How to lose body-fat healthily.

Previous blog posts have been about Carbohydrates, Fats & Proteins. However, when you go shopping, you buy food. So this blog post is going to be about food. Updated!

1) If you're eating a high-carb diet, eat 6 small meals or 3 meals and 3 snacks per day to keep your blood glucose relatively stable. I used to believe that it also kept your metabolic rate high, but I now know this to be a myth. If you're the type of person who gets lowish blood glucose in the mornings (which may make you ravenously hungry and therefore highly likely to buy junk food when you're away from home), skipping breakfast is not advisable. If you're the type of person who isn't satisfied by small meals/snacks, a small number of large meals (Intermittent Fasting) is a better option.

2) Meals and snacks should contain proteins, fats and fibrous carbs.

3) Slow sugary/starchy carbs can be eaten in meals/snacks at breakfast and before/after workouts/exercise/intense activity. If/when you are sedentary, keep slow sugary/starchy carbs to a minimum. Keep fast sugary/starchy carbs to a minimum (except for the occasional treat or post-workout) as they can cause large fluctuations in blood glucose and insulin levels. The more intense exercise you do, the more slow sugary/starchy carbs you can eat.

4) Drink >1.5 litres of no-added-sugar watery drinks per day. If your urine is darker than straw, drink more. If you're weeing too often, drink less.

5) Balance your omega-6 and omega-3 essential fatty acids (EFAs) by eating about 100g of omega-3 rich oily fish (sild, sardines, pilchards, mackerel, herring, salmon, trout, fresh tuna etc) per day or supplement with fish oil capsules such that you get at least 2g of EPA+DHA per day. Please note that tinned tuna contains virtually zero omega-3 fat.

If you're vegetarian or vegan, see Vegetarians & vegans, listen up!

6) Eat 2 to 3 portions of low-sugar fruits per day - preferably before meals/snacks. Minimise your consumption of high-sugar fruits.

Proteins are:- Meats, poultry, fish, eggs, cheese, Quorn, seeds, nuts, legumes (peas, beans & lentils).

Fibrous carbs are:- All vegetables that grow above ground level, bulbs (onions, leeks, garlic etc) and "vegetable" fruits (tomatoes, peppers, cucumbers/courgettes, aubergines, avocados, olives etc).
Slow sugary/starchy carbs are:- All-bran, no-added-sugar muesli, oats, sweet potatoes, lightly-boiled new potatoes eaten hot, cold or refrigerated, Basmati rice, non-overcooked legumes & root veggies, lumpy wholegrain rye breads, Burgen/Vogel's soya & linseed breads.

Fast sugary/starchy carbs are:- White wheat breads, wholemeal wheat breads, most breakfast cereals including Shredded Wheat, Weetabix, Cheerios, Grapenuts etc, sugar, sweets, chocolate, cakes, biscuits, cereal bars, sweetcorn, overcooked tubers e.g. jacket potatoes, overcooked root veggies, overcooked legumes e.g. baked beans.

High sugar fruits are:- Ripe & over-ripe bananas, grapes, pineapples, sweet apples, sweet pears, sultanas, raisins, currants and any dried fruits with added sugar.

Low sugar fruits are:- Berries, stone fruits, citrus, Granny Smith apples, Conference pears. Dried apple rings, apricots, pear halves, peach halves and prunes without added sugar are high in sugar but they release that sugar very slowly.

Fats are sats, monos and the EFAs mentioned above. Butter is high in sats and monos. Olive oil & spreads are high in monos. Sunflower/safflower/corn oils & spreads are very high in omega-6 EFAs - minimise your consumption of these. Don't fry or roast with high-EFA oils as they oxidise and convert into trans-fats too quickly. Meats contain sats, monos and some EFAs. Minimise your consumption of anything with the word "hydrogenated" in the ingredients list.

Some foods fall in-between categories like yellow bananas which are medium speed sugary/starchy carbs. Green bananas are slow carbs and black bananas are fast carbs.

Depending on your insulin sensitivity, speed of metabolism and exercise levels, you may get away with eating fast sugary/starchy carbs - you'll just have to "suck it and see".

If eating makes you feel drowsy followed by hunger, you probably have Insulin Resistance. See Insulin Resistance: Solutions to problems. for ways to reverse Insulin Resistance.

One final bijou tip-ette:- Avoid walking down "dodgy" supermarket aisles (confectionery, cereals, booze, fizzy drinks) as "What the eye don't see, the heart don't grieve over".

Happy New Year folks!

Cont'd on How to lose body-fat healthily, Part 2.

Proteins: Dogs' Doodads.

"Mmmm! These Korean meatballs really are the dogs' b*llocks!" said Hugh Dennis on "Mock the Week" as "Things you don't hear on TV cookery programmes".

For an overview on Protein, see http://en.wikipedia.org/wiki/Protein.
For an overview on Protein in nutrition, see http://en.wikipedia.org/wiki/Protein_in_nutrition.

I'm not going to write any more about protein, as somebody else already has. So, I am referring you to Lyle McDonald's protein articles, as what Lyle doesn't know about protein fits on a postage stamp........a very small one!

I shall now take a break. Merry Christmas everyone!

Fats: Spawn of Satan or Dogs' Doodads?

From http://ajcn.nutrition.org/content/65/5/1628S.full.pdf

Fats get a lot of bad press in the media. There are so many adverts with "X% fat-free" or "only 1g of fat per Jaffa Cake" as if that's going to stop you from getting fat when you "om nom nom" your way through a whole box of the things!

Saturated fats are usually described as "bad" and polyunsaturates are usually described as "good". This is simplistic. Everything is bad in excess, even polyunsaturates. The thing about fats is that there are four basic types (saturates, monounsaturates, ω-6 polyunsaturates and ω-3 polyunsaturates) and they need to be consumed in roughly the right proportions for optimum health. Suffice it to say, the majority of people in the West do not eat them in anywhere near the right proportions. So, what exactly are fats?


Fats

Fats are an ester of glycerol (CH₂OH-CHOH-CH₂OH) & 3 fatty acids, and are also known as triglycerides (TG's) or triacylglycerols (TAG's).

1 molecule of glycerol + 3 molecules of fatty acid = 1 molecule of triglyceride + 3 molecules of water.

It's the fatty acids that determine whether a fat is saturated, monounsaturated etc. The four different types of fatty acid have a CH₃ at one end and a COOH at the other. The difference is in the middle section.

Saturated fatty acids have a middle section consisting of CH₂'s. Here's a diagram for Stearic acid (the predominant fatty acid in beef):-

__H H H H H H H H H H H H H H H H H O
H-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H


Monounsaturated fatty acids have one C=C bond in the middle, which is usually (but not always) 9 from the left-hand end, resulting in monounsaturates often being referred to as ω-9's, as ω is the last letter of the Greek alphabet. Here's a diagram for Oleic acid (the predominant fatty acid in olive oil):-

__H H H H H H H H_____H H H H H H H O
H-C-C-C-C-C-C-C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H


ω-6 polyunsaturated fatty acids have two or more C=C bonds in the middle, with the last one always being 6 from the left-hand end. Here's a diagram for Linoleic acid (the predominant fatty acid in sunflower oil):-

__H H H H H_____H_____H H H H H H H O
H-C-C-C-C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H


ω-3 polyunsaturated fatty acids have three or more C=C bonds in the middle, with the last one always being 3 from the left-hand end. Here's a diagram for Alpha-linolenic acid (the predominant fatty acid in flax-seed oil):-

__H H_____H_____H_____H H H H H H H O
H-C-C-C=C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H H H H H H H H H H H


These diagrams are slightly misleading. Where there is a C=C bond, there are two H's on the "underside" only of the molecule. This asymmetry causes the H's to repel each other and bend the molecule into a V-shape at each C=C bond. C=C bonds with H's on the same side are known as "cis" bonds. The above molecule is really cis, cis, cis (c,c,c) Alpha-linolenic acid. The other type of C=C bond is known as "trans" and looks like the following diagram:-

__H H H___H H___H H___H H H H H H H O
H-C-C-C=C-C-C=C-C-C=C-C-C-C-C-C-C-C-C-O-H
__H H___H H___H H___H H H H H H H H


This is a diagram of trans, trans, trans (t,t,t) Alpha-linolenic acid. As the H's are on opposite sides of the molecule, they do not repel each other and the molecule is straight, as shown above. Note that saturated fatty acid molecules are naturally straight. Therein lies the problem with trans-fatty acids. They're straight, like saturated fatty acids, but they have unsaturated bonds, which are prone to peroxidation. See http://www.cyberlipid.org/perox/oxid0002.htm WARNING! Heavy-duty organic chemistry!

Our bodies take trans-fatty acids and incorporate them into cell membranes as if they were saturated fatty acids. This results in atherogenicity (artery-clogging), damage to the immune system and other health problems. Trans-fatty acids are found in partially-hydrogenated vegetable oils, so any cooking/spreading fats which have the word "hydrogenated" high-up in the ingredients list should be avoided. These are bad fats.

There are naturally-occurring trans-fatty acids made by bacteria in the stomachs of ruminant animals, like Conjugated Linoleic Acid (CLA). This looks a bit like the diagram below:-

__H H H H H_____H___H H H H H H H H O
H-C-C-C-C-C-C=C-C=C-C-C-C-C-C-C-C-C-C-O-H
__H H H H H H H___H H H H H H H H H


This has one of the C=C bonds shifted to the left and also has one cis bond and one trans bond, so the molecule is always bent. CLA has possibly beneficial properties, but human trials show mixed results. It's certainly not artery-clogging, so don't let anyone put you off eating butter from grass-fed cows (e.g. Anchor or Kerrygold butter) by saying that it has trans-fats in it. CLA is a harmless trans-fat.


