Good Science: Doubly-labeled water

I was reading an interview with Rudolph L. Leibel and doubly-labeled water was mentioned. This sort of stuff fascinates me. Using doubly-labeled water, a mass spectrometer, loads of measurements and some mathematics, it's possible to work out how many kcals someone is burning. This method costs an arm & a leg. So, how does doubly-labeled water work?

Chemistry 101:

Water has the formula H2O. H stands for Hydrogen and O stands for Oxygen.

Elements have isotopes. Hydrogen has two isotopes, Deuterium and Tritium. Deuterium oxide, or D2O is known as heavy water and one use for heavy water is the manufacture of atomic bombs, if you recall the film "The heroes of Telemark". Deuterium is non-radioactive, as is heavy water. Tritium is radioactive.

Oxygen has three stable non-radioactive isotopes one of which is O-18. This can be used to make labeled water H2O-18. Mix D2O with a bit of H2O-18 and you have doubly-labeled water. Now what? To quote Leibel:-

"The interesting thing is that when you give somebody water like this, the deuterium comes out of the body which is determined by water turnover in the individual. The O-18 is in equilibrium with carbon dioxide, so the O-18 comes out by two mechanisms: first with normal water by transpiration, perspiration and urine, but also in the breath.

The difference between those two decay curves (the O-18 comes out faster), which we obtain by getting urine from these patients every day for 10 days-that gap is proportional to carbon dioxide production in that individual. By doing this, we can figure out how much carbon dioxide this person made over a period of 10 days. Knowing that, and knowing what the so-called diet quotient is - in other words, what the ratio of carbohydrates to fat in their diet is - you can back-calculate the amount of oxygen used to produce that amount of carbon dioxide.

So by some simple algebra using the rate of carbon dioxide excretion, you can actually calculate how much oxygen their body used in the process of oxidative metabolism. That is a very critical number because it tells you how much energy they burned. Oxygen consumption can be immediately converted into calories.

So we measure caloric expenditure both by figuring out how many calories it takes to make their body weight absolutely stable, and checking that number by also using this double-doped water excretion technique using mass spectroscopy. It's quite expensive: the isotopes to do such a study cost about $500, not including the spectroscopy."

See A comparative study of different means of assessing long-term energy expenditure in humans.

Ain't science wonderful?

The key to happiness

AC-CENT-TCHU-ATE THE POSITIVE (Mister In-Between)

(Johnny Mercer/Harold Arlen, sung by Bing Crosby)

You've got to accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between

You've got to spread joy up to the maximum
Bring gloom down to the minimum
Have faith or pandemonium
Liable to walk upon the scene

(To illustrate his last remark
Jonah in the whale, Noah in the ark
What did they do
Just when everything looked so dark)

Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No, do not mess with Mister In-Between
Do you hear me, hmm?

(Oh, listen to me children and-a you will hear
About the elininatin' of the negative
And the accent on the positive)
And gather 'round me children if you're willin'
And sit tight while I start reviewin'
The attitude of doin' right

(You've gotta accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between)

You've got to spread joy (up to the maximum)
Bring gloom (down) down to the minimum
Otherwise (otherwise) pandemonium
Liable to walk upon the scene

To illustrate (well illustrate) my last remark (you got the floor)
Jonah in the whale, Noah in the ark
What did they say (what did they say)
Say when everything looked so dark

Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No! Don't mess with Mister In-Between

When good science goes bad

I was rummaging through PubMed (as you do) and it occurred to me that there's a problem.

1) The conclusions in the abstracts don't always tie-up with the data in the full studies.
2) There is no mention of who funded the studies.
3) There is no mention of any conflict of interest for the authors.

Some abstracts link to a free full study and some don't. This makes it difficult to know which studies have been "fixed" to achieve a desired outcome by tweaking the methodology. For example, here are some studies involving Hunter SJ, in chronological order:-

Elderly women in northern New England exhibit seasonal changes in bone mineral density and calciotropic hormones which is about seasonal variations in Vitamin D status affecting bone density and was co-authored by Michael Holick.

