasing unsaturated fat or decreasing total fat intake, so it's not perfect.

I'm not going to review the epidemiological data because they are contradictory and they are "lesser evidence" compared to the controlled trials that have been conducted. However, I will note that Dr. Ancel Keys' major epidemiological study linking saturated fat consumption to heart disease, the "Seven Countries" study, has been thoroughly discredited due to the omission of contradictory data (read: the other 15 countries where data were available). This was the study that sparked the anti-saturated fat movement. Older epidemiological studies and those conducted internationally tend to find nonexistent or weak links between saturated fat and health problems, while more recent American studies, such as the Nurses' Health study, have sometimes found strong associations. I'll address this phenomenon in another post.

In the next post, I'll get into the meaty data: the controlled trails evaluating the effect of saturated fat on health.

Thanks to Rockies for the CC photo.

Saturated Fat and Health: a Brief Literature Review, Part I

Even years ago, when I watched my saturated fat intake, I always had a certain level of cognitive dissonance about it. I knew that healthy non-industrial cultures often consumed large amounts of saturated fat. For example, the Masai of East Africa, who traditionally subsist on extremely fatty milk, blood and meat, do not appear to experience heart attacks. Their electrocardiogram readings are excellent and they have the lowest level of arterial plaque during the time of their lives when they are restricted (for cultural reasons) to their three traditional foods. They get an estimated 33% of their calories from saturated animal fat.

Then there are the Pacific islanders, who often eat large amounts of highly saturated coconut. Kitavans get 17% of their calories from saturated fat (Americans get about 10% on average), yet show no trace of heart disease, stroke or overweight. The inhabitants of the island of Tokelau, who I learned about recently, eat more saturated fat than any other culture I'm aware of. They get a whopping 55% of their calories from saturated fat! Are they keeling over from heart attacks or any of the other diseases that kill people in modern societies? Apparently not. So from the very beginning, the theory faces the problem that the cultures consuming the most saturated fat on Earth have an undetectable frequency of heart attacks and other modern non-communicable diseases.

Humans have eaten saturated animal fat since our species first evolved, and historical hunter-gatherers subsisted mostly on animal foods. Our closest recent relatives, neanderthals, were practically carnivores. Thus, the burden of proof is on proponents of the theory that saturated fat is unhealthy.

There have been countless studies on the relationship between saturated fat and health. The first studies were epidemiological. Epidemiological studies involve collecting data from one or more populations and seeing if any specific factors associate with the disease in question. For example, the Framingham Heart study collected data on diet, lifestyle and mortality from various diseases and attempted to connect diseases to lifestyle factors. This type of study is useful for creating hypotheses, but it can only determine associations. For example, it can establish that smokers tend to die more often from heart disease than non-smokers, but it can't determine that smoking is actually the cause of heart disease. This is because multiple factors often travel together. For example, maybe smokers also tend to take care of themselves less in other ways, sleeping less, eating more sugar, etc.

Epidemiological data are often incorrectly used to demonstrate causality. This is a big problem, and it irritates me to no end. There's only one way to show conclusively that a diet or lifestyle factor actually causes something else: a controlled trial. In a controlled trial, researchers break participants into two groups: an intervention group and a control group. If they want to know the effect of saturated fat on health, they will advise the participants in each group to eat different amounts of saturated fat, and keep everything else the same. At the end of the trial, they can determine the effect of saturated fat on health because it was the only factor that differed between groups. In practice, reducing saturated fat also involves either increasing unsaturated fat or decreasing total fat intake, so it's not perfect.

I'm not going to review the epidemiological data because they are contradictory and they are "lesser evidence" compared to the controlled trials that have been conducted. However, I will note that Dr. Ancel Keys' major epidemiological study linking saturated fat consumption to heart disease, the "Seven Countries" study, has been thoroughly discredited due to the omission of contradictory data (read: the other 15 countries where data were available). This was the study that sparked the anti-saturated fat movement. Older epidemiological studies and those conducted internationally tend to find nonexistent or weak links between saturated fat and health problems, while more recent American studies, such as the Nurses' Health study, have sometimes found strong associations. I'll address this phenomenon in another post.