Saturated fat consumption should be about 10% of total calories. This is because, even though saturated fats are not essential (our bodies can synthesise them), this guarantees adequate synthesis of sex hormones. Total polyunsaturate consumption should be about 5% of total calories, with a ω-6:ω-3 ratio of between 1:2 and 4:1. As ω-3's are found in greater quantities than ω-6's only in flax-seeds (a.k.a. linseeds) and oily fish, and many people eat way too little or no oily fish (and who, other than body-builders and some vegetarians/vegans, eats flax-seeds?), the ω-6:ω-3 ratio in the West is ~20:1. This is due to the widespread consumption of meats, eggs & milk from grain-fed animals, grains, nuts and seeds. There are high rates of heart disease and other inflammatory diseases in the West, as ω-6's end up in series 1 & 2 prostaglandins, and series 2 prostaglandins are pro-inflammatory. ω-3's end up in series 3 prostaglandins, which are anti-inflammatory.

So eat up yer oily fish if you're not vegetarian or vegan. Otherwise, eat up yer ground-up flax-seeds!

Monounsaturates can make up about 15% to 35% of total calories, depending on activity levels. From the histogram in Everyone is Different, sedentary people, on average, burn twice as much energy from fats as from carbohydrates.

So, if 25% of energy comes from protein say, 25% of energy can come from carbohydrates, and 50% can come from fats, i.e. a 2:1 ratio of fats:carbs. The cyclists at the left-hand end of the histogram in Chapter 1 would do best on 25% protein, 15% carbohydrate, 60% fat, when sedentary, whereas the cyclist at the right-hand end of the histogram would do best on 25% protein, 60% carbohydrate, 15% fat, when sedentary. When active, more carbs are needed by everyone.

Which fats contain which fatty acids? See https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQcYggz8ORx7mdTT7_ngR-jKOG-2FB4sm5HZWFyJF7xFYlNn-XCkbs4tSIuFFaJFVUdFTw13Q5M2-Adu_jeVnu3O37NhPlK_XWrxIACJ_QT1KmVElpl1YoLO4nfBBoqJNI5FQlhSDh/s640/comparison-of-fats.gif for a Comparison of Dietary Fats.

For high-temperature cooking, saturates are the least likely to oxidise (when they're on fire, they're oxidising!), followed by monounsaturates, then ω-6's, with ω-3's being the most likely to oxidise. An oil doesn't have to be smoking, to be oxidising. Alpha-linolenic acid oxidises to varnish at room temperature without smoking, which is why linseed oil is used to varnish cricket bats and dilute putty. The best non-animal fat for high-temperature cooking is Coconut Oil, followed by Palm Oil and then Olive Oil.

Extra-Virgin Olive Oil (EVOO) has a lower smoke point than refined Olive Oil (due to higher levels of free fatty acids), but has higher levels of polyphenol antioxidants, which makes it heart-healthy.

Oils high in polyunsaturates shouldn't be heated to temperatures greater than 100°C, as polyunsaturates can change from the cis configuration to the trans configuration at 102°C. See http://www.harricksci.com/sites/default/files/pdf/application_notes/FatIR_App-Notes_ATR_Oil-Analysis.pdf

Carbohydrates: Dogs' Doodads or Spawn of Satan?

Depending on which side of the fence you're on, Carbohydrates are either the Dogs' Doodads or the Spawn of Satan. As I get older, I prefer to sit on the fence. Let's start with the basics.


What are Carbohydrates?

Carbohydrates are so named because they have the generic formula (CH2O)n. C is carbon and H2O is water hence Carbo-Hydrate. There are several different types.

1) Sugars. There are monosaccharides, the most common being Glucose (a.k.a. Dextrose), Fructose and Galactose. There are disaccharides, the most common being Sucrose, Lactose and Maltose. Disaccharides are 2 monosaccharides linked by a glycosidic bond formed by a condensation reaction (removal of a water molecule, usually by an enzyme). Disaccharides have to be hydrolysed (have a water molecule added back in, usually by an enzyme) into monosaccharides before they can be absorbed in the gut.
Sugars are simple carbohydrates.

2) Starches. These are chains of glucose molecules linked by glycosidic bonds. Starches have to be hydrolysed into glucose molecules before they can be absorbed. There are unbranched chains like amylose which is also known as resistant starch. There are branched chains like amylopectin and maltodextrin. Glycogen is a branched chain "animal starch" that is synthesised inside muscle and liver cells and which can be rapidly converted back into glucose inside cells.

3) Non-Starch Polysaccharides (NSPs). These are also known as fibre/fiber and there are 2 types: soluble (e.g. pectin, beta-glucan & cellulose) and insoluble (e.g. bran). These aren't absorbed, but gut bacteria can feed on soluble fibre/fiber. Starches and NSPs are complex carbohydrates.

For more information, see http://en.wikipedia.org/wiki/Carbohydrate

The amount of carbohydrate that someone needs varies from person to person and increases with the intensity and volume of exercise done. See Everyone is Different. What are the best carbs to eat? "Complex" ones from "wholegrain" cereals? Not necessarily.


Simple vs Complex

TV ads for breakfast cereals bang on about the wholegrain goodness of complex carbohydrates releasing energy slowly. The terms "Simple" and "Complex" actually refer purely to the chemical structure of a carbohydrate and have nothing to do with how quickly they turn into blood glucose in the body. The Glycaemic Index (GI) (or Glycemic Index if you're American) relates to how quickly carbohydrates turn into blood glucose in the body. See http://www.mendosa.com/gilists.htm for a list of 750 foods and their GI & GL (GL = Glycaemic Load = GI/100 x carb content per serving). Here are a few extracts. Note: a GI of 55 is low; a GL of 10 is low.

The last three items in the list are all simple carbohydrates. As you can see, some wholegrain complex carbohydrates turn into blood sugar faster than simple carbs. This is because the wholegrains have been ground into powder which is rapidly digested and absorbed, despite the presence of fibre/fiber.

As fructose has such a low GI, does this mean that we can eat as much of it as we like? No! When we eat fructose, it passes from the small intestine into the portal vein and goes straight to the liver. As liver cells contain an enzyme called fructokinase (which has a high affinity for fructose), all dietary fructose is absorbed by the liver where it tops-up liver glycogen. Liver glycogen is also topped-up by glucose (obtained from the digestion of starchy carbohydrates). Once liver glycogen stores are full, any further fructose is converted into fats, which are stored as ectopic liver fat and also exported as triglycerides. High serum triglycerides are heart-unhealthy. See Cholesterol And Coronary Heart Disease.

Why is GI important? When we eat carbohydrates, they raise blood glucose levels. Pancreatic beta cells secrete a hormone called insulin, which allows more glucose to pass into cells (by moving Glu-T4 transporters inside the cells). When more glucose enters cells, glucose levels in the blood fall. It's a negative feedback loop. For millions of years, we lived on a diet of natural, unrefined carbohydrates and so the secretion of insulin never had to change blood glucose levels very rapidly.

When unnatural, refined, high-GI carbs are eaten, blood glucose levels rise much faster. This results in over-secretion of insulin (hyperinsulinaemia). This shuttles too much glucose into cells and results in.......low blood glucose, followed by low blood insulin. Rapidly-falling and low blood insulin levels cause feelings of severe hunger and cravings to eat more carbs. It's a vicious circle. Hyperinsulinaemia also has other bad effects on the body. See http://www.mercola.com/2001/jul/14/insulin.htm to learn about Insulin and its Metabolic Effects.

GI has a weakness because adding fats and some proteins to high-GI foods lowers the GI but can increase the insulin response. Saturated fats, monounsaturates and omega-6 polyunsaturates raise the insulin response to carbs.

There is another index called the Insulin Index (II). See http://www.mendosa.com/insulin_index.htm.
The II contains a few surprises. Some proteins (e.g. the whey in milk & yoghurt) produce a large insulin response. Insulinogenic proteins are also glucogenic, so they don't cause low blood glucose.

On the other hand, refrigerating some foods lowers their GI & II by changing the starch in them into resistant starch, even if the food is subsequently re-heated. Rice & potatoes are two such foods.

As the terms "simple" and "complex" are meaningless in terms of carbohydrates' effects in the body, I prefer to use the terms "slow" and "fast". In a nutshell, slow carbs are good and fast carbs are bad. These terms can be applied to proteins, too. Egg is slow and whey is fast. Sticking to mostly slow foods keeps blood glucose and insulin levels stable, which results in better appetite control and better health, too.

It was soaring serum insulin levels that were sending me to sleep after carby meals years ago. Postprandial hyperinsulinaemia results in amino acids from digested foods being shuttled into cells. However, L-tryptophan isn't shuttled into cells, so the level of this amino acid in the blood rises relative to others. As L-tryptophan competes with other amino acids to cross the blood-brain barrier, now that the competition has been removed, more L-tryptophan enters the brain. It's converted into 5-hydroxytryptophan (5-HTP), then serotonin & melatonin. High melatonin levels in the brain cause sleepiness.

So remember, "Right carbs, right amounts, right times."

Everyone is Different.

If there's one thing I've learned over the years of research into Diet and Nutrition, it's this: Everyone is Different. When I first discovered low-carbohydrate diets (thanks to the late Dr Robert C. Atkins M.D.), I thought that it was the One True Diet, and I became a bit of an "Atkins bore" telling everyone how wonderful it was and suggesting that everyone should be on it. I now know that what suits me* doesn't necessarily suit everyone else.

*It only suited me because I had Insulin Resistance/Metabolic Syndrome/Syndrome-X. I reversed it in 2008. See Insulin Resistance: Solutions to problems for how I did it.

Here's Fig. 2 from Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Used with permission.

