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, eat 25g (women) or 50g ( men) of powdered linseeds (a.k.a. flaxseeds) per day with lots of fluids or supplement with flaxseed oil in bottles/capsules such that you get at least 10g (women) or 20g (men) of flaxseed oil per day.

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".

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.

Gluten-Free Appetizers + Snacks

Baked Grape Tomatoes with Basil and Cornbread Crumbs
Basil Pesto
Brown Rice Tortilla Chips
Buttermilk Flatbread

Cilantro Pesto de Esteban
Crispy Potato Sticks with Roasted Tomato Salsa
Crunchy White + Sweet Potato Chips

Easy Guacamole with Lime
Green Chile Quesadilla
Greenwiches Lettuce Cups and Wraps
Hummus Tahini with Spiced Oil

Jalapeño Lime Hummus

Joey's Kicked Up Rockin' Guac

Nachos Fabuloso
Parmesan Crisps
Pecan Crackers

Quick + Easy Garlic Shrimp Pizzas
Roasted Eggplant Tapenade
Roasted Red Pepper Hummus
Roasted Tomato Salsa
Roasted Yellow Tomato Salsa
Roasted Vegetable Salsa

Savory Grain Free Crackers
Spinach and Cheddar Quesadilla
Three Ways To Dress a Naked Salad (Gluten-Free Dressings)
Winter Pesto

A blast from the past.

Look who's turned up on the BBC food boards after a 4-5 years absence. A big "Welcome back" to Zoë Harcombe, who has the site 'Why do you overeat? When all you want is to be slim' and The Harcombe Diet.

We agree on most things. The problem with counting Calories is that, if you reach your Calorie limit by 6pm, what do you do? Spend the rest of the evening hungry and go to bed with a rumbling tummy & hunger pangs? Or just have one teensy-weensy bite to eat, which turns into a "nom-a-thon"? I know what I would do, as I can resist anything.......except temptation!

What we don't agree on is that Calories don't count. I say that they do. So does Lyle McDonald and Anthony Colpo. For people who are restrained to a hospital bed, changing the relative proportions of carbohydrate & fat (keeping protein constant) in their diet makes no difference whatsoever to their long-term weight gain/loss (ignoring glycogen + water weight differences). What it does make a difference to is how much these restrained people would beg for food. On a high-carb diet, I was much hungrier than when I was on a low-carb diet. This is why I ate way too much on the former diet (& got fat) and ate much less on the latter diet (& got slim).

It's thought that Insulin is the only hormone responsible for body-fat storage. This isn't correct.

Insulin makes the body store glucose (from dietary carbohydrates) and amino acids (from dietary proteins) and stops the body from burning fats. Therefore, having chronically-high serum insulin levels (hyperinsulinaemia) is not desirable for people wishing to burn body-fat for fuel.

As we all know, dietary carbohydrate raises serum insulin levels by raising blood glucose. See http://www.mendosa.com/gilists.htm.

However, dietary protein also raises serum insulin levels. See http://www.mendosa.com/insulin_index.htm.

Eating most fats with carbohydrates raises serum insulin levels even higher still, although fats lower the glucose response. See http://jn.nutrition.org/cgi/reprint/133/8/2577.pdf. What do junk foods mostly consist of? High-GI carbohydrates + fats. However, omega-3 fats reduce the hyperinsulinaemia caused by the other fats. See http://diabetes.diabetesjournals.org/cgi/reprint/53/suppl_1/S166.pdf.

Eating fat on its own does not raise serum insulin levels. See http://intl.ajcn.org/cgi/reprint/75/3/505.pdf. However, it's still possible to gain body-fat by eating too many Calories of dietary fat. Acylation Stimulating Protein (ASP) makes the body store dietary fat as body-fat. See http://www.jlr.org/cgi/reprint/30/11/1727.pdf.

The amount of food that free-living people (i.e. people who are not restrained to a hospital bed) eat depends mostly on their appetites. This is affected by the food that they eat (the low blood glucose that follows hyperinsulinaemia causes severe hunger pangs) and also advertisements. Watch this Google video of Adam Curtis' BBC documentary The Century Of The Self - Part 1 of 4.

I hope that you all had a good Christmas.