In the next post, I'll get into the meaty data: the controlled trails evaluating the effect of saturated fat on health.

Thanks to Rockies for the CC photo.

Yoga And Weight Loss

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Abs Yoga Workout for Beginners



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Most Toxic Foods(Buy Organic) - Peaches, Apples, Sweet Bell Peppers,Celery, Nectarines, Cherries, Potatoes, pears, lettuce, Grapes(imported), Strawberries, Tomatoes, Spinach

Weight Loss Story

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Do you have a weight loss story or weight loss tips that you would like to share ? Your story will inspire others to help them lose weight and live a healthier lifestyle. Give others the motivation to succeed with their weight loss goals.

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

Beef Tallow: a Good Source of Fat-Soluble Vitamins?

Suet is a traditional cooking fat in the US, which is a country that loves its cows. It's the fat inside a cow's intestinal cavity, and it can be rendered into tallow. Tallow is an extremely stable fat, due to its high degree of saturation (56%) and low level of polyunsaturated fatty acids (3%). This makes it ideal for deep frying. Until it was pressured to abandon suet in favor of hydrogenated vegetable oil around 1990, in part by the Center for Science in the Public Interest, McDonald's used tallow in its deep fryers. Now, tallow is mostly fed to birds and feedlot cows.

I decided to make pemmican recently, which is a mixture of pulverized jerky and tallow that was traditionally eaten by native Americans of many tribes. I bought pasture-raised suet at my farmer's market. It was remarkably cheap at $2/lb. No one wants it because it's so saturated. The first thing I noticed was a yellowish tinge, which I didn't expect.

I rendered it the same way I make lard. It turned into a clear, golden liquid with a beefy aroma. This got me thinking. The difference between deep yellow butter from grass-fed cows and lily-white butter from industrial grain-fed cows has to do with the carotene content. Carotene is also a marker of other nutrients in butter, such as vitamin K2 MK-4, which can vary 50-fold depending on what the cows are eating. So I thought I'd see if suet contains any K2.

And indeed it does. The NutritionData entry for suet says it contains 3.6 micrograms (4% DV) per 100g. 100g is about a quarter pound of suet, more than you would reasonably eat. Unless you were really hungry. But anyway, that's a small amount of K2 per serving. However, the anonymous cow in question is probably a grain-finished animal. You might expect a grass-fed cow to have much more K2 in its suet, as it does in its milkfat. According to Weston Price, butter fat varies 50-fold in its K2 content. If that were true for suet as well, grass-fed suet could conceivably contain up to 180 micrograms per 100g, making it a good source of K2.

Tallow from pasture-raised cows also contains a small amount of vitamin D, similar to lard. Combined with its low omega-6 content and its balanced n-6/n-3 ratio, that puts it near the top of my list of cooking fats.

Sneaky...

Found a neat way to stop myself weighing before my weigh in day... Take a pint of squash to bed and then when I wake up drink it down. That puts any hint of weighing straight out of my mind. Good huh!

Ok, yesterday was good. I didn't celebrate with food, or anything else for that matter. I had my granola for breakfast, a Nakd food bar for what ended up as lunch, a slice - nay - a bite of cake at TB's house ( excessive consumption avoided due to the chocolate and chilli flake flavour! Not good, trust me), 2 large beetroot with salad cream for dinner and some pea and ham soup from the diet chef delivery box as a supper.

So that was a sweet day, eating wise. It was a crap day in other ways owing to the presence of Felix, our lodger's cat. This cat can pee and crap around the house for England. I found 6 huge dumps under the kitchen cupboards. We have a little bit of skirting missing at the bottom of our kitchen cupboards next to the dishwasher. Its hardly big enough to get my arm in, so after dismantling the skirting boards around my whole kitchen, I located 6 turn outs by the said little cat - Felix. I then neat bleached the floor and sealed it all back up again, including the 'hole' where the little sod was sneaking in and crapping.