Respiratory Exchange Ratio (RER) (a.k.a. Respiratory Quotient (RQ)) is the ratio of carbon dioxide breathed out to oxygen breathed in. This ratio depends on the fuels that the body is burning for energy. For example, if the body is burning 100% fats, RER = 0.7. If the body is burning 100% carbohydrates aerobically, RER=1.0. If the body is burning 100% carbohydrates, with some aerobically and some anaerobically (e.g. sprinting flat-out), RER > 1.0. To understand why this is so, see Respiratory Exchange Ratio (RER) explained.

RER varies with intensity of exercise, food intake (increasing protein &/or carbohydrate intake increases it and fasting or reducing protein &/or carbohydrate intake reduces it) and cardiovascular fitness. Increasing cardiovascular fitness reduces RER.

The top diagram is a histogram of fasted RER and % fat oxidation vs. number of subjects. At the left-hand end of the histogram, there are two cyclists with a fat oxidation of 93 - 100%. At the right-hand end of the histogram, there is one cyclist with a fat oxidation of 20 - 27%. Average fat oxidation is ~60%.

As exercise intensity increases, the peak in the histogram shifts to the right as shown in the lower diagram. At 25% of maximum intensity, mean fat oxidation is ~53%. At 50% of maximum intensity, mean fat oxidation is ~37% and at 75% of maximum intensity, mean fat oxidation is ~13%. At maximum intensity, mean fat oxidation is ~0% i.e. 100% of energy is obtained from carbohydrates when sprinting flat-out. Somebody on a very-low-carbohydrate, high fat ketogenic diet e.g. Atkins induction (~20g net carbs/day) could keel over with hypoglycaemia if they exercise for too long at too high an intensity.

As there is variation from person to person, you must find out for yourself your own optimum proportions of proteins, fats & carbohydrates, and these depend upon the intensity & volume of exercise you do. It sounds complicated, but it isn't really.

Apply the principle of "Eat, monitor & adjust accordingly" as Toxic Toffee (ex-Muscletalk member) always used to say. The eating bit will be covered in future Blog posts. The monitoring bit doesn't necessarily involve bathroom scales.

Hang on. Isn't "dieting" all about losing excess weight? Not necessarily. Remember the old joke?
Q. What's the best way to lose 5lbs of ugly flab?
A. Cut off your head.
As your body contains water, muscle, bodyfat, bones, cartilage, tendons, organs, glycogen, skin etc and your scales can't tell the difference between them, losing weight the wrong way can make you less healthy. However, losing weight the right way will make you more healthy.

If you starve, skip breakfast or go for a long run before breakfast, as your body is lacking glycogen reserves & amino acids, a large amount of a corticosteroid hormone called cortisol is secreted, which increases the conversion of muscle into amino acids, then glucose. As muscle has an energy density of ~600kcal/lb, a deficit of 3,500kcal (which would result in a bodyfat loss of 1lb) results in a muscle loss of 5.8lb. For more information, see The Energy Balance Equation.

Chronically-high cortisol also suppresses the immune system and weakens skin & bones.

Unless you have a lot of muscle mass to spare, it's bodyfat that you should be losing, and to monitor this, either use a tape-measure around your waist, check how loose/tight your clothes are, or strip-off and jump up & down in front of a full-length mirror. As Big Les (Muscletalk Moderator) says, "If it jiggles, it's fat.".

2016 EDIT: Scales that can calculate bodyfat % etc are now inexpensive, e.g. Body Analysis Scale.

So, what happens if you eat too much carbohydrate but your body doesn't burn it fast enough? Initially, carbohydrate intake tops-up liver and muscle glycogen stores, which increases carbohydrate-burning to compensate. The liver can store about 70g of glycogen and muscles can store about 400g of glycogen. If, despite increased carbohydrate-burning, more carbohydrate is consumed than is burned, glycogen stores continue to fill. When glycogen stores become full, RER increases to 1.0 and 100% of energy is derived from carbohydrate. Getting 100% of energy from carbohydrate means that zero fat is burned, so keeping glycogen stores filled to the brim by chronically overeating carbohydrate is not a good idea if you want to burn some body-fat.

Once glycogen stores are full, any additional intake of carbohydrate beyond that which is burned passes through the lipogenesis pathway - this basically means that carbs are turned into fat - which may end up as liver fat. But there's even worse news. Fat is secreted by the liver into the blood as triglycerides. This is bad for the cholesterol particles in your blood. See Cholesterol and Coronary Heart Disease. What happens if you eat too few carbs? As stated above, someone exercising at a highish intensity taking in insufficient carbohydrates could get hypoglycaemia & keel over.

How many grams of carbohydrate per day does it take to promote lipogenesis? Someone at rest burns ~1kcal/minute. If this is derived 100% from carbohydrate, this is equivalent to 0.25g of carbohydrate/minute, or 15g of carbohydrate/hour, or 360g of carbohydrate/day. Therefore, sedentary people who chronically consume more than 360g of carbohydrate/day may produce significant triglycerides. People who have The Metabolic Syndrome/Syndrome-X (a high proportion of people who have excess belly fat) have increased lipogenesis and higher serum triglycerides than healthy people.

Discussing weight again for a moment, it's often said that all diets are the same, as weight loss is all about calories. This is true. See Is a Calorie a Calorie? However, body composition is determined by a combination of macro-nutrient proportions (i.e. the relative amounts of proteins, carbohydrates and fats in the diet) and the intensity & volume of exercise. Health is determined by a combination of micro-nutrient proportions (i.e. vitamins, minerals & anutrients) and exercise. See On burning, storing and recomposing.

If you're only interested in weight loss, just count calories. If  you wish to lose bodyfat without losing muscle mass, you need to know what proportions of proteins, carbohydrates & fats to eat (it's really not that critical, but many people get it wrong). You need to know the difference between good carbs & bad carbs, and good fats & bad fats. You need to know the best times to eat proteins, carbohydrates & fats relative to exercise (it's also really not that critical, but many people get it wrong). You need to know the difference between good exercise & bad exercise.

Continued on We are not all the same.

It's all about ME, baby! (1997 - present)

If you're wondering "Who is this Nige geezer and why is he wittering on about Cholesterol, Diabetes & Vitamin D?", read on...

This story starts in 1997. I'd just come through an acrimonious divorce and I was tired, bloated, 17st 7lb and depressed. Then a pamphlet dropped through my letterbox. It was from Agora Lifestyles, promoting a book by a Dr. Robert C. Atkins (never heard of him!). I didn't buy his book, but I read the pamphlet from cover to cover, and it described postprandial sleepiness followed by ravenous hunger after eating meals high in carbohydrate. Since childhood, I used to feel very sleepy after eating starchy meals but I never knew why. So, despite my disbelief that Atkins' diet could work, I cut out bread, pasta, potatoes, rice, cereals etc - all of the things that we are constantly told are good for us because they are "low-fat".

Within days, I felt like a new man. The postprandial sleepiness & ravenous hunger were gone, my weight slowly decreased and the heartburn I used to get was also gone. I was a total convert. By nature I'm very curious (which is why I became an Engineer), so I wondered how Atkins' diet worked. In 1999, I got Internet access at work and was delighted to see that there were people out there (some of them doctors) other than Atkins who were saying much the same thing.

In 2001, I got a shock when the company for which I'd worked for 24 years lost a "must win" contract and I was put on the redundancy list. My health began to deteriorate. My body temperature fell and in November 2002 I was admitted to hospital with renal colic caused by a uric acid kidney stone. I got to see an endocrinologist, who did tests and found that my pituitary gland wasn't secreting TSH, causing secondary hypothyroidism. I was prescribed levothyroxine. The upside is that I am now exempt from prescription charges. I also get annual blood tests, so that I can see the results of any diet/supplement/exercise change on my blood-work.

As well as having a dysfunctional pituitary, I also had "Metabolic Syndrome" (a.k.a. "Syndrome-X" in the US). This is a fancy name for pre-type 2 diabetes and it's caused by Insulin Resistance (IR). This meant that my fasting serum glucose, triglycerides, total cholesterol, LDL & uric acid were high and my HDL was low. A diet lower in sugary & starchy carbohydrates suits people with this condition.

I didn't know how Atkins's diet worked, so I studied some biochemistry web-sites to get a better understanding of human metabolism. In November 2002, I joined the Muscletalk forum after e-mailing James Collier B.Sc. (Hons) - Moderator and Contributor to Muscletalk as an Expert in Nutrition, criticising his negative article on ketogenic diets. Username "Nigeepoo" was born. Why Nigeepoo? I have a rather odd sense of humour and think that putting "poo" on the end of a word is hilarious. It also suits my warm & fluffy nature!

This was the beginning of a new phase in my learning. From there, I found a US & then a Canadian (now closed) body-building forum which allowed me to learn even more about nutrition. In January 2003, the BBC series "Diet Trials" studied the Atkins diet amongst others. At the end of the series, viewers were referred to a BBC Nutrition & Fitness board (now closed) and a Healthy eating board (now a Food Q&A board) where I posted. As a result of various recommendations, I bought some books on running, diet & nutrition, metabolism and biochemistry. I also surfed PubMed and various journals, looking for studies on ketogenic diets and the effects of different proteins, fats and carbohydrates on subjects. See How stuff works.

In 2004, my pituitary stopped secreting sufficient LH & FSH and in 2005 it stopped secreting sufficient GH, so I decided to take early retirement and take things a bit easier as I was having trouble with my memory & concentration. I decided to dump my nutritional knowledge to hard-copy before I forgot it, so I wrote an e-book, "Nigee's Guide to Losing Body-fat Healthily". That's not the only reason why I wrote it....you'll have to read it to find out the other one. Was that hint subtle enough? Please note that the information in the e-book is frozen and is now completely out-of-date. The information in this blog is kept up-to-date.