Demonstration of Glycated Insulin in Human Diabetic Plasma and Decreased Biological Activity Assessed by Euglycemic-Hyperinsulinemic Clamp Technique in Humans which is about how high blood glucose glycates insulin before it's even secreted, resulting in it working less well in muscle cells.

Reduced prevalence of limited joint mobility in type 1 diabetes in a U.K. clinic population over a 20-year period which pretty much does what it says on the tin.

Then, Hunter starts working for The Sugar Bureau and begins co-authoring studies like this:-

Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, scrutinised in Who pays the piper

Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial, scrutinised in Who pays the piper part 2

and

Session 4: CVD, diabetes and cancer Diet, insulin resistance and diabetes: the right (pro)portions, which concludes "based on the results of diabetes prevention trials focusing on lifestyle measures, evidence favours low-fat diets as the preferred approach for weight loss and diabetes prevention."

Evidence favours low-fat diets for weight loss and diabetes prevention, huh? See Low-carb diet pitted against low-fat PLUS medication (low-carb still wins) and Diabetes Update

So, getting paid by an organisation which promotes the consumption of sugar makes good science go bad.

Ghrelin, the other "in"

Having just written about Leptin, it's Ghrelin's turn now. When your stomach is empty, serum ghrelin level is high and when your stomach is full, serum ghrelin level is low. Interestingly, high serum ghrelin has a beneficial effect on the hippocampus (responsible for learning stuff) so do your studying when you're hungry!

As a full stomach reduces serum ghrelin and thus reduces appetite, anything that keeps the stomach full for longer reduces appetite for longer. This is where enterogastrones come in. The most useful one in terms of appetite control is cholecystokinin, the secretion of which is stimulated by proteins & fats. This is one reason why diets high in proteins & fats keep you full for longer. Another useful filler is fibre/fiber, of course. As shown on the BBC programme "The Truth about Food", blending a meal with water or some other low-calorie liquid like soup also slows stomach emptying.

Finally, sleep deprivation raises ghrelin so I must try harder to spend less time on my computer and get some shut-eye.

Don't fight it, if you like it.

I was listening to "Scream" by Timbaland in the car today and the first part of the title made me think of dieting. Sometimes our bodies fight our every effort to change our weight. This is a particular problem for people who are trying to lose weight. They feel cold, hungry & listless and they really want to EAT SOMETHING, damn it! It's because they are trying to change their set point weight. For information about set point weight, see Good Science: Dr. Leibel Explains Metabolic Slowdown with Weight Loss.

The problem with getting fat is that adipocytes (fat cells) can only hypertrophy (become larger in size) so much. When they reach a certain size, they secrete something (I don't know how this works so don't ask) that stimulates preadipocytes to become adipocytes. A larger number of something is called hyperplasia. Once adipocyte hyperplasia has occurred, we are stuck with them for life depending on what part of the body they've formed in. Visceral fat (the harmful fat around your internal organs) cannot be removed by liposuction. Only sub-cutaneous fat can. Losing weight & bodyfat results in adipocytes becoming smaller. However, the more of them there are, the smaller they have to become to achieve a given fat mass.

Adipocytes secrete leptin, the amount secreted reducing with reducing size. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP). Reducing serum leptin level acts on the hypothalamus, increasing our appetites and reducing our energy expenditures. When adipocytes become smaller than normal, leptin secretion reduces considerably and even though there are more of them, net serum leptin decreases and the end result is feeling cold, hungry & listless.

There's another problem that can occur with leptin. In the above example, there's a lack of leptin and the body doesn't work properly. This is analogous to type 1 diabetes. In some people, the hypothalamus becomes insensitive to leptin. Leptin resistance is analogous to type 2 diabetes in that the stuff's present at the correct level but it doesn't have the desired effect and the body doesn't work properly. The end result is also feeling cold, hungry & listless.