That disgusting moment of my life over with, I decide to put on some washing and as I dump the laundry on the floor I see one of my nice shirts suddenly wick wetness from the floor... Yes, you guessed it, it was a nice pool of cat pee. *sigh* so I bunged all the washing in the machine with some detol and cleaned up the pee. I came back to get the washing from the machine 40 minutes later and there was a mahoosive great turd right there in front of the machine!!

Ok, so that's all done and then I hear a wail from DS... "Oh mum...? Think you better come here...!"

Yes, another nice present on all the leads to DS's PS2. Yummy. Have you ever had to wipe cat crap from a bundle of leads. It ain't fun and it ain't pretty. There is absolutely no way to avoid touching the stuff. Oh my it's grim. Of course, its bad enough when its your own cat, but when its someone elses little precious its just foul.

Right then, well if that hasnt put you off your lunch, nothing will.

Vitamin D: It's Not Just Another Vitamin

If I described a substance with the following properties, what would you guess it was?

-It's synthesized by the body from cholesterol
-It crosses cell membranes freely
-It has its own nuclear receptor
-It causes broad changes in gene transcription
-It acts in nearly every tissue
-It's essential for health

There's no way for you to know, because those statements all apply to activated vitamin D, estrogen, testosterone and a number of other hormones. Vitamin D, as opposed to all other vitamins, is a steroid hormone precursor (technically it's a secosteroid but it's close enough for our purposes). The main difference between vitamin D and other steroid hormones is that it requires a photon of UVB light for its synthesis in the skin. If it didn't require UVB, it would be called a hormone rather than a vitamin. Just like estrogen and testosterone, it's involved in many processes, and it's important to have the right amount.

The type of vitamin D that comes from sunlight and the diet is actually not a hormone itself, but a hormone precursor. Vitamin D is converted to 25(OH)D3 in the liver. This is the major storage form of vitamin D, and thus it best reflects vitamin D status. The kidney converts 25(OH)D3 to 1,25(OH)D3 as needed. This is the major hormone form of vitamin D. 1,25(OH)D3 has profound effects on a number of tissues.

Vitamin D was originally identified as necessary for proper mineral absorption and metabolism. Deficiency causes rickets, which results in the demineralization and weakening of bones and teeth. A modest intake of vitamin D is enough to prevent rickets. However, there is a mountain of data accumulating that shows that even a mild form of deficiency is problematic. Low vitamin D levels associate with nearly every common non-communicable disorder, including obesity, diabetes, cardiovascular disease, autoimmune disease, osteoporosis and cancer. Clinical trials using vitamin D supplements have shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

It all makes sense if you think about how humans evolved: in a tropical environment with bright sun year-round. Even in many Northern climates, a loss of skin pigmentation and plenty of time outdoors allowed year-round vitamin D synthesis for most groups. Vitamin D synthesis becomes impossible during the winter above latitude 40 or so, due to a lack of UVB. Traditional cultures beyond this latitude, such as the Inuit, consumed large amounts of vitamin D from nutrient-rich animal foods like fatty fish.

The body has several mechanisms for regulating the amount of vitamin D produced from sunlight exposure, so overdose from this source is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

Here's how to become vitamin D deficient: stay inside all day, wear sunscreen anytime you go out, and eat a low-fat diet. Make sure to avoid animal fats in particular. Rickets, once thought of as an antique disease, is making a comeback in developed countries despite fortification of milk (note- it doesn't need to be fortified with fat-soluble vitamins if you don't skim the fat off in the first place!). The resurgence of rickets is not surprising considering our current lifestyle and diet trends. In a recent study, 40% of infants and toddlers in Boston were vitamin D deficient using 30 ng/mL as the cutoff point. 7.5% of the total had rickets and 32.5% showed demineralization of bone tissue! Part of the problem is that mothers' milk is a poor source of vitamin D when the mother herself is deficient. Bring the mothers' vitamin D level up, and breast milk becomes an excellent source.