Discovering Vitamin D3 at the beginning of 2007 was a major breakthrough, in terms of memory, concentration, mood and the Metabolic Syndrome. My endocrinologist was so pleased with my last set of blood and urine tests (all normal except for slightly raised cholesterol) that I don't need to see him any more. I still have annual blood tests, to monitor my condition.

Discovering the bad effects of a sedentary lifestyle at the end of 2010 was another major breakthrough in terms of tackling IR. See Insulin Resistance: Solutions to problems.

Right, that's enough about me, baby! Tomorrow, it's back to boring old nutritional stuff again.

Cheers, Nige.

Cholesterol And Coronary Heart Disease

From http://www.health-heart.org/

Cholesterol & coronary heart disease are mentioned a lot in the media. Unfortunately, most of what you see & hear is either completely wrong, or dumbed-down so much that it's inaccurate.

Fat & cholesterol don't stick to the insides of artery walls like grease on the inside of a drainpipe. This article explains what cholesterol is, how arteries get blocked and how to minimise the risk of having a heart attack or ischaemic stroke.


What is cholesterol?

Cholesterol is a large, waxy molecule (C₂₇H₄₅OH) consisting of a hydrocarbon (fat-soluble) tail, a middle section consisting of four carbon rings (the steroid bit) and an alcohol (water-soluble) group on the end. Cholesterol is a powerful anti-oxidant and is what bile acids, mineralcorticoids, glucocorticoids and sex hormones are made from.

Cholesterol is "chauffeured" around the body in lipoprotein "limousines". Lipoproteins are lipo (fat-soluble) at one end, protein (water-soluble) at the other end and they form a spherical shell around their contents with the lipo end pointing inwards and the protein end pointing outwards. The shell is like the body of the limousine. In the shell, there are apo(lipo)proteins which are like the chauffeur, as they determine where the particles are taken up. HDL has apo A in its shell which makes it get taken up by receptors in the liver. LDL has apo B in its shell which makes it get taken up by receptors in cells, artery walls etc. The passengers are cholesterol, cholesteryl esters, phospholipids and triglycerides. These limousines have different types, like chylomicrons, VLDL, LDL, IDL & HDL, the difference being the type & amount of apo(lipo)protein and the relative proportions of cholesterol & the other passengers. There are also sub-groups of each type.

The different variants are affected by serum triglycerides. High serum triglycerides (caused by a chronic over-consumption of sugary & starchy carbohydrates for activity level) result in cholesterol-depleted, triglyceride-rich particles and low serum triglycerides result in cholesterol-rich, triglyceride-depleted particles. As cholesterol is a powerful antioxidant, smaller cholesterol-depleted particles (Type B) oxidise faster than larger cholesterol-rich ones (Type A).

Oxidised LDL particles are "bad cholesterol" and are swallowed by scavenger macrophages. These expand into foam cells, which become embedded in the intima of artery walls. Other processes occur which cause cholesterol & calcium to accumulate as a plaque inside the media of artery walls. To see a cross-section through an artery wall, see the top of this page. Unoxidised LDL particles are not swallowed by scavenger macrophages, so unoxidised LDL particles are not "bad cholesterol". In young people, plaques of cholesterol with no calcium can accumulate within artery walls, making Coronary Artery Calcium (CAC) scans ineffective. See Stenosis Can Still Exist in Absence of Coronary Calcium.

Plaques force the inner artery wall inwards, making the artery narrower, impeding the flow of blood through it. This can cause angina pectoris (pain in the chest) as the heart is starved of oxygen, or vascular dementia as the brain is starved of blood. The cap covering the plaque may rupture, causing chunks of plaque to circulate and block coronary arteries (causing a heart attack), or cerebral arteries (causing an ischaemic stroke).

It's possible to reduce serum triglycerides significantly by eating lots of long-chain omega-3 fats from oily fish. These inhibit the conversion of glucose into triglycerides. Inhibiting the conversion of glucose into triglycerides can result in increased blood glucose levels (not good - see below) if sugary/starchy carbohydrate intake is too high. Solution? Reduce sugary/starchy carbohydrate intake to suit activity level.


Why do foam cells embed themselves into the intima of artery walls?

Arteries are elastic, muscular tubes which stretch a bit each time the heart pumps and contract again between beats. They also relax & constrict to control the flow of blood through them. When you get cold, they constrict to reduce the flow of blood to the skin to prevent excessive heat loss. When you get hot, they open to increase the flow of blood to the skin to increase heat loss.

Foam cells don't go just anywhere. They embed themselves into damaged areas of artery walls. This is a good thing, otherwise damaged artery walls could rupture, causing a haemorrhage.


What damages artery walls?

Chronically high blood pressure.
Chronically high blood glucose.
Chronically high blood free radicals.
Chronically high blood homocysteine.
Chronically low blood antioxidants.
Chronically high blood pro-oxidants.
Chronically low blood anti-inflammatories.
Chronically low Vitamin K2.
Chronically high LDL due to hypothyroidism or other factors.


How can I reduce damage to my artery walls?

1) Have blood pressure (BP) tested regularly. There's one problem with having your BP taken in a GP's surgery and that is 'white-coat hypertension' where the stress of having your arm squeezed by the cuff sends your BP up! If you buy your own BP monitor (Lloyds pharmacy sell a fully automatic BP monitor with standard cuff for £9.99), you can become accustomed to using it and overcome white-coat hypertension. 5,000iu/day of Vitamin D3 can reduce BP by making artery walls more elastic. 4g/day of Epsom Salts provides 400mg/day of Magnesium, which acts as a smooth muscle relaxant, reducing BP & cardiac arrhythmias.

2) Have blood glucose (BG) tested regularly. If you're lucky, you may be able to get a HbA1c test. This shows accumulated damage to red blood cells by blood glucose.

3) Don't smoke! Apart from lung cancer, chronic obstructive pulmonary disease & emphysema, smoking speeds the oxidation of LDL.

4) Take a B-complex containing B6, B12 & folic acid, which lowers serum homocysteine levels.

5) Eat a diet rich in anti-oxidants from coloured veggies (beta-carotene), fruits (Vitamin C + bioflavonoids), tomatoes (lycopene), nuts & seeds (gamma-tocopherol & copper), Brazil nuts (selenium), beer/wine in moderation (muscle relaxant), green tea (polyphenols), cocoa/dark chocolate (polyphenols & copper), onions/garlic (quercetin) etc. See Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50.

6) In men and non-menstruating women, too much iron in the blood relative to copper is pro-oxidant, so don't supplement with iron. Menstruating women have the opposite problem.

7) Take about 2g/day of long-chain omega-3 fats from oily fish, or about 20g/day of flaxseed oil if male, or about 10g/day of flaxseed oil if female. Please note that tinned tuna contains very little omega-3 fats. See Clinical nutrition: 4. Omega-3 fatty acids in cardiovascular care.

8) Eat a diet rich in Vitamin K2, to make calcium go into bones & teeth, instead of into artery walls, kidneys & brain. For good sources of Vitamin K2, see HERE. Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective.

9) If you're feeling tired and are gaining weight for no obvious reason, get serum thyroid hormone levels tested (TSH, FT4 & FT3 preferably), as low thyroid hormones down-regulate LDL receptors, resulting in LDL particles lingering in the blood for longer than usual. This increases LDL-C, LDL-P (particle count) and the oxidation of the particles. See Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis.


What about Benecol & Flora Pro-Activ?

These yoghurts & spreads contain plant sterols/stanols, which reduce total serum cholesterol by up to 15%. However, LDL quality is more important than LDL quantity (up to a point) and there is no evidence that these foods save lives.


What about statins?

Statins (HydroxyMethylGlutarate Coenzyme-A Reductase inhibitors) reduce serum cholesterol. They also have anti-inflammatory & anti-clotting effects by reducing levels of the non-sterol derivative mevalonate and subsequent products. Click HERE to see the cholesterol synthesis pathway. Statins save lives in people who have had a heart attack and in men between the ages of 30 and 60. However, younger & older men and women do not get a significant reduction in deaths, (though heart-attack deaths may be reduced) and there can be undesirable side-effects (muscle pains, memory loss etc). I strongly recommend that anyone taking statins, supplements with at least 100mg/day of Co-Q10, as the synthesis of this vital substance is reduced. Note that fish oils have anti-inflammatory, anti-clotting and anti-arrhythmia actions, but don't suppress the production of Co-Q10.


What about dietary cholesterol?

When cholesterol is eaten, the liver produces less cholesterol. An average egg contains about 250mg of cholesterol. The vast majority of people (who don't have genes for familial hypercholesterolaemia) can eat two eggs a day without significantly affecting their serum cholesterol & triglyceride levels. See Effect of dietary egg on human serum cholesterol and triglycerides. People with the ApoE4/E4 polymorphism are more sensitive to dietary fat & cholesterol raising serum LDL, and cannot eat fat & cholesterol willy-nilly.

There are a couple of sites that have CVD risk calculators, JBS2 and QRISK®2-2013. The National Institute for Clinical Excellence (NICE) no longer recommends the use of JBS2, as it's overly-pessimistic.

Blood Glucose, Insulin & Diabetes

Diabetes is afflicting an increasing percentage of the population as time goes by. Even athletes like Sir Steven Redgrave can get it. This article tries to explain the workings of the body's blood glucose (BG) regulation system and what can go wrong with it.


How does the body regulate blood glucose?

At any given moment, there's ~4.5g of glucose in your blood (5mmol/L x 180g x 5L). As the brain alone uses about 6g of glucose per hour in the absence of ketones, blood glucose (BG) level could fall to zero within an hour if we ate no sugary/starchy carbs. If we ate a mere 5g of glucose, BG level could double. As very low BGs are fatal and very high BGs damage proteins by a process called glycation (a bit like caramelisation), the body keeps BG levels within fairly tight limits by the use of a negative feedback (NFB) control system.