It's supposedly possible to restore the sensitivity of the hypothalamus to leptin, but that's for another blog post. So a fat person could say "I'm not fat, I'm hypothalamically-challenged!"

Ban Butter, Part 4,400?

By the time I've finished typing this, there will probably be over 4,400 blogs containing the phrase "Ban Butter". I'm not going to call Shyam Kolvekar rude names. He's a heart surgeon so he's probably very good at cutting people's chests open, removing clogged coronary arteries and grafting in veins removed from legs or whatever it is they do. I don't really wanna know!

He obviously doesn't read our blogs, or he wouldn't have said what he did. If he didn't get any money from Unilever for saying it, that's rather foolish. If I'm going to risk being called every rude name under the sun, I want it to be worth my while.

Anyway, in case you missed it, here's Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

See also Fats and Fatty Acids in Human Nutrition and specifically Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials.

I personally use Anchor Spreadable (kept in the 'fridge) or Anchor/Kerrygold (kept out of the 'fridge) as they're from grass-fed cows.

Finally, for a little light relief, see Butter vs Margarine.

Update: From Hartke Is Online!

Good Calories, Bad Calories by Gary Taubes

I haven't yet fully read the book mentioned in the title, but I've read the Cliff Notes. I have the following comments, based on these notes:-

1) Do I really need to buy Good Calories, Bad Calories?
2) I completely disagree with the following:-

a) Fattening Diets
▪ it's impossible to fatten people on high-fat, high-protein diets: they just can't eat enough
▪ in one experiment, the volunteers would sit staring at "plates of pork chops a mile high" and refuse to eat enough to get an excess thousand cal/day

b) The Carbohydrate Hypothesis, II: Insulin
▪ so: carbs = glucose = glycerol phosphate = trigs = fattening

a) There's an obvious problem with trying to fatten someone using "plates of pork chops a mile high" and that is BOREDOM. Even I, who loves meat, would baulk at eating pork chops washed down with more pork chops plus a side helping of even more pork chops. However, if I had a plateful of fatty roast beef, pork, lamb & duck with all of the crackling/skin plus lashings of juices, I wouldn't have any difficulty in getting thousands of excess kcals/day. Om, nom, nom!

b) See I have a theory and Enzymes.

P.S. Today's featured article on Wikipedia is....The ketogenic diet!

Enzymes

I've started to discuss my hypothesis with Gary Taubes by email and this blog post is intended to go into a bit more detail about how stuff works. Trying to explain the following over the phone with hand-waving is very difficult, especially when I forget things!

Firstly, see Enzyme. Their name always ends in "ase". The thing about enzymes is that their activity can be increased & decreased by the level of substrate i.e. how much "stuff" there is going in to the reaction and how much "stuff" there is coming out of the reaction. Activation & inhibition can also be produced by other substances not directly involved in the reaction.

To get from Glucose (assuming muscle cells) to Pyruvate involves a multi-step process involving lots of different enzymes and other substances. Here's the first step.

Glucose + 1 molecule of ATP (Adenosine Tri-Phosphate) is converted by Glucokinase (with the aid of 2 Magnesium ions) into Glucose-6-phosphate + 1 molecule of ADP (Adenosine Di-Phosphate) + 1 Hydrogen ion. Here's the last step.

Phosphoenolpyruvate + 1 molecule of ADP is converted by Pyruvate kinase (with the aid of 2 Magnesium ions and 1 Potassium ion) into 1 molecule of Pyruvate + 1 molecule of ATP.

As stated in Everyone is Different , muscle cells at rest derive most of their energy from fat (Tri-Palmitin). Inside the cell mitochondria, molecules of Palmitoyl CoA (from Palmitate from hydrolysed Tri-Palmitin) produce energy starting with a process called beta-oxidation, where Acetyl CoA is repeatedly "snipped-off" yielding a fatty acid that's shorter by 2 carbon groups, 1 molecule of Acetyl CoA, 1 molecule of FADH2 + 1 molecule of NADH+H+ (don't ask!) until all that's left is Acetyl CoA. The molecules of Acetyl CoA enter the Krebs Cycle which produces more energy.