Here's how to optimize your vitamin D status: get plenty of sunlight without using sunscreen, and eat nutrient-rich animal foods, particularly in the winter. The richest food source of vitamin D is high-vitamin cod liver oil. Blood from pasture-raised pigs or cows slaughtered in summer or fall, and fatty fish such as herring and sardines are also good sources. Vitamin D is one of the few nutrients I can recommend in supplement form. Make sure it's D3 rather than D2; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. Vitamin D3 supplements are typically naturally sourced, coming from sheep lanolin or fish livers. A good regimen would be to supplement every day you get less than 10 minutes of sunlight.

People with dark skin and the elderly make less vitamin D upon sun exposure, so they should plan on getting more sunlight or consuming more vitamin D. Sunscreen essentially eliminates vitamin D synthesis, and glass blocks UVB so indoor sunlight is useless. Vitamin D toxicity from supplements is possible, but exceptionally rare. It only occurs in cases where people have accidentally taken grotesque doses of the vitamin. As Chris Masterjohn has pointed out, vitamin D toxicity is extremely similar to vitamin A deficiency. This is because vitamin A and D work together, and each protects against toxicity from the other. Excess vitamin D depletes vitamin A, thus vitamin D toxicity is probably a relative deficiency of vitamin A.

I know this won't be a problem for you because like all healthy traditional people, you are getting plenty of vitamin A from nutrient-dense animal foods like liver and butter. Vitamin K2 is the third, and most overlooked, leg of the stool. D, A and K2 form a trio that act together to optimize mineral absorption and use, aid in the development of a number of body structures, beneficially alter gene expression, and affect many aspects of health on a fundamental level.

Thanks to horizontal.integration for the CC photo.

Vitamin D: It's Not Just Another Vitamin

If I described a substance with the following properties, what would you guess it was?

-It's synthesized by the body from cholesterol
-It crosses cell membranes freely
-It has its own nuclear receptor
-It causes broad changes in gene transcription
-It acts in nearly every tissue
-It's essential for health

There's no way for you to know, because those statements all apply to activated vitamin D, estrogen, testosterone and a number of other hormones. Vitamin D, as opposed to all other vitamins, is a steroid hormone precursor (technically it's a secosteroid but it's close enough for our purposes). The main difference between vitamin D and other steroid hormones is that it requires a photon of UVB light for its synthesis in the skin. If it didn't require UVB, it would be called a hormone rather than a vitamin. Just like estrogen and testosterone, it's involved in many processes, and it's important to have the right amount.

The type of vitamin D that comes from sunlight and the diet is actually not a hormone itself, but a hormone precursor. Vitamin D is converted to 25(OH)D3 in the liver. This is the major storage form of vitamin D, and thus it best reflects vitamin D status. The kidney converts 25(OH)D3 to 1,25(OH)D3 as needed. This is the major hormone form of vitamin D. 1,25(OH)D3 has profound effects on a number of tissues.

Vitamin D was originally identified as necessary for proper mineral absorption and metabolism. Deficiency causes rickets, which results in the demineralization and weakening of bones and teeth. A modest intake of vitamin D is enough to prevent rickets. However, there is a mountain of data accumulating that shows that even a mild form of deficiency is problematic. Low vitamin D levels associate with nearly every common non-communicable disorder, including obesity, diabetes, cardiovascular disease, autoimmune disease, osteoporosis and cancer. Clinical trials using vitamin D supplements have shown beneficial and sometimes striking effects on cancer, hypertension, type 1 diabetes, bone fracture and athletic performance. Vitamin D is a fundamental building block of health.

It all makes sense if you think about how humans evolved: in a tropical environment with bright sun year-round. Even in many Northern climates, a loss of skin pigmentation and plenty of time outdoors allowed year-round vitamin D synthesis for most groups. Vitamin D synthesis becomes impossible during the winter above latitude 40 or so, due to a lack of UVB. Traditional cultures beyond this latitude, such as the Inuit, consumed large amounts of vitamin D from nutrient-rich animal foods like fatty fish.