How does a negative feedback control system work?

NFB systems consist of a non-inverting (more in → more out) part, which in this case are the islet cells of Langerhans (a.k.a. pancreatic beta cells), as increasing BG level results in increasing insulin secretion. It's actually more complicated than that. Beta cells can store insulin and dump it into the blood if there is a sudden increase in BG level. This is analogous to the accelerator pump in a carburettor, which dumps petrol into the engine if you slam your foot on the accelerator pedal, i.e. it produces a rapid response. The dumping of insulin from beta cell storage is known as the 1st Phase insulin response. If this (or the accelerator pump) fails, there is a lag in the response; this will become significant below.

Increasing BG level results in increasing insulin secretion from beta cells and is known as the 2nd Phase insulin response.

The other part of a NFB system is the inverting (more in → less out) feedback part, which in this case is split into three parts, all working in parallel. They are:

1. Liver - increasing insulin level results in decreasing Hepatic Glucose Production.
2. Muscle cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.
3. Fat cells - increasing insulin level shifts GLU-T4 transporters which shuttle glucose from the blood into cells, decreasing BG level.

What can go wrong?

There are three main types of diabetes:

1) Type 2 diabetes. This is by far the most common (about 95% of all cases) and is usually caused by abdominal obesity. Type 2 diabetes has two main mechanisms going on. The first is a progressive insulin resistance (IR) of target tissues, possibly caused by increased levels of saturated fatty acids being fed to the liver from abdominal fat stores, chronically-high BG and insulin levels caused by chronically over-consuming high glycaemic load carbohydrates, possibly accompanied by large amounts of saturated fat and/or large amounts of omega-6 fat. A sedentary lifestyle lowers the sensitivity of muscle cells to insulin. Insulin resistance also has a hereditary link. IR is reversible. See Insulin Resistance: Solutions to problems.

Insulin resistance weakens the feedback in the NFB system, resulting in increased BG level (hyperglycaemia) and increased insulin level (hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective. Increased BG level causes increased damage to beta cells by glycation. Increased insulin level gradually causes further insulin resistance as target tissues become increasingly insensitive (a bit like louder and louder music making you progressively deafer and deafer). Eventually, beta cells become too damaged to secrete sufficient insulin and insulin levels begin to fall. This results in a massive rise in BG level and this is now full-blown Type 2 diabetes. There are five main treatments for Type 2 diabetes:

1. Lifestyle interventions - reduced intake of high glycaemic load carbohydrates and/or increased intake of omega-3 fats and/or increased intake of Vitamin D3 and/or increased intense exercise and/or loss of abdominal fat.
2. Sulphonylureas - drugs which stimulate beta cells to secrete even more insulin. Unfortunately, that's a bit like flogging a dying horse as it doesn't address the problems caused by weakened feedback and eventual beta cell failure is inevitable, resulting in the need for insulin injections.
3. Biguanide drugs such as Metformin - increase insulin sensitivity in target tissues. This strengthens the feedback in the NFB system, which results in reduced BG and insulin levels. This combined with lifestyle interventions can return the NFB system to normal operation.
4. Thiazolidinediones - also increase insulin sensitivity in target tissues, e.g. muscle and fat, as well as possibly improving the secretory function of beta cells. Increases the number of new, empty fat cells.
5. Insulin injections take the strain off beta cells, but may worsen insulin resistance.

2) Type 1 diabetes. This is much less common (about 5% of all diabetes cases) and is caused by an autoimmune disease. One possible mechanism is as follows: Due to an increase in Zonulin, the gut becomes more permeable than it should (a.k.a. Leaky Gut), which allows protein fragments to pass into the blood. These are locked-onto by antibodies, and destroyed by the immune system. However, if a protein fragment happens to have the same sequence of amino acids as a protein in your body, the immune system sets about destroying parts of your own body. Examples of this are gluten (proteins found in wheat, rye, barley and oats) producing antibodies in the blood that can destroy the gut causing Coeliac Disease, or skin cells causing Dermatitis Herpetiformis, or mucous membranes causing Sjogren's Syndrome, or brain cells causing Cerebellar Ataxia. As there's an association between the consumption of cows' milk and the incidence of type 1 diabetes (see here ), it's possible that, in susceptible individuals, casein protein fragments enter the blood, resulting in auto-immune destruction of pancreatic beta cells. Another possible mechanism is autoimmune attack after a viral infection. Once all beta cells have been destroyed, no insulin is secreted and insulin injections are required. If some beta cells survive, there's a possibility that normal BG levels can be maintained if sugary/starchy carbohydrate intake is reduced.

3) Latent Autoimmune Diabetes of Adulthood (LADA). This is a slow developing diabetes that is more like type 1 in origin (autoimmune with antibodies) but is often misdiagnosed as type 2 because of the age at diagnosis and the relatively slow progression of the disease (slow compared to type 1 but fast compared to type 2). It is believed that Sir Steven Redgrave has this. Whether or not his autoimmune disease was triggered by a huge intake of milk (to build those Olympic-winning muscles), we'll never know. To minimise your risk of developing autoimmune diseases, see Keep 'em tight.



What else can go wrong?

As stated earlier, loss of the 1st Phase insulin response can occur. This usually happens when beta cells are chronically over-secreting insulin due to a chronically-high intake of sugary/starchy carbs and are unable to store any. This results in a lag in insulin response. This isn't a problem if low glycaemic load carbs are eaten and BG levels change only a little or very slowly. However, if high glycaemic load carbs are eaten, this produces a rapid rise in BG level. If a NFB loop with a lag in it is presented with a step response change in input level, its output overshoots. This results in too much insulin being secreted (a.k.a. postprandial hyperinsulinaemia), which causes feelings of postprandial sleepiness and also down-regulates insulin receptors in the ventromedial hypothalamus (VMH), resulting in an eventual normal insulin level being interpreted by the VMH as rebound hypoinsulinaemia, which causes feelings of ravenous hunger (as insulin acts as a satiety/satiation hormone in the brain). The solution? Stick to low glycaemic load carbs.


Where does blood glucose come from if I haven't eaten?

When no sugary/starchy carbs are being digested, BG starts to fall. Adrenaline and noradrenaline (catecholamine hormones) are secreted by the adrenal medulla into the blood and also by sympathetic neurons. Like glucagon (see below), they stimulate the mobilisation of glycogen and triacylglycerols (stored fats) by triggering the production of cyclic AMP (adenosine mono-phosphate). Adrenaline and noradrenaline differ from glucagon in that their glucose-producing effect is greater in muscle glycogen than in liver. They also inhibit the uptake of glucose by muscle. Instead, fatty acids released from adipose tissue are used as fuel. Adrenaline also stimulates the secretion of glucagon and inhibits the secretion of insulin. Thus, catecholamines such as adrenaline and noradrenaline increase the amount of glucose released into the blood by the liver and decrease the utilization of glucose by muscle.

Pancreatic alpha cells secrete glucagon. This hormone mobilises the conversion of liver glycogen into glucose. The liver only stores about 70g of glycogen, but when combined with water, a larger mass of glucose is generated. Eventually, liver glycogen stores become depleted and BG level falls again. Glucagon also stimulates gluconeogenesis in the liver & kidneys, which is the production of glucose from non-carbohydrate precursors, like the conversion of glucogenic amino acids, such as glutamine, into glucose. This causes slow muscle wastage unless there is sufficient protein intake to provide the necessary amino acids. When BG falls to about 3.3mmol/L, the pituitary kicks-in and secretes ACTH (adrenocorticotropic hormone) which stimulates the release of cortisol from the adrenal cortex. Cortisol further stimulates gluconeogenesis in the liver & kidneys by catabolising (breaking down) muscle mass. When BG level falls to about 2mmol/L, the pituitary secretes GH (Growth Hormone) which has an anti-insulin effect.


What else does insulin do?

Insulin has many metabolic effects in the body apart from lowering BG level. It's a very anabolic hormone and an insulin spike is usually desired post workout to maximise the uptake of glucose and amino acids by muscle cells. There's nothing wrong with the occasional short-term insulin spike. It's chronically-high insulin levels due to chronic overconsumption &/or insulin resistance that cause long-term health problems like high blood pressure and clogging of arteries.

Vitamin D

A 77% reduction in new all-cause cancers in women over the age of 55.

From https://academic.oup.com/ajcn/article/85/6/1586/4633053

Vitamin D is known as the "Sunshine Vitamin" and it was once thought that a deficiency in it was rare and that it was only involved in calcium homoeostasis in bones and that a lack of it caused only Rickets. Recent research has shown that not only is Vitamin D involved in a whole host of bodily processes, but also that an insufficiency in it is very common, leading to an increased risk factor for a whole host of degenerative diseases, such as Coronary Heart Disease and Cancer.


What is Vitamin D?

There's a good overview on Vitamin D here.
See also University Lecture: The D-Lightful Vitamin D for Health by Michael F. Holick.


How common is Vitamin D deficiency?

According to Hyppönen and Power, in a large sample of the white British population born in 1958, 60.9% of subjects had serum 25(OH)D (the active metabolite of Vitamin D) of less than 75nmol/L in Summer & Autumn, and 87.1% had serum 25(OH)D of less than 75nmol/L in Winter & Spring. To convert units from nmol/L to ng/mL, divide by 2.5.

Here's my experience of Vitamin D3. For many years, I was struggling to cope with my job and I eventually took early retirement on the grounds of ill-health. In mid-2006 I was given a serum 25(OH)D test and the result was 73nmol/L. As the Reference Range for serum 25(OH)D is 50-200 nmol/L, I was technically not deficient in Vitamin D. Subsequent events suggested otherwise.