Cranberry Buffalo Roast Stew

A hearty gluten-free Crock Pot stew to warm your celiac soul.

What could be more comforting as we face the chilly New Year than a slow roasted one-dish supper? Not to mention, easier. Especially after all the hustle and bustle of last week's holiday celebrations. All the sugar. And latkes. And eggnog. And hoopla. I'm exhausted just imagining it. So I'll stop. And share a recipe instead- a tasty little number I tossed together in my trusty Crock Pot over the weekend- a cranberry laced stew that cooked its sweet 'n savory heart out while I worked on creating more print-friendly recipes for you.

Read more + get the recipe >>

Butter, Margarine and Heart Disease

Shortly after World War II, margarine replaced butter in the U.S. food supply. Margarine consumption exceeded butter in the 1950s. By 1975, we were eating one-fourth the amount of butter eaten in 1900 and ten times the amount of margarine. Margarine was made primarily of hydrogenated vegetable oils, as many still are today. This makes it one of our primary sources of trans fat. The consumption of trans fats from other sources also likely tracked closely with margarine intake.


Coronary heart disease (CHD) resulting in a loss of blood flow to the heart (heart attack), was first described in detail in 1912 by Dr. James B. Herrick. Sudden cardiac death due to CHD was considered rare in the 19th century, although other forms of heart disease were diagnosed regularly by symptoms and autopsies. They remain rare in many non-industrial cultures today. This could not have resulted from massive underdiagnosis because heart attacks have characteristic symptoms, such as chest pain that extends along the arm or neck. Physicians up to that time were regularly diagnosing heart conditions other than CHD. The following graph is of total heart disease mortality in the U.S. from 1900 to 2005. It represents all types of heart disease mortality, including 'heart failure', which are non-CHD disorders like arrhythmia and myocarditis.

The graph above is not age-adjusted, meaning it doesn't reflect the fact that lifespan has increased since 1900. I couldn't compile the raw data myself without a lot of effort, but the age-adjusted graph is here. It looks similar to the one above, just a bit less pronounced. I think it's interesting to note the close similarity between the graph of margarine intake and the graph of heart disease deaths. The butter intake graph is also essentially the inverse of the heart disease graph.

Here's where it gets really interesting. The U.S. Centers for Disease Control has also been tracking CHD deaths specifically since 1900. Again, it would be a lot of work for me to compile the raw data, but it can be found here and a graph is in Anthony Colpo's book The Great Cholesterol Con. Here's the jist of it: there was essentially no CHD mortality until 1925, at which point it skyrocketed until about 1970, becoming the leading cause of death. After that, it began to fall due to improved medical care. There are some discontinuities in the data due to changes in diagnostic criteria, but even subtracting those, the pattern is crystal clear.

The age-adjusted heart disease death rate (all forms of heart disease) has been falling since the 1950s, largely due to improved medical treatment. Heart disease incidence has not declined substantially, according to the Framingham Heart study. We're better at keeping people alive in the 21st century, but we haven't successfully addressed the root cause of heart disease.

Was the shift from butter to margarine involved in the CHD epidemic? We can't make any firm conclusions from these data, because they're purely correlations. But there are nevertheless mechanisms that support a protective role for butter, and a detrimental one for margarine. Butter from pastured cows is one of the richest known sources of vitamin K2. Vitamin K2 plays a central role in protecting against arterial calcification, which is an integral part of arterial plaque and the best single predictor of cardiovascular death risk. In the early 20th century, butter was typically from pastured cows.

Margarine is a major source of trans fat. Trans fat is typically found in vegetable oil that has been hydrogenated, rendering it solid at room temperature. Hydrogenation is a chemical reaction that is truly disgusting. It involves heat, oil, hydrogen gas and a metal catalyst. I hope you give a wide berth to any food that says "hydrogenated" anywhere in the ingredients. Some modern margarine is supposedly free of trans fats, but in the U.S., less than 0.5 grams per serving can be rounded down so the nutrition label is not a reliable guide. Only by looking at the ingredients can you be sure that the oils haven't been hydrogenated. Even if they aren't, I still don't recommend margarine, which is an industrially processed pseudo-food.