The body has several mechanisms for regulating the amount of vitamin D produced from sunlight exposure, so overdose from this source is impossible. Sunlight is also the most effective natural way to obtain vitamin D. To determine the optimal blood level of vitamin D, it's instructive to look at the serum 25(OH)D3 levels of people who spend a lot of time outdoors. The body seems to stabilize between 55 and 65 ng/mL 25(OH)D3 under these conditions. This is probably near the optimum. 30 ng/mL is required to normalize parathyroid hormone levels, and 35 ng/mL is required to optimize calcium absorption.

Here's how to become vitamin D deficient: stay inside all day, wear sunscreen anytime you go out, and eat a low-fat diet. Make sure to avoid animal fats in particular. Rickets, once thought of as an antique disease, is making a comeback in developed countries despite fortification of milk (note- it doesn't need to be fortified with fat-soluble vitamins if you don't skim the fat off in the first place!). The resurgence of rickets is not surprising considering our current lifestyle and diet trends. In a recent study, 40% of infants and toddlers in Boston were vitamin D deficient using 30 ng/mL as the cutoff point. 7.5% of the total had rickets and 32.5% showed demineralization of bone tissue! Part of the problem is that mothers' milk is a poor source of vitamin D when the mother herself is deficient. Bring the mothers' vitamin D level up, and breast milk becomes an excellent source.

Here's how to optimize your vitamin D status: get plenty of sunlight without using sunscreen, and eat nutrient-rich animal foods, particularly in the winter. The richest food source of vitamin D is high-vitamin cod liver oil. Blood from pasture-raised pigs or cows slaughtered in summer or fall, and fatty fish such as herring and sardines are also good sources. Vitamin D is one of the few nutrients I can recommend in supplement form. Make sure it's D3 rather than D2; 3,000- 5,000 IU per day should be sufficient to maintain blood levels in wintertime unless you are obese (in which case you may need more and should be tested). I feel it's preferable to stay on the low end of this range. Vitamin D3 supplements are typically naturally sourced, coming from sheep lanolin or fish livers. A good regimen would be to supplement every day you get less than 10 minutes of sunlight.

People with dark skin and the elderly make less vitamin D upon sun exposure, so they should plan on getting more sunlight or consuming more vitamin D. Sunscreen essentially eliminates vitamin D synthesis, and glass blocks UVB so indoor sunlight is useless. Vitamin D toxicity from supplements is possible, but exceptionally rare. It only occurs in cases where people have accidentally taken grotesque doses of the vitamin. As Chris Masterjohn has pointed out, vitamin D toxicity is extremely similar to vitamin A deficiency. This is because vitamin A and D work together, and each protects against toxicity from the other. Excess vitamin D depletes vitamin A, thus vitamin D toxicity is probably a relative deficiency of vitamin A.

I know this won't be a problem for you because like all healthy traditional people, you are getting plenty of vitamin A from nutrient-dense animal foods like liver and butter. Vitamin K2 is the third, and most overlooked, leg of the stool. D, A and K2 form a trio that act together to optimize mineral absorption and use, aid in the development of a number of body structures, beneficially alter gene expression, and affect many aspects of health on a fundamental level.

Thanks to horizontal.integration for the CC photo.

What is Metabolism ?

Metabolism is the rate at which your body burns calories in order to maintain itself. Whether you are walking, eating, drinking, sleeping etc. your body is constantly burning calories . Even while we sleep our metabolism is working. Metabolism is a constant process that begins when we're conceived and ends when we die. It is an important process for all life forms. If it stops, a living thing dies.
Total Daily Energy Expenditure or Metabolic Rate Graph

The body burns calories in three ways : Basal Metabolic Rate (BMR) , physical activity , and the thermic effect of food.