In January 2007, after reading the above study and a study by Vieth, Kimball, Hu and Walfish, I began to supplement with 2,000iu/day of Vitamin D3 and also used a UVB+IR lamp for 3 minutes each night. At first, nothing happened and I was pretty sceptical about getting any improvement. However, after about 8 weeks, I began to notice an awakening in my brain. This continued, and by March 2007, I was feeling quite perky. Friends commented on the fact that I had become very chatty and I was also waking early in the morning raring to go, totally unlike my former self. In May 2007, I had another serum 25(OH)D test and the result was 115nmol/L. Another interesting result was my serum triglycerides, something that's usually always higher than desirable. My TGs were 1.4mmol/L (RR less than 1.8mmol/L). This was the lowest result since tests began in 2002.

I began to get bored with standing around stark naked in front of a UV lamp for 3 minutes each night and I stopped doing this. Slowly, my brain began to go back to sleep. I couldn't understand why as I thought that 2,000iu/day of Vitamin D3 (5 x RDA) was more than enough.

In November 2007, I had another serum 25(OH)D test. When I saw my endocrinologist in December 2007, I was quite shocked to see that the result was now 70nmol/L. I immediately increased my Vitamin D3 intake to 5,000iu/day (12.5 x RDA) and within 2 weeks, my brain started to wake up again. In May 2008, serum 25(OH)D was 173nmol/L and in September 2008 it was 163nmol/L. I'm still taking 5,000iu/day.

See also The urgent need to recommend an intake of vitamin D that is effective.


What foods contain it?

For a list of the foods highest in Vitamin D, see here. Beware of foods that have been supplemented, as Vitamin D2 may have been used. This is less effective than Vitamin D3 according to Armas, Hollis and Heaney. Vegetarians and vegans may not want to eat foods containing Vitamin D3 as this is sourced from animals (e.g. the lanolin from a sheep's coat). Eating the Standard English Diet, it is difficult to obtain 5,000iu/day of Vitamin D. The cheapest way to get a lot of it is by going out in the sun in a swimsuit for 20 or so minutes in the middle of the day in Summer and Autumn, which costs absolutely nothing. As Vitamin D is fat-soluble, the body can build up stores to keep itself supplied during Winter and Spring.


Vitamin D deficiency, Insulin Resistance and The Metabolic Syndrome and Type 2 Diabetes

According to Hyppönen and Power, there is a strong association between decreasing 25(OH)D, increasing Body Mass Index (BMI) and increasing HbA1c (glycated haemoglobin).

According to Khaw, Wareham, Bingham, Luben, Welch and Day, increasing HbA1c is associated with increasing Relative Risk of mortality, summarised here.

According to Chiu, Chu, Go and Saad, there is a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher Relative Risk of Insulin Resistance and The Metabolic Syndrome.

In January 2003, I had Impaired Glucose Tolerance (fasting serum glucose = 6.0mmol/L and 2 hours post-75g glucose load serum glucose = 8.7mmol/L). A sandwich used to send me to sleep.

By September 2008, I had Normal Glucose Tolerance (fasting serum glucose = 5.0mmol/L and 2 hours post-75g glucose load serum glucose = 3.7mmol/L). I also no longer suffered from hyperinsulinaemic sleeps. Result!


Vitamin D deficiency and Cancer

According to Lappe, Travers-Gustafson, Davies, Recker and Heaney, subjects receiving 1400-1500mg/day supplemental calcium and 1100iu/day supplemental Vitamin D3 have a Relative Risk of getting any type of cancer of 0.402 which is equivalent to a 60% reduction in the risk of getting cancer compared to the non-supplementing group.

If the first 12 months results are discarded (to exclude any subjects who already had cancer when they started the study), the RR is 0.232 which is equivalent to a 77% reduction in the risk of getting cancer. I wonder what the result would have been had 5,000iu/day of Vitamin D3 been used.
See also Diaz, Paraskeva, Thomas, Binderup and Hague.


Vitamin D deficiency and Mental function

According to Vieth, Kimball, Hu and Walfish as mentioned above, supplementing with 4,000iu/day of Vitamin D3 produces a large reduction in the "Miserableness Factor" without affecting serum Calcium levels.

According to Wilkins, Sheline, Roe, Birge and Morris, Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults.

According to Gloth, Alam and Hollis, Improvement in 25(OH) D is significantly associated with improvement in depression scale scores in a group of 15 subjects with SAD.

According to Cherniack, Troen, Florez, Roos and Levis, Hypovitaminosis D is prevalent among older adults, and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.


Vitamin D deficiency and High Blood Pressure

According to Forman, Giovannucci, Holmes, Bischoff-Ferrari, Tworoger, Willett and Curhan, plasma 25(OH)D levels are inversely associated with the risk of incident hypertension.


Vitamin D deficiency and the Immune System

According to Cannell, Vieth, Umhau, Holick, Grant, Madronich, Garland and Giovannucci, Vitamin D deficiency predisposes children to respiratory infections.

According to Ginanjar, Sumariyono, Setiati and Setiyohadi, The active form of vitamin D produces and maintains self immunologic tolerance.


Vitamin D Deficiency and Falls

According to Dharmarajan, Akula, Kuppachi and Norkus, in the pilot study of older adults with gait imbalance and falls, vitamin D deficiency was observed in 54% of patients tested and previously unrecognised.


Vitamin D Deficiency and Chronic Pain

According to Plotnikoff and Quigley, all patients with persistent, non-specific musculoskeletal pain are at high risk for the consequences of unrecognised and untreated severe hypovitaminosis D.
According to Al Faraj and Al Mutairi, Vitamin D deficiency is a major contributor to chronic low back pain in areas where vitamin D deficiency is endemic.
According to Gloth, Lindsay, Zelesnick and Greenough, there may be a pain syndrome associated with vitamin D depletion that appears as hyperaesthesia worsened by light, superficial pressure or even small increments of movement.


NEW! Vitamin D deficiency and Autism

Autism spectrum disorder and low vitamin D at birth: a sibling control study.


But doesn't the sun damage the skin and cause skin cancer?

Inappropriate sun exposure can certainly damage the skin.  

Chronic overexposure to the sun (e.g. farmers and other outdoor workers) causes wrinkly, leathery skin and skin cancers such as Basal Cell Carcinoma and Squamous Cell Carcinoma. These are benign skin cancers which are removable and rarely fatal.

Acute overexposure to the sun (e.g. people getting severe sunburn on foreign holidays) causes the much more serious Malignant Melanoma. This condition, if not caught early enough, has a very high risk of mortality.

However, sensible sun exposure has more benefits than hazards. See Does solar exposure, as indicated by the non-melanoma skin cancers, protect from solid cancers: vitamin D as a possible explanation. EDIT: See also Is Vitamin D Shooting Me in the Foot?


Is it possible to get too much Vitamin D?

It is possible to overdose with Vitamin D by supplementation. According to Vieth, published cases of vitamin D toxicity with hypercalcaemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intakes of greater than 40,000iu/day. See also Pharmacokinetics of vitamin D toxicity.

People suffering from Sarcoidosis, Primary Hyperparathyroidism, a history of Calcium Kidney Stones and Milk-Alkali Syndrome need to consult their GP before supplementing with Vitamin D. People prescribed Warfarin also need to be careful, as Warfarin is a Vitamin K recycling antagonist, which can result in calcification of tissues.

It isn't possible to overdose by sun exposure, as the metabolic processes down-regulate when ~10,000iu has been produced. To find out when the sun is strong enough to produce Vitamin D in your skin, see the Vitamin D Synthesis in Human Skin Calculator.

EDIT: Insufficient Vitamin A can result in Vitamin D toxicity. See Is Vitamin D Safe? Still Depends on Vitamins A and K! Testimonials and a Human Study.

EDIT: Vitamins A & D are synergistic, not antagonistic. See New Evidence of Synergy Between Vitamins A and D: Protection Against Autoimmune Diseases.

I've found a cheap source of 5,000iu Vitamin D3 gelcaps. See https://uk.iherb.com/pr/vitamin-d3-5-000-iu-360-softgels/18335 That's a 1 year supply for about £10 including postage. You can use discount code NIG935 to get 5% off your first order.

10,000iu Vitamin D3 gelcaps are also available. See https://uk.iherb.com/pr/Healthy-Origins-Vitamin-D3-10-000-IU-360-Softgels/21298

Addendum:- Some editorials, meta-studies and human Randomised Controlled Trials on Vitamin D and Vitamin D3 from 2005.