One of the strongest explanations of CHD is the oxidized LDL hypothesis. The idea is that LDL lipoprotein particles ("LDL cholesterol") become oxidized and stick to the vessel walls, creating an inflammatory cascade that results in plaque formation. Chris Masterjohn wrote a nice explanation of the theory here. Several things influence the amount of oxidized LDL in the blood, including the total amount of LDL in the blood, the antioxidant content of the particle, the polyunsaturated fat content of LDL (more PUFA = more oxidation), and the size of the LDL particles. Small LDL is considered more easily oxidized than large LDL. Small LDL is also associated with elevated CHD mortality. Trans fat shrinks your LDL compared to butter.

In my opinion, it's likely that both the decrease in butter consumption and the increase in trans fat consumption contributed to the massive incidence of CHD seen in the U.S. and other industrial nations today. I think it's worth noting that France has the highest per-capita dairy fat consumption of any industrial nation, along with a comparatively low intake of hydrogenated fat, and also has the second-lowest rate of CHD, behind Japan.

The Fundamentals

I heard an interview of Michael Pollan yesterday on Talk of the Nation. He made some important points about nutrition that bear repeating. He's fond of saying "don't eat anything your grandmother wouldn't recognize as food". That doesn't mean your grandmother specifically, but anyone's grandmother, whether she was Japanese, American or African. The point is that commercial food processing has taken us away from the foods, and traditional food preparation methods, on which our bodies evolved to thrive. At this point, we don't know enough about health to design a healthy synthetic diet. Diet and health are too complex for reductionism at our current level of understanding. For that reason, any departure from natural foods and traditional food processing techniques is suspect.

Mainstream nutrition science has repeatedly contradicted itself and led us down the wrong path. This means that traditional cultures still have something to teach us about health. Hunter-gatherers and certain other non-industrial cultures are still the healthiest people on Earth, from the perspective of non-communicable disease. Pollan used the example of butter. First we thought it was healthy, then we were told it contains too much saturated fat and should be replaced with hydrogenated vegetable margarine. Now we learn that trans fats are unhealthy, so we're making new margarines that are low in trans fats, but are still industrially processed pseudo-foods. How long will it take to show these new fats are harmful? What will be the next industrial fat to replace them? This game can be played forever as the latest unproven processed food replaces the previous one, and it will never result in something as healthy as real butter.

The last point of Pollan's I'll mention is that the world contains (or contained) a diversity of different cultures, living in dramatically different ways, many of which do not suffer from degenerative disease. These range from carnivores like the Inuit, to plant-heavy agriculturalists like the Kitavans, to pastoralists like the Masai. The human body is adapted to a wide variety of foodways, but the one it doesn't seem to like is the modern Western diet.

Pollan's new book is In Defense of Food. I haven't read it, but I think it would be a good introduction to the health, ethical and environmental issues that surround food choices. He's a clear and accessible writer.

Merry Christmas, happy Hanukkah, and happy holidays to everyone!

Seasons Greetings from New Mexico!

Bunny tracks and a low flannel sky sifting snow. My view today. We have a buffalo roast with cranberries and wine in the slow cooker. A fire in the kiva. A quiet-as-a-field-mouse day here in northern New Mexico.

Sending out a bundle of wishes for a safe and warm holiday to all- be it Christmas, Hanukkah, Yule, or simply Thursday. Be well, Dear Readers. And thank you for your comment love this past year. I appreciate every kind word, your recipe tweaks and stories shared.

One more glimpse of snow in New Mexico- our view. 

My New Year's gift to you? During the next week- or two- I'll be busy behind the scenes creating printable recipes. 

Be safe, be healthy, and be good to one another.

All images & content are copyright protected, all rights reserved. Please do not use our images or content without prior permission. Thank you. 

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?

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, omega-6 polyunsaturates and omega-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 and three fatty acids and are also known as triglycerides or triacylglycerols.

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 sat, mono etc. The four different types of fatty acid all 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 all 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 OH-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 HMonounsaturated 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 usually being referred to as omega-9's, as omega is the letter at the end 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 OH-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

Omega-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 OH-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

Omega-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 OH-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 OH-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 have unsaturated bonds which are prone to oxidation. 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 and so any processed foods or cooking/spreading fats which has the word "hydrogenated" high-up in the ingredients list should be avoided. These truly are bad fats. There are also 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 medical studies 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. New Zealand butter) by saying that it has trans-fats in it. CLA is a harmless trans-fat.