Basal Metabolic Rate (BMR)	This is a measure of the energy that your body uses when it is inactive. It represents the minimum amount of energy required to keep your body functioning, including your heart beating, lungs breathing, brain working and body temperature normal. BMR accounts for 60-75% of daily calories burned. This means you burn the most calories while at rest. The faster your metabolic rate the more calories you burn. The number of calories required for basal metabolism varies with sex, age, body size, lean muscle mass and hormones. People with a high percentage of muscle mass burn more calories while at rest. This means it is important to not only lose fat but to gain muscle in the weight loss process. By increasing your total muscle mass, you can increase your metabolic rate which helps in weight loss.
Physical activity	It accounts for around 20% of calorie expenditure .You can determine the amount of calories you burn according to your workout and intensity. Also, you can control the number of calories burned depending on the duration, frequency and intensity of your physical activities.
Thermic Effect of Food	It accounts for about 10% of the total energy used by an average person. It is the energy used by our body when we eat and digest food so that it can be metabolised by the body. In other words our body needs energy to breakdown and process the food.

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Proper Random

Ok, I have no idea what goes on with my body.

I weighed in this morning at I was 16 stone 4lbs.

I mean... What?

I have no idea how my body can lose 3 pounds in 24 hours, but evidently it did.

I don't know about you, but this just seems to make a mockery of the weighing machine. To reiterate... I weigh in at 9:20 after using the loo, naked - bar my leg and armpit fuzz and before I eat or drink anything. If yesterday was my weigh in day, I would have been completely gutted and probably had a take away and a bottle of wine, puked it up and had something else and then been completely bad all week because of feeling so rubbish about a.) the lack of weight loss and b.) the fact that I am eating like a hog. That is why losing weight is such a nightmare.
But, as luck would have it, yesterday was NOT my weigh in day, and thankfully it was today and I am happy... disturbed, but happy.

It would seem that whether you have a good day or a bad day, you just have to keep with the programme. I am going to try - yes TRY - and remember this the next time I don't see the results on the scales that I want to. If I try and remember this incident, it might stop me going completely off the rails for a day, let alone a week.

So, I am moving. I am off the mark again. Wont be long until I am back in those 15's again and not feeling quite so bad. I am committing to another week of weightloss and that's how I am going to attack it. I cant focus on how much I need to lose, because its just too big a number. I think its something like 70 pounds. Even 7 pounds is too much to focus on. The best way I think is to focus week by week on my eating rather than the weight I will lose. Means that every Wednesday is a little bit more interesting too. So, I'm signing up to another week on my band behaviour bond.

The bond is thus:

I will eat 3 regular meals plus 2 healthy snacks
I will think about what I am eating before I eat it
I will stop eating when I am full
I will not drink alcohol
I will not drink with meals
I will keep active and do all my lessons
I will feel positive about myself and my skills
I will complete tasks that I must do
I will be in bed before midnight every night this week

Its now 11:15am and I have already completed DH's Tax return for him and arranged an extra lesson today. I have been in and fed Mary, played with the kittens and am about to attack the garden as it is now a jungle and small children from the area could get lost in some of those brambles!

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Today's round-up

Breakfast - granola and milk
Lunch - raw food bar
snack - banana
dinner - 5 pieces of tortellini in sauce
snack - McDonalds vanilla milkshake.

Total cals... well the milkshake has 420 alone. The bar is 100, the granola and milk 235 and a banana is about 100. The tortellini...about 100 aswell.

So roughly 1000 cals.

Feel like crud.

Went to see the film IGOR. It was ok, but came away wondering how I can claw back the wasted hour and 30 minutes of my life. Guessing I'll probably not be getting the DVD.

Work = Hmmm Good knowing that tomorrow I only have 1 pupil, even if it does mean that the 6 that have cancelled because of 6th form parents meetings, vomiting bug, colds and other assorted ills means I have lost £70.

Pessimistic? Who me?