The Role of Vitamin D in Cancer Prevention
Estimates of optimal vitamin D status.
Prevalence of Vitamin D inadequacy among postmenopausal North American women receiving osteoporosis therapy.
Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials.
The re-emerging burden of rickets: a decade of experience from Sydney.
An excess of widespread pain among South Asians: are low levels of vitamin D implicated?
Vitamin D is associated with improved survival in early-stage non-small cell lung cancer patients.
Vitamin D and prevention of colorectal cancer.
Should older people in residential care receive vitamin D to prevent falls? Results of a randomized trial.
Effect of vitamin D replacement on musculoskeletal parameters in school children: a randomized controlled trial.
Effect of cholecalciferol plus calcium on falling in ambulatory older men and women: a 3-year randomized controlled trial.
Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial.
Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes.
Risk factors for vitamin D inadequacy among women with osteoporosis: an international epidemiological study.
A system for improving vitamin D nutrition in residential care.
Impact of dietary and lifestyle on vitamin D in healthy student girls aged 11-15 years.
How much vitamin D3 do the elderly need?
Lower levels of plasma 25-hydroxyvitamin D among young adults at diagnosis of autoimmune type 1 diabetes compared with control subjects: results from the nationwide Diabetes Incidence Study in Sweden (DISS).
A meta-analysis of second cancers after a diagnosis of nonmelanoma skin cancer: additional evidence that solar ultraviolet-B irradiance reduces the risk of internal cancers.
Risk assessment for vitamin D.
Supplementation with calcium + vitamin D enhances the beneficial effect of weight loss on plasma lipid and lipoprotein concentrations.
Serum 25(OH)D levels, dietary intake of vitamin D, and colorectal adenoma recurrence.
The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults.
Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis.
A higher dose of vitamin d reduces the risk of falls in nursing home residents: a randomized, multiple-dose study.
Potentially modifiable determinants of vitamin D status in an older population in the Netherlands: the Hoorn Study.
Fracture prevention with vitamin D supplementation: considering the inconsistent results.
A prospective study of plasma vitamin D metabolites, vitamin D receptor polymorphisms, and prostate cancer.
The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis.
A single dose of vitamin D enhances immunity to mycobacteria.
Does solar exposure, as indicated by the non-melanoma skin cancers, protect from solid cancers: vitamin D as a possible explanation.
Vitamin D intake and breast cancer risk in postmenopausal women: the Iowa Women's Health Study.
Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial.
Bone mineral density and bone markers in patients with a recent low-energy fracture: effect of 1 y of treatment with calcium and vitamin D.
Vitamin D deficiency in multicultural primary care: a case series of 299 patients.
Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials.
Efficacy of different doses and time intervals of oral vitamin D supplementation with or without calcium in elderly nursing home residents.
Vitamin D status and response to Vitamin D(3) in obese vs. non-obese African American children.
Vitamin D and skin physiology: a D-lightful story.
Additive benefit of higher testosterone levels and vitamin D plus calcium supplementation in regard to fall risk reduction among older men and women.
Rapid correction of low vitamin D status in nursing home residents.
Effects of a long-term vitamin D and calcium supplementation on falls and parameters of muscle function in community-dwelling older individuals.
Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease.
Exploration of association of 1,25-OH2D3 with augmentation index, a composite measure of arterial stiffness.
Vitamin D and prevention of colorectal adenoma: a meta-analysis.
The tolerability and biochemical effects of high-dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insufficiency.
Administration of oral vitamin D induces cathelicidin production in atopic individuals.
Estimation of the dietary requirement for vitamin D in healthy adults.
Changes in 25-Hydroxyvitamin D3 to oral treatment with vitamin D3 in postmenopausal females with osteoporosis.
Vitamin D or hormone D deficiency in autoimmune rheumatic diseases, including undifferentiated connective tissue disease.
High-dose oral vitamin D3 supplementation in the elderly.
A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men.
Vitamin D deficiency in older men.
Serum vitamin D and risk of pancreatic cancer in the prostate, lung, colorectal, and ovarian screening trial.
Vitamin D supplementation during Antarctic winter.
Vitamin D insufficiency and treatment with oral vitamin D3 in northern-dwelling patients with chronic kidney disease.
Long-term effects of giving nursing home residents bread fortified with 125 microg (5000 IU) vitamin D(3) per daily serving.
Effects of vitamin D and calcium supplementation on markers of apoptosis in normal colon mucosa: a randomized, double-blind, placebo-controlled clinical trial.
Estimation of the dietary requirement for vitamin D in free-living adults >=64 y of age.
Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.
Plasma 25-hydroxyvitamin D concentration and metabolic syndrome among middle-aged and elderly Chinese individuals.
Meta-analysis: longitudinal studies of serum vitamin D and colorectal cancer risk.
Effect of vitamin D supplementation in the institutionalized elderly.
Calcitriol ointment 3 microg/g is safe and effective over 52 weeks for the treatment of mild to moderate plaque psoriasis.
Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men.
Low parathyroid hormone levels in bedridden geriatric patients with vitamin D deficiency.
Increased levels of 25 hydroxyvitamin D and 1,25-dihydroxyvitamin D after rosuvastatin treatment: a novel pleiotropic effect of statins?
Effect of vitamin D deficiency and replacement on endothelial function in asymptomatic subjects.
Vitamin D and depressive symptoms in women during the winter: a pilot study.
Treatment of vitamin D deficiency increases lower limb muscle strength in institutionalized older people independently of regular physical activity: a randomized double-blind controlled trial.
Vitamin D, parathyroid hormone and the metabolic syndrome in middle-aged and older European men.
Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.
Fall prevention with supplemental and active forms of vitamin D: a meta-analysis of randomised controlled trials.
Meta-analysis of vitamin D, calcium and the prevention of breast cancer.
Effects of vitamin d and calcium on proliferation and differentiation in normal colon mucosa: a randomized clinical trial.
Combination of alfacalcidol with calcium can improve quadriceps muscle strength in elderly ambulatory Thai women who have hypovitaminosis D: a randomized controlled trial.
Vitamin D(3) induces expression of human cathelicidin antimicrobial peptide 18 in newborns.
Levels of vitamin D and cardiometabolic disorders: systematic review and meta-analysis.
No significant effect on bone mineral density by high doses of vitamin D3 given to overweight subjects for one year.
Effects of supplemental vitamin D and calcium on oxidative DNA damage marker in normal colorectal mucosa: a randomized clinical trial.
Vitamin D levels, lung function, and steroid response in adult asthma.
Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations:a nested case-control study.
Pandemic preparedness for swine flu influenza in the United States.
Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren.
Vitamin D supplementation suppresses age-induced bone turnover in older women who are vitamin D deficient.
Suppression of C-terminal telopeptide in hypovitaminosis D requires calcium as well as vitamin D.
A phase I/II dose-escalation trial of vitamin D3 and calcium in multiple sclerosis.
Milk fortified with the current adequate intake for vitamin D (5 microg) increases serum 25-hydroxyvitamin D compared to control milk but is not sufficient to prevent a seasonal decline in young women.
Vitamin D-vitamin K interaction: effect of vitamin D supplementation on serum percentage undercarboxylated osteocalcin, a sensitive measure of vitamin K status, in Danish girls.
Vitamin D status and impact of vitamin D3 and/or calcium supplementation in a randomized pilot study in the Southeastern United States.
Calcium/vitamin D supplementation and coronary artery calcification in the Women's Health Initiative.
Circulating 25-hydroxyvitamin D and risk of pancreatic cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers.*
A 16-week randomized clinical trial of 2000 international units daily vitamin D3 supplementation in black youth: 25-hydroxyvitamin D, adiposity, and arterial stiffness.
The effect of narrowband UV-B treatment for psoriasis on vitamin D status during wintertime in Ireland.
Effects of vitamin D supplementation to children diagnosed with pneumonia in Kabul: a randomised controlled trial.
Dairy calcium intake, serum vitamin D, and successful weight loss.
Atorvastatin increases 25-hydroxy vitamin D concentrations in patients with polycystic ovary syndrome.
A randomized controlled trial of the effects of vitamin D on muscle strength and mobility in older women with vitamin D insufficiency.
Serum 25-hydroxyvitamin D concentration is associated with functional capacity in older adults with heart failure.
Effect of vitamin D supplementation on testosterone levels in men.
Vitamin D production depends on ultraviolet-B dose but not on dose rate: a randomized controlled trial.
Vitamin D(3) is more potent than vitamin D(2) in humans.
Nutrients and foods for the primary prevention of asthma and allergy: systematic review and meta-analysis.
High-dose vitamin D(3) during intensive-phase antimicrobial treatment of pulmonary tuberculosis: a double-blind randomised controlled trial.
Circulating 25-hydroxyvitamin D levels and frailty in older men: the osteoporotic fractures in men study.
Association of low serum 25-hydroxyvitamin D levels and mortality in the critically ill.
Effects of vitamin D supplementation on 25-hydroxyvitamin D, high-density lipoprotein cholesterol, and other cardiovascular disease risk markers in subjects with elevated waist circumference.
Changes in balance, functional performance and fall risk following whole body vibration training and vitamin D supplementation in institutionalized elderly women. A 6 month randomized controlled trial.
Diet induced thermogenesis, fat oxidation and food intake following sequential meals: influence of calcium and vitamin D.
The response of elderly veterans to daily vitamin D3 supplementation of 2,000 IU: a pilot efficacy study.
Meta-analysis: Circulating vitamin D and ovarian cancer risk.
Relation of vitamin D level to maximal oxygen uptake in adults.
Vitamin D status in patients with stage IV colorectal cancer: findings from Intergroup trial N9741.
Circulating levels of vitamin D and colon and rectal cancer: the Physicians' Health Study and a meta-analysis of prospective studies.
Burning daylight: balancing vitamin D requirements with sensible sun exposure.
Relationships between vitamin D status and cardio-metabolic risk factors in young European adults.
Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis.
Vitamin D status and early age-related macular degeneration in postmenopausal women.
Vitamin D and clinical disease progression in HIV infection: results from the EuroSIDA study.
Annual high-dose vitamin D3 and mental well-being: randomised controlled trial.