As muscle cells at rest derive most of their energy from Acetyl CoA rather than Pyruvate, Pyruvate accumulates. This inhibits the enzyme Pyruvate kinase causing an accumulation of Phosphoenolpyruvate. This inhibits the enzyme that produces Phosphoenolpyruvate etc etc. This results in an accumulation of Glucose-6-phosphate. This inhibits the enzyme Glucokinase causing an accumulation of Glucose. This inhibits the Glu-T4 transporters making muscle cells temporarily insulin resistant. Blood glucose stops entering muscle cells.

Things change when muscle cells undergoing anaerobic exercise use Pyruvate instead of Acetyl CoA. A lack of Pyruvate activates the enzyme Pyruvate kinase causing a lack of Phosphoenolpyruvate. This activates the enzyme that produces Phosphoenolpyruvate etc etc. This results in a lack of Glucose-6-phosphate. This activates the enzyme Glucokinase causing an lack of Glucose. This activates the Glu-T4 transporters making muscle cells temporarily insulin sensitive. Blood glucose enters muscle cells even if blood insulin level is normal.

The same principle applies to fat cells regarding glycerol-3-phosphate. In conclusion:
Within cells, the biochemical processes that produce "stuff" are not static but vary according to the needs of the cells.

I need a break!

While waiting to get hold of Taube's book Good Calories Bad Calories, I'm reading Toban Wiebe's Complete Notes to Good Calories, Bad Calories by Gary Taubes.

I'm also reading Anthony Colpo's latest articles on http://www.anthonycolpo.com/ . This guy doesn't mince his words!

An apple a day...

Once upon a time, there were Crab Apples. They were extremely sour (except perhaps for the Chestnut Crabapple) and contained a lot of Pectin, a soluble fibre/fiber. Then, we clever humans selectively bred apple trees over a large number of years and voila! We have the modern-day apple. Note that this contains on average 10.4g of sugar/100g of apple and only 2.4g of fibre/100g of apple. The British Dental Association claims that the Pink Lady, Braeburn and Fuji contain so much sugar that they cause tooth decay.

Different types of fruit vary hugely in their sugar content. Some fruits (blueberries & cranberries) also contain mannose. Bananas also contain starch, which turns into sugars as the banana changes colour from green to yellow to black.

Don't eat/drink too much fructose, as that goes straight to your liver where it tops-up liver glycogen and, once your liver glycogen stores are full, overspills as triglycerides a.k.a. fats into your liver & blood.

For more on fructose, see Sugar: The Bitter Truth by Robert H. Lustig, M.D.

As glucose and fructose have very different effects on the body, this is a situation where "a calorie isn't a calorie".

Awwwww, CRAP!

I've just read Dr A's latest post and it had a link to Jezwyn's Girl Gone Primal. In Australia, they're having a heatwave and as for the food.....................................well!

In the South of England, the weather's like this:-

Mmm. These oxymorons are absolutely delicious!

I like the word oxymoron. I just saw it in Richard's Blog. As you've probably figured out from reading my Blog, the phrase "healthy low-fat" (usually found just before the word "diet") is to me, a presumptuous oxymoron.

If I type the phrase "healthy low-fat" into Google, I get about 148,000 results. Oh, dear! However...

If I type the phrase "healthy low-carb" into Google, I get about 64,400 results. Yee-haw!

So low-fat may be winning the diet war right now, but the tide is definitely turning. Slowly, slowly, catchee monkey.

Forget Fad Diets.