Anyway, back to diet. Saturated fat consumption should be about 10% of total calories. This is because, even though sat fats are not essential (our bodies can manufacture them), this guarantees adequate levels of sex hormones in the body. Total polyunsaturate consumption should be about 5% of total calories, with a ratio of omega-6 (O6) to omega-3 (O3) of between 1:2 and 4:1. As O3's are only found in greater quantities than O6's 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 O6:O3 ratio in the West is about 20:1. This is due to the widespread consumption of meats, eggs & milk from grain-fed animals, grains, nuts and seeds. So, it’s not surprising that there are high rates of heart disease and other inflammatory diseases in the West, as O6's end up in series 1 & 2 prostaglandins and series 2 prostaglandins are pro-inflammatory. O3 fats 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 15% to 35% of total calories, depending on activity levels. Remember from the histogram in the Blog post Everyone is Different, sedentary people on average burn twice as much energy from fats as from carbs. So, if energy from protein is 25% say, 25% of energy can come from carbs 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, 5% carbs, 70% fat when sedentary, whereas the cyclist at the right-hand end of the histogram would do best on 25% protein, 60% carbs, 15% fat when sedentary. When active, more carbs are needed by everyone.

Which fats contain which fatty acids? See http://homepage.ntlworld.com/nigel.kinbrum/comparison-of-fats.gif for a Comparison of Dietary Fats chart. Click http://www.apag.org/oleo/fatsoils.pdf for tables of Properties & Composition of Vegetable & Special Oils and Properties & Composition of Animal & Marine Fats & Oils.

For high-temperature cooking, saturates are the least likely to oxidise (when they're on fire, they're oxidising!), followed by monos, then omega-6's with omega-3's being the least stable. An oil doesn't have to be smoking to be oxidising. Alpha-linolenic acid oxidises at room temperature, which is why linseed oil is used to varnish cricket bats and soften 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 smoking temperature than refined Olive Oil (due to higher levels of free fatty acids), but has higher levels of polyphenol antioxidants, which makes it pretty heart-healthy.

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

Sweet Potato Latkes

Sweet potato latkes and ruby applesauce.

The shortest day of the year is finally upon us. The darkest point in the turning of the seasons will tomorrow tilt toward light. The balance in power has shifted. Daylight gains. The darkness recedes, inch by inch, minute by minute. Light is reborn. Pretty powerful stuff. No wonder so many cultures have celebrated the Winter Solstice in a myriad of ways.

For Hanukkah- no matter how you spell it- it's also about light. An eight day Festival of Lights, in fact, and food is intricately woven into the tradition. Because Hanukkah celebrates the fortuitous finding of a flask of olive oil (a small amount that would, maybe, last a day, but miraculously burned for eight dark nights) recipes for celebrating the miracle of light are cooked in oil.

And that brings to me to one of my all-time favorite foods on Earth.

Latkes.

Read more + get the recipe >>

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 fast they turn into blood glucose in the body. The Glycaemic Index (GI) (or Glycemic Index if you're American) relates to how fast 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 carbs. As you can see, some wholegrain complex carbs turn into blood sugar faster than simple carbs. This 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 carbs). Once liver glycogen stores are full, any further fructose is converted into.......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. Rapidly-falling and low blood glucose 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. As over-secretion of insulin can cause low blood glucose which causes severe hunger pangs, it's not something that someone who wants to lose body-fat really wants. Therefore,the consumption of foods with an II greater than 60 should be minimised for optimum fat loss. So take it easy with the baked beans ("my carbohydrates are exceedingly complex"). Overcooking foods raises their GI & II and baked beans are well-overcooked in a sugary sauce. EDIT: I now know that insulinogenic proteins are also glucogenic, so there is no 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 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.

Updated text in bold green.
If there is one thing that I have learned over the years of research into Diet and Nutrition, it's this: Everyone is Different. When I first discovered Low-carb Diets (thanks to the late Dr Atkins), I thought that it was the One True Diet, and I became a bit of an "Atkins Diet" 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 someone else. So why do "Healthy Eating" guidelines assume that everyone is the same and tell everyone to get 15% of their total calories from proteins, 55% from carbohydrates and 30% from fats?