Vitamin D status and outcomes in heart failure patients.
The impact of vitamin D status on periodontal surgery outcomes.
The role of paricalcitol on proteinuria.
Effects of weight loss on serum vitamin D in postmenopausal women.
Vitamin D status and mortality risk in CKD: a meta-analysis of prospective studies.
Vitamin D intake and risk of cardiovascular disease in US men and women.
Meta-analysis: Serum vitamin D and colorectal adenoma risk.
Calcium plus vitamin D supplementation and the risk of nonmelanoma and melanoma skin cancer: post hoc analyses of the women's health initiative randomized controlled trial.
Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial.
Vitamin D supplementation for prevention of mortality in adults.
The effect of calcium plus vitamin D on risk for invasive cancer: results of the Women's Health Initiative (WHI) calcium plus vitamin D randomized clinical trial.
New clinical trials with vitamin D and analogs in renal disease.
The relation between vitamin D deficiency and fibromyalgia syndrome in women.
Interventions for latent autoimmune diabetes (LADA) in adults.
Calcium and vitamin D supplementation is associated with decreased abdominal visceral adipose tissue in overweight and obese adults.
Effect of vitamin D supplementation on muscle strength, gait and balance in older adults: a systematic review and meta-analysis.
Vitamin D3 and the risk of CVD in overweight and obese women: a randomised controlled trial.
Low 25-hydroxyvitamin D is associated with increased mortality in female nursing home residents.
Improvement of vitamin D status resulted in amelioration of biomarkers of systemic inflammation in the subjects with type 2 diabetes.
Vitamin D supplementation in infants with chronic congestive heart failure.
Vitamin D reduces musculoskeletal pain after infusion of zoledronic acid for postmenopausal osteoporosis.
Consumption of vitamin D-and calcium-fortified soft white cheese lowers the biochemical marker of bone resorption TRAP 5b in postmenopausal women at moderate risk of osteoporosis fracture.
Vitamin D improves viral response in hepatitis C genotype 2-3 naïve patients.
Vitamin D supplementation in the treatment of atopic dermatitis: a clinical trial study.
Effect of vitamin D repletion on urinary calcium excretion among kidney stone formers.
25-Hydroxyvitamin D levels and the risk of stroke: a prospective study and meta-analysis.
Improvement of vitamin D status via daily intake of fortified yogurt drink either with or without extra calcium ameliorates systemic inflammatory biomarkers, including adipokines, in the subjects with type 2 diabetes.
Treatment of vitamin D insufficiency in children and adolescents with inflammatory bowel disease: a randomized clinical trial comparing three regimens.
Therapeutic effects of calcium & vitamin D supplementation in women with PCOS.
Higher vitamin D dietary intake is associated with lower risk of alzheimer's disease: a 7-year follow-up.
Vitamin D3 supplementation at 4000 international units per day for one year results in a decrease of positive cores at repeat biopsy in subjects with low-risk prostate cancer under active surveillance.
Comparison of narrowband ultraviolet B exposure and oral vitamin D substitution on serum 25-hydroxyvitamin D concentration.
The relation between sunscreen layer thickness and vitamin D production after ultraviolet B exposure: a randomized clinical trial.
Circulating 25-hydroxyvitamin D concentration and the risk of type 2 diabetes: results from the European Prospective Investigation into Cancer (EPIC)-Norfolk cohort and updated meta-analysis of prospective studies.
Vitamin D3 therapy corrects the tissue sensitivity to angiotensin ii akin to the action of a converting enzyme inhibitor in obese hypertensives: an interventional study.
The effect of combined calcium and cholecalciferol supplementation on bone mineral density in elderly women with moderate chronic kidney disease.
Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis.
Relative effectiveness of oral 25-hydroxyvitamin D3 and vitamin D3 in raising wintertime serum 25-hydroxyvitamin D in older adults.
Vitamin D supplementation and depression in the women's health initiative calcium and vitamin D trial.
Vitamin D with calcium reduces mortality: patient level pooled analysis of 70,528 patients from eight major vitamin D trials.
An open label, randomized controlled study of oral calcitriol for the treatment of proteinuria in patients with diabetic kidney disease.
Ergocalciferol from mushrooms or supplements consumed with a standard meal increases 25-hydroxyergocalciferol but decreases 25-hydroxycholecalciferol in the serum of healthy adults.
Narrowband ultraviolet B three times per week is more effective in treating vitamin D deficiency than 1600 IU oral vitamin D₃ per day: a randomized clinical trial.
Vitamin D intake is inversely related to risk of developing metabolic syndrome in African American and white men and women over 20 y: the Coronary Artery Risk Development in Young Adults study.
Vitamin D and gestational diabetes: a systematic review and meta-analysis.
Associations between 25-hydroxyvitamin D and weight gain in elderly women.
Effect of cholecalciferol as adjunctive therapy with insulin on protective immunologic profile and decline of residual β-cell function in new-onset type 1 diabetes mellitus.
A pooled analysis of vitamin D dose requirements for fracture prevention.
Determinants and effects of vitamin D supplementation on serum 25-hydroxy-vitamin D levels in patients with rheumatoid arthritis.
Vitamin D is a major determinant of bone mineral density at school age.
Effect of vitamin D and inhaled corticosteroid treatment on lung function in children.
Serum 25-hydroxyvitamin D3 and D2 and non-clinical psychotic experiences in childhood.
Vitamin D deficiency in postmenopausal, healthy women predicts increased cardiovascular events: a 16-year follow-up study.
Randomized trial of vitamin D supplementation and risk of acute respiratory infection in Mongolia.
25-hydroxyvitamin d levels and risk of ischemic heart disease, myocardial infarction, and early death: population-based study and meta-analyses of 18 and 17 studies.
Association of low serum 25-hydroxyvitamin D levels and acute kidney injury in the critically ill.
A 12-week double-blind randomized clinical trial of vitamin D₃ supplementation on body fat mass in healthy overweight and obese women.
Circulating 25-hydroxy-vitamin D and risk of cardiovascular disease: a meta-analysis of prospective studies.
Relation of severe deficiency of vitamin D to cardiovascular mortality during acute coronary syndromes.
Vitamin D reduces left atrial volume in patients with left ventricular hypertrophy and chronic kidney disease.
Interventions for preventing falls in older people in care facilities and hospitals.
Vitamin D and risk of death from vascular and non-vascular causes in the Whitehall study and meta-analyses of 12,000 deaths.
Calcium plus vitamin D3 supplementation facilitated fat loss in overweight and obese college students with very-low calcium consumption: a randomized controlled trial.
Randomized controlled trial of vitamin D supplement on endothelial function in patients with type 2 diabetes.
Effect of vitamin D supplementation on progression of knee pain and cartilage volume loss in patients with symptomatic osteoarthritis: a randomized controlled trial.
Lipoprotein lipase links vitamin D, insulin resistance, and type 2 diabetes: a cross-sectional epidemiological study.
The effect of different doses of vitamin D supplementation on insulin resistance during pregnancy.
Vitamin D and dental caries in controlled clinical trials: systematic review and meta-analysis.
Vitamin D deficiency and depression in adults: systematic review and meta-analysis.
Improving the vitamin D status of vitamin D deficient adults is associated with improved mitochondrial oxidative function in skeletal muscle.
Low 25-OH vitamin D is associated with benign prostatic hyperplasia.
Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial.
Vitamin D levels in Alzheimer's and Parkinson's diseases: a meta-analysis.
Supplemental vitamin D and physical performance in COPD: a pilot randomized trial.
Vitamin D and risk of future hypertension: meta-analysis of 283,537 participants.
Randomized clinical trial of vitamin D3 doses on prostatic vitamin D metabolite levels and ki67 labeling in prostate cancer patients.
Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease.
Anti-inflammatory effect of vitamin D on gingivitis: a dose-response randomised control trial.
Role of vitamin D in children with respiratory tract infection.
Effect of vitamin D supplementation and ultraviolet B exposure on serum 25-hydroxyvitamin D concentrations in healthy volunteers: a randomized, crossover clinical trial.
Vitamin D and multiple sclerosis: what is the clinical impact?
Is hypovitaminosis D associated with abdominal aortic aneurysm, and is there a dose-response relationship?
Plasma vitamin D levels, menopause, and risk of breast cancer: dose-response meta-analysis of prospective studies.
Impact of vitamin D on chronic kidney diseases in non-dialysis patients: a meta-analysis of randomized controlled trials.
Serum 25-hydroxyvitamin D levels and the risk of depression: a systematic review and meta-analysis.
The effect of vitamin D-related interventions on multiple sclerosis relapses: a meta-analysis.
Vitamin D status and physical function in nursing home residents: a 1-year observational study.
Maternal vitamin D status and risk of pre-eclampsia: a systematic review and meta-analysis.
Meta-analysis: vitamin D and non-alcoholic fatty liver disease.
Serum 25-hydroxyvitamin D and breast cancer risk: a meta-analysis of prospective studies.
Treatment with oral active vitamin D is associated with decreased risk of peritonitis and improved survival in patients on peritoneal dialysis.
Vitamin D supplementation affects serum high-sensitivity C-reactive protein, insulin resistance, and biomarkers of oxidative stress in pregnant women.
The role of vitamin D supplementation in the risk of developing pneumonia: three independent case-control studies.
Short-term vitamin D3 supplementation lowers plasma renin activity in patients with stable chronic heart failure: an open-label, blinded end point, randomized prospective trial (VitD-CHF trial).
Vitamin D and psychosis: mini meta-analysis.
Meta-analysis of memory and executive dysfunctions in relation to vitamin D.
Vitamin D intake and lung cancer risk in the Women's Health Initiative.
Association of low serum 25-hydroxyvitamin D levels and sepsis in the critically ill.
Vitamin D favorably alters the cancer promoting prostaglandin cascade.
Vitamin D intake and risk of type 1 diabetes: a meta-analysis of observational studies.
Effect of vitamin D supplementation on antibiotic use: a randomized controlled trial.
Effects of vitamin D supplementation on glucose metabolism, lipid concentrations, inflammation, and oxidative stress in gestational diabetes: a double-blind randomized controlled clinical trial.
Improvement in high-density lipoprotein cholesterol levels in argentine Indian school children after vitamin D supplementation.
Vitamin D supplementation for prevention of mortality in adults.
Beneficial role for supplemental vitamin D3 treatment in chronic urticaria: a randomized study.
Vitamin D3 supplementation during weight loss: a double-blind randomized controlled trial.
Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies.


*See https://www.slideshare.net/TedHutchinson/ow-to-optimize-vitamin-d-supplementation-to-prevent-cancer-based-on-cellular-adaptation-and-hydroxylase-enzymology for an explanation.

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