"Müller Rice makes the perfect low fat snack. Healthy and tasty, it keeps hunger at bay at any time of the day." says Müller Dairy. Let's take a look at the Nutritional information for Müller Rice Apple Flavour (from http://www.mullerdairy.co.uk/) :-

Nutritional information:
	Per 100g				Per 200g serving
Energy	464 KJ				928 KJ
	110 kcal				220 kcal
Protein	3.2g				6.4g
Carbohydrates	19.3g				38.6g
of which sugars	13.7g				27.4g
Fat	2.2g				4.4g
of which saturates	1.3g				2.6g
Fibre	0.4g				0.8g
Sodium	0.1g				0.2g
RDA (per serving)
Calcium	190 mg				23 %
Ingredients:

Milk, Sugar, Rice (7%), Apples (5%), Apple Juice from Concentrate (2%), Egg, Modified Maize Starch, Stabilisers: Carob Bean Gum, Guar Gum; Salt, Acidity Regulators: Ascorbic Acid, Sodium Citrates, Citric Acid; Flavourings.

There's more sugar in it than rice. One 200g serving contains about 6 teaspoonfuls of sugar. Enjoy!

How stuff works.

My preceding post got rather technical and delved into the finer points of cell biochemistry. For those who want to learn more about how cells work, I thoroughly recommend Metabolism at a Glance (Paperback) by Jack G Salway, Sen. Lecturer in Medical Biochemistry, University of Surrey. It's crammed with metabolic pathway diagrams.

I also recommend Medical Biochemistry at a Glance (Paperback) by Jack G Salway.

For general information on nutrition and metabolism, I recommend Introduction to Nutrition and Metabolism (Paperback) by David A Bender, Sen. Lecturer in Biochemistry, UCL.

A good site for information on fat loss, muscle gain etc is https://www.bodyrecomposition.com/.

A good site for nutrient data is https://nutritiondata.self.com/

A good site for peer-reviewed evidence is https://www.ncbi.nlm.nih.gov/pubmed/

A good site for searching textbooks is NCBI Bookshelf

A good site for clinical studies is https://clinicaltrials.gov/ 

A good site for enzyme structures is https://www.ebi.ac.uk/thornton-srv/databases/enzymes/.

Here's a searchable version of Biochemistry, by L Stryer.
It's a bit dry, but of interest is:-
Food Intake and Starvation Induce Metabolic Changes and
Phosphatidate Is a Common Intermediate in the Synthesis of Phospholipids and Triacylglycerols.

Here's a YouTube video of ATP Synthase, which takes a proton gradient and, using a molecular motor-generator, converts ADP + Phosphate into ATP, the energy source that cells use.

Happy reading and viewing!

I have a hypothesis.

I was keeping quiet about this, as it contradicts Gary Taubes, Michael R Eades & Richard D Feinman and Eugene J Fine.

Please note: This post is not criticising low-carb, high-fat diets. I'm pointing out that if someone on a low-carb, high-fat diet exercises as much gluttony as they want on roast lamb/pork/duck etc, they may not lose as much weight/body fat as they expected & they may even gain.

I don't want to start a shit-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied and pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.

"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.

Consider muscle cells undergoing anaerobic activity:-

Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.

This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.

Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."

In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.

Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.

There. I've said it. I expect comments. Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.

EDIT: Here's evidence that dietary fat can be stored in the absence of dietary carbohydrate. It involves doing maths on an Oral Fat Tolerance Test:- On burning, storing and recomposing.

EDIT: Here's evidence that a calorie is a calorie (where weight change is concerned):- Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
 
As a lot of people report that they can eat dietary fat without getting fat (& actually getting lighter & slimmer), there appears to be something "magical" going on. It's generally accepted that fat is the least thermogenic of all the macronutrients & protein is the most thermogenic. I wonder if this is the case for all types of fat and all types of people.

See Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance.

From Battle of the Weight Loss Diets: Who's Winning (at losing):-
Insulin Resistant people lose more weight on low-carb, high-fat (LCHF) diets than high-carb, low-fat (HCLF) diets.  
Insulin Sensitive people lose more weight on high-carb, low-fat (HCLF) diets than low-carb, high-fat (LCHF) diets.

According to Gary Taubes's Carbohydrate Insulin Hypothesis, everyone should lose more weight on low-carb, high-fat (LCHF) diets than on high-carb, low-fat (HCLF) diets. Therefore, Gary Taubes's Carbohydrate Insulin Hypothesis is false.