To illustrate just how different people are, 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 fuel that the body is burning for energy. For example, if the body is burning 100% fat, RER = 0.7. If the body is burning 100% carbohydrate aerobically, RER=1.0. If the body is burning 100% carbohydrate anaerobically (flat-out sprinting), RER > 1.0. RER goes up and down depending on intensity of exercise, food intake (eating protein and/or carbohydrate increases it and extended fasting reduces it). 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%.

There's a helluva big difference between burning 93 - 100% fat at rest and burning 20 - 27% fat at rest. Interestingly, average fat oxidation is 66%, which means that average carb oxidation is 34%. So, on average, at rest, people burn twice as much energy from fat as from carbs. So why do current "Healthy Eating" guidelines recommend almost twice as much energy from carbs as from fats for everyone, including sedentary people?

As exercise intensity increases, the peak in the histogram shifts to the right as shown in the lower diagram. At 25% full work-load, mean fat oxidation is ~53%. At 50% full work-load, mean fat oxidation is ~37% and at 75% full work-load, mean fat oxidation is ~13%.

I suspect that at 100% full work-load, mean fat oxidation is 0% i.e. 100% of energy is obtained from carbs when sprinting flat-out. Somebody on a very low carb diet like Atkins induction (~20g net carbs/day) could keel over with hypoglycaemia if they exercise for any length of time at this rate.

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

Just apply the principle of "Eat, monitor and adjust accordingly" as Toxic Toffee (ex-Muscletalk member) always used to say. The eating bit I will advise on in future Blog posts. The monitoring bit does not involve the use of 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 your head off! As your body is made up of water, muscle, fat, 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 yourself or skip breakfast or go for a fast run before eating breakfast, as your body is lacking in glycogen and amino acids, a large amount of a corticosteroid hormone called cortisol is secreted which converts muscle into amino acids, then glucose. It also suppresses your immune system and weakens your skin and bones.

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

So, what happens if you eat too many carbs but your body doesn't burn them fast enough? Initially, carbohydrate intake tops-up liver and muscle glycogen stores, which increases carb-burning to compensate. The liver can store about 70g of glycogen and muscles can store about 400g of glycogen. If, despite increased carb-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 filling glycogen stores by eating loads of carbohydrate is not a good idea if you want to burn 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 you end up wearing as body-fat. But there's even worse news. On the way to being worn as body-fat, fat is in the blood as triglycerides. This is bad for the cholesterol particles in your blood. See the Blog on Cholesterol and Coronary Heart Disease. What happens if you eat too few carbs? As stated above, a "carb-burner" taking in insufficient carbs could get hypoglycaemia.

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 consistently eat more than 360g of carbohydrate /day will 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.

Just 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 protein, carbohydrates and fat that you eat) and the intensity and volume of exercise.

So, if all you're interested in is weight loss, just count calories. If however, you wish to lose body-fat without losing muscle, you need to know how to determine what proportions of proteins, carbs and fats to eat (it's not that critical, but many people get it totally wrong). You need to know the difference between good carbs and bad carbs and good fats and bad fats. You need to know the best times to eat proteins, carbs and fats (it's not that critical, but many people get it totally wrong). You need to know the difference between good exercise and bad exercise.

Cont'd on We are not all the same.

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

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

The 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 sleepiness after eating meals high in carbohydrate. Since childhood, I would 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 (oo-er, missus!) The sleepiness was 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 and I was referred to an endocrinologist. It turned out that my pituitary gland was failing and it was no longer secreting enough TSH to stimulate my thyroid gland to secrete thyroxine. I was therefore prescribed levothyroxine. The upside to all this is that I am now exempt from all prescription charges. I also get regular blood tests, so that I can see the results of any diet/supplement/exercise change on my bloodwork.

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 higher than they should have been and my HDL was lower than it should have been. It just so happens that a diet low in sugary & starchy carbohydrates suits people with this condition.

I still didn't understand how Atkins' 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 BSc (Hons) - Moderator and Contributor to Muscletalk as an Expert in Nutrition, criticising the article on ketogenic diets that he had written. 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) bodybuilding 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 anymore. I'll 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.

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

Cheers, Nige.