Ok... positive stuff:

DAD CAME HOME YESTERDAY!!! Yes, he is back on the ranch and feeling ok. His wound/hole in gut is now the size of a small tea plate rather than a dinner plate which is good news. There is a lot of new skin growing. His old stoma site his like a woman's breast and he jokingly says that he doesn't need Mum any more now that he has it!! Its so swollen underneath where his old bag was, but healing. Apparently its 'normal'. Must say i haven't seen anyone else with a breast growing out the side of their tummy, but there we go. His new stoma is working well, and everything is ok by the sounds of it. He is wired up to a battery charger on one side of him, and the vac wound suction machine on the other, so he wont be doing any hiking any time soon - which is a seriously good thing! He is so hyperactive that he cant sit still usually, so this will put paid to that and force him to chillax.

Another cool thing... We now have 7 kittens... yes 7! Our 6 kittens have all been named now - BOB by the Moore family, LOLA but the Green family, SUMMER by the Elliot family, OREO and KIMBA by Steph and Nick and SQUIGGLES by Ally and Dan. However, SQUIGGLES gained a sister today. At work, Ally could hear squeaking and found a little stray feral kitten about 2 weeks old abandoned under a prickly hedge. It was not too well and she took it to the vet. He had to remove two pieces of plastic from its little throat and then give it treatment for a week. They gave it back to them on Friday and they had been feeding it every two hours and helping it go for a poo and a wee (normally the mum does this you see by licking). They brought Her - called PRICKLES - to visit her brother when I came up with a plan. PRICKLES has been adopted by Mary. We placed her near to Mary and Mary licked her all over and didn't show any signs of a problem at all. Prickles then joined her brothers and sisters, who are all a bit older and more boisterous as they are 4 weeks old today, but seems no problem. I kept a close eye on them all morning and then saw her have her first feed. She was straight in there and latched on for a full 7 minutes same as all the rest of them... well except one which I kept swapping over on rotation seeing as Mary only has 6 nipples!! Then I left them alone for a bit. I came back just before I went to work and weighed all the kittens. The fattest was Summer at 15oz, and Prickles was 10.7 oz. I thought this would be a good indicator of her growth in comparison to the others or if we have to top it up a little bit. Anyway, then Mary laid down again ready to feed, so I let her feed them and Prickles was straight in there again. I weighed her again and she had taken 0.3oz milk on board which is perfect. As its from Mary as opposed to formula its got to be more nutritious for her. So far, so good! I looked in on them a minute ago and they were all cuddles up together in a big pile with Prickles in the centre. Ahhh

Ok, this is it... dont get scared now

I am getting those jitters again guys...

Its been 6 days since starting to really work with the band again, so tomorrow is weigh in time.

I jumped on the scales today and it said 16st 7lb. Thats EXACTLY the same as last wedensday when I started doing my UTMOST to get going.

Only... on Saturday morning it said 16st 4lb...

I AM GUTTED. I am trying very hard not to stuff my face because of feeling so rubbish about this.

Maybe saturday was a wrong read... (although it was same time, same clothes, post toilet, pre breakfast/foodstuff consumption and they are elcectronic things -so thats not sitting too well in my logical mind)

Maybe I put on 3 pounds in the last 3 days (although I have done nothing other than eat the stuff that came with the pack, and have reasonable snacks and have stayed well within ALL limits and not cheated AT ALL - so that doesnt sit in my logical mind)

Maybe I just am not supposed to be thin

Maybe I cant do this

I feel like a piece of scum and I want chocolate, sweets and tasty treats to eat.

stuff it all.

HOWEVER > I am not going to do those things (oh man I so want to though!)

I am going to weigh in properly tomorrow as I should do and see what it says. I will decide how to celebrate or commiserate after tomorrows weigh in.

Now, to those of you who are gonna tell me it takes my body some time to adjust - DON'T BOTHER. Its junk. If you don't eat, you lose weight.

I went to slimming world WITHOUT a band and lost weight eating far more than I did this week. I even lost weight when I used to pig out on all kinds of stuff (see previous posts of about 3 years ago if you don't believe me).

So, my body is not in starvation, or holding water or some rubbish. I obviously am doing something wrong or need less calories.