It's possible that in people who do well on LCHF diets, kcals out on the right hand side of the Energy Balance Equation increase significantly. So keep on keeping on.

EDIT: With the benefit of four more years of knowledge, here's why LCHF & ketogenic diets have an advantage for people who have Insulin Resistance. How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See also:-
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?

See also How stuff works & Enzymes.

Look after your brain, Part 4.

Ketogenic Diet REALLY WORKS!!!
WHAT IF THERE WAS A CURE FOR ALZHEIMER’S DISEASE AND NO ONE KNEW?
High fat, low carb diet may help Alzheimer's sufferers.

The above popped-up when I Googled for "ketogenic diet" alzheimer's.

See also
D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease ,
D-β-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease ,
Ketones: Metabolism's ugly duckling ,
Ketone bodies, potential therapeutic uses ,
Neuroprotective and disease-modifying effects of the ketogenic diet ,
Ketone bodies as a therapeutic for Alzheimer's disease ,
Altered lipid metabolism in brain injury and disorders ,
The ketogenic diet: uses in epilepsy and other neurologic illnesses and
Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis.

EDIT: Ketones give the brain two fuels to run on instead of one (glucose). This improves mental function considerably. However, it can't repair the damage done to the brain by amyloid plaques, protein tangles etc. Sadly, this damage is progressive and permanent. Therefore, coconut oil can't cure Alzheimer's Disease, Lewy Body Dementia etc. It just delays the inevitable.

It's mum's 80th Birthday today so I'm off to see her now.

Continued on Look after your brain, Part 5.

Look after your computer.

I don't know what I'd do if my lap-top were to die. For starters, I'd stop being an internet smart-arse. I'm on-line virtually all day (& some of the night, too!). I often talk to people on the 'phone with the 'phone in my left hand and my right hand doing 1-finger typing/mousing.

When my 2nd cousin asked me "Can you find out about the osteopath Paul that works in the Foot Pain Clinic, Winchmore Hill?", within a minute I'd found Paul Costin. When my ex-G/F asked me "who's the bloke that was in such & such TV programme?", I immediately went to The Internet Movie Database.

I therefore take PC security very seriously. As I mentioned in a previous blog post, my lap-top has limited memory and, being over 6 years old, limited CPU & graphics processing power. So, anything that can improve what I have is worth a try.

The first utility I shall mention is one that I've been using for ages. It's a watch-dog program called WinPatrol. It prevents programs from altering critical system files and installing start-up programs & services without your permission.

On 1st Jan, I installed Malwarebytes' Anti-Malware (MBAM). It found a load of dodgy stuff in the registry (MyWebSearch & SelectRebates) and deleted it all. The end result was more free memory and a bit more free disk space.

On 2nd Jan, I installed ESET Smart Security 4 (& uninstalled Virgin PCguard) after trying NOD32 Antivirus 4 which detected stuff that Virgin PCguard had missed. I gained ~160MB of free memory and my lap-top ran a bit faster, too.

I test my Firewall from the outside using GRC | ShieldsUP! and from the inside using LeakTest.exe, which I renamed to IEXPLORE.EXE, to try and trick the software. ESET Smart Security 4's firewall, once set to Interactive mode, passed all of the tests.

If I find any other useful programs, I'll let you know.

Mum says....

....that Alpro Soya is full of soya bean goodness. Yes, it's another TV advert! I saw it loads of times in the ad-breaks of a programme I was watching on ITV Player. It looks like Alpro aren't allowed to tell us that their soya (soy in just about every other country) milk is full of soya bean goodness, so they have to use argumentum ad verecundiam/ipse dixit.

Alpro. A tasty blend of water, organic soya beans and concentrated organic apple juice. Watch out for all that sugar. You don't want to become addicted, or get tooth decay!

So, do you trust mum? I would rather trust Drew Price BSc, MASc HFI (ACSM).