Gluten-Free Layer Bars: Coconut Chocolate Nirvana

Gluten-free coconut chocolate layer bars.

This is a quickie bonus post. Chocolate-coconut layered cookie bar bliss --- just in time for the holidays. A wink and a nudge to the retro cookie  layer bar recipe I posted two years ago. This newer version is non-dairy using condensed coconut milk, so you lactose-free folks don't miss out on all the fun.

Now get ready to party.

Read more + get the recipe >>

Cholesterol And Coronary Heart Disease

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, small cholesterol-depleted particles (Type B) oxidise faster than large 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, click HERE and scroll down to the bottom of the 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, 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. Eventually, the cap covering the plaque can 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 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. See The unusual suspects.

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 virtually zero 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 arteries, 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 the oxidation of these particles.

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 should supplement 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, and Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism. People with ApoE4/E4 are more sensitive to dietary cholesterol raising serum LDL, and cannot eat 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. Note that CVD mortality isn't the same thing as overall mortality. Higher than "normal" total cholesterol level is associated with lower overall mortality, according to Research finds ‘raised’ cholesterol to be associated with a reduced risk of death.

Gluten-Free Sweet Potato Coffee Cake- and a love story

Winter in Northern New Mexico- my view.

It's been snowy, windy, cold- you name it. From all the tweets I've been reading over on Twitter lately, I'm not alone. Far from it. This has been one crazy snowy month. So what does a gluten-free goddess do when she gets stuck in the middle of the desert with no buckwheat flour, no sorghum, and no four-wheel drive? (Note to self- if you're going to live in rural Northern New Mexico, Darling, a cute and thrifty little Honda Fit won't cut it.)

Snowed in and hungry she does the only sensible thing.

She scans the pantry and pulls out a Whole Foods gluten-free cake mix and starts stirring things up. She starts imagining dirt bombs. And bakes up a coffee cake worthy of the winter holidays.

The love part of the story?

Read more + get the recipe >>

A big shout out to to the guys & gals from forums.ebay.co.uk

I don't know how you found this Blog as I get the message "Error: you do not have permission to view the requested forum or category." when I click on the link from whence you came. So, how did you find me?

EDIT: Now I know how you found me and why. If you want to lose some flab or stop falling asleep after lunch, read Nigee's Guide to Losing Body-Fat Healthily. If your get up and go has got up and left, see the Vitamin D article.

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 about 4.5g of glucose circulating 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 a bit more sophisticated 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 Phase 1 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 Phase 2 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 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. It may also be linked to a Vitamin D deficiency, see here.

Insulin resistance weakens the feedback in the NFB system, resulting in further increased BG and insulin levels (hyperinsulinaemia). Increased BG level causes increased damage to beta cells by glycation. Increased insulin level 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.
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 cases) and is caused by an autoimmune disease. One possible mechanism is as follows: Due to an increase in Zonulin (see here ), the gut becomes more permeable than it should (a.k.a. Leaky Gut Syndrome) and allows protein fragments to pass into the blood. These are destroyed by antibodies. However, if a protein fragment happens to have the same sequence of amino acids as a protein in our own body, the antibodies then set about destroying parts of our 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 is an association between the consumption of cows' milk and the incidence of type 1 diabetes (see here ), it's quite possible that, in susceptible individuals, fragments of casein protein enter the blood in this way resulting in antibodies that destroy pancreatic beta cells. Another possible mechanism is autoimmune attack after a viral infection. Once all of the beta cells are destroyed, no insulin is secreted and insulin injections are required. If some beta cells survive, there is a possibility that normal BG level can be maintained if sugary/starchy carbohydrate intake is reduced.

3) Latent Autoimmune Diabetes of Adulthood (LADA). The percentage of cases with this is unknown as it is often misdiagnosed as type 2 diabetes. 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). See here. 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 will never know.

What else can go wrong?
As stated earlier, loss of the Phase 1 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 large and rapid rise in BG level. If a NFB loop with a lag in it is presented with a sudden change in input level, its output overshoots. This results in too much insulin being secreted, which eventually results in low BG levels! This is known as rebound hypoglycaemia. 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 monophosphate). 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. See Liver and Kidneys Synthesize 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 gland 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. 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 that cause long-term health problems like high blood pressure and clogging of arteries.