I am in a seriously foul mood, so responders to this post beware I might BITE!!! GRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRRR

DART: Many Lessons Learned

The Diet and Reinfarction Trial (DART), published in 1989, is one of the most interesting clinical trials I've had the pleasure to read about recently. It included 2,033 British men who had already suffered from an acute myocardial infarction (MI; heart attack), and tested three different strategies to prevent further MIs. Subjects were divided into six groups:

• One group was instructed to reduce total fat to 30% of calories (from about 35%) and replace saturated fat (SFA) with polyunsaturated fat (PUFA).
• The second group was told to double grain fiber intake.
• The third group was instructed to eat more fatty fish or take fish oil if they didn't like fish.
• The remaining three were control groups that were not advised to change diet; one for each of the first three.
  

Researchers followed the six groups for two years, recording deaths and MIs. The fat group reduced their total fat intake from 35.0 to 32.3% of calories, while doubling the ratio of PUFA to SFA (to 0.78). After two years, there was no change in all-cause or cardiac mortality. This is totally consistent with the numerous other controlled trials that have been done on the subject. Here's the mortality curve:

Here's what the authors have to say about it:

Five randomised trials have been published in which a diet low in fat or with a high P/S [polyunsaturated/saturated fat] ratio was given to subjects who had recovered from MI. All these trials contained less than 500 subjects and none showed any reduction in deaths; indeed, one showed an increase in total mortality in the subjects who took the diet.

So... why do we keep banging our heads against the wall if clinical trials have already shown repeatedly that total fat and saturated fat consumption are irrelevant to heart disease and overall risk of dying? Are we going to keep doing these trials until we get a statistical fluke that confirms our favorite theory? This DART paper was published in 1989, and we have not stopped banging our heads against the wall since. The fact is, there has never been a properly controlled clinical trial that has shown an all-cause mortality benefit for reducing total or saturated fat in the diet (without changing other variables at the same time). More than a dozen have been conducted to date.

On to fish. The fish group tripled their omega-3 intake, going from 0.6 grams per week of EPA to 2.4 g (EPA was their proxy for fish intake). This group saw a significant reduction in MI and all-cause deaths, 9.3% vs 12.8% total deaths over two years (a 27% relative risk reduction). Here's the survival chart:

Balancing omega-6 intake with omega-3 has consistently improved cardiac risk in clinical trials. I've discussed that here.

The thing that makes the DART trial really unique is it's the only controlled trial I'm aware of that examined the effect of grain fiber on mortality (without simultaneously changing other factors). The fiber group doubled their grain fiber intake, going from 9 to 17 grams by eating more whole grains. This group saw a non-significant trend toward increased mortality and MI compared to its control group. Deaths went up from 9.9% to 12.1%, a relative risk increase of 18%. I suspect this result was right on the cusp of statistical significance, judging by the numbers and the look of the survival curve:

You can see that the effect is consistent and increases over time. At this rate, it probably would have been statistically significant at 2.5 years. This result is consistent with short term trials I've found showing that wheat bran causes insulin resistance. In one, feeding five healthy subjects wheat bran for 7 weeks in addition to a controlled diet initially reduced blood glucose levels but resulted in insulin resistance, insulin hypersecretion and reactive hypoglycemia by the end of the seven weeks. Other trials show a non-significant trend toward insulin resistance on a whole-grain rich diet. The longer the trial, the stronger the effect.

I think the problem with whole grains is that the bran and germ contain a disproportionate amount of toxins, among which are the lectins. I've speculated before that grain lectins could contribute to leptin and insulin resistance. The bran and germ also contain a disproportionate amount of nutrients. To have your cake and eat it too, soak, sprout or ferment grains. This reduces the toxin load but preserves or enhances nutritional value. Wheat may be a problem whether it's treated this way or not.

Subjects in the studies above were eating grain fiber that was not treated properly, and so they were increasing their intake of some pretty nasty toxins while decreasing their nutrient absorption. Healthy non-industrial cultures would never have made this mistake. Grains must be treated with respect, and whole grains in particular.