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

It's all about ME, baby! (1997 - present) is my story after discovering the Atkins Diet. This is my story up to that point. I was born one snowy Winter's day. Mum told me that my cot was placed next to an open window in Central Middlesex Hospital. That explains a lot! Here's mum, me and my sister.


I don't remember much about my early years. As we were relatively poor (dad was a tailor and mum did typing for a solicitor), getting regular French Fancies & Corona lemonade deliveries was considered a status symbol. I ran around in the street with other kids of my age but I was fat. I was also very short for my age (insufficient GH from my pituitary?) and was rubbish at sports in primary school. Here's a photo taken when I was about 9 or 10. I'm the shortest boy in the picture.


Stripy shirts were all the rage, apparently. Even at this tender age, I used to regularly fall asleep after eating a plate of chips (that's fries, to Americans).

In secondary school, sports was dreadful what with having to play cricket using a cricket ball (instead of a tennis ball), contact sports, swimming and showers. Being short, fat & under-developed, I was embarrassed to get undressed in front of my peers, so I developed the art of forging sick notes in my mum's handwriting. I was a very sickly child! ;-D

My forging skills resulted in the total avoidance of swimming (also contact sports, cross-country running etc) and a big improvement in the quality of my handwriting! With tennis, I had to travel to a tennis court by train. I didn't mind doing that, as there were no showers at the tennis courts and I could play the game for a while until I overheated. Secondary school was where I developed a total hatred for almost all sports and when I left, that was the end of exercise as far as I was concerned. When I left secondary school at the age of 18, I was 4 feet 10 inches tall.

At university, I would have a cheese & ham salad baguette washed down with a can of Coke (non-diet in those days) for lunch, followed by a snooze.

At work, I would have a cheese & raw onion roll washed down with a can of Coke for tea-break, followed by a snooze. Here's me at the age of 26. At some point, my pituitary gland "woke up" and secreted GH, as I grew to 6 feet 1 inch tall in my late twenties.


I did manage to get some work done!

When I was dating, I jogged/walked for over 4 miles a day to see my girlfriend. I got slim. After I married, that stopped and as I was a skint Electronic Engineer and Lesley was a skint Cake Decorator, my diet was predominantly cheap carbohydrates, like bread, pasta, potatoes & rice. The result? Lots of snoozes + lots of weight gain. I was a lazy git, apparently.

In 1992, Lesley left me to live with her mother. In 1994, I started dating Eileen. At parties, I became (in)famous for falling asleep after eating nibbles made from refined carbohydrates.

How many working brain cells do researchers have?

Apparently (according to a Japanese study referred to in Am I Missing Something??? ), eating/drinking lots of sugary & starchy carbohydrate causes postprandial hyperglycemia (high blood glucose after meals) in people with type 2 Diabetes. No sh*t, Sherlock! Postprandial hyperglycemia "causes damage to blood vessels, inflammation and oxidation and these cause clogged vessels and heart attacks." I think we're all in agreement that postprandial hyperglycemia is BAD. So, how to tackle this thorny problem? By pharmacological approaches i.e. drug therapies. Like, Duh!
And what is Diabetes-UK's (& the ADA's) dietary advice to people with type 2 Diabetes?
"The actual amount of carbohydrate that the body needs varies depending on your age, weight and activity levels, but it should make up about half of what you eat and drink." & under Ten steps to eating well:
"At each meal include starchy carbohydrate foods
Examples include bread, pasta, chapatis, potatoes, yam, noodles, rice and cereals. The amount of carbohydrate you eat is important to control your blood glucose levels." Like, Duh!


I've been doing a bit of research on methylglyoxal (MG) as a result of reading Methylglyoxal on Atkins... Uh oh! Apparently it's very toxic, therefore ketogenic diets are BAD, mmm-kay? MG causes Insulin Resistance and Advanced Glycation End-products which are both deemed to be undesirable.

Consider this: MG is a glycolysis (conversion of glucose to pyruvate) inhibitor. As MG inhibits glycolysis in cells, uptake of Blood Glucose by cells decreases. Oh, look. Cells have become Insulin Resistant! As uptake of Blood Glucose by cells decreases, Blood Glucose rises. Oh, look. Increased Advanced Glycation End-products! It's bleedin' obvious (to anyone with a sufficient number of working brain cells) that, on a high-carb diet, MG is toxic. It's a no-brainer that MG's toxicity disappears on a low-carb/keto diet, when you actually want cells to burn fatty acids/ketones rather than glucose. Like, Duh!

In fact, strangulating the glucose pathway in cells may have benefits. See Cancer.


Here's another one. According to Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet (KD), "The KD resulted in progressive loss of BMC." And yet, just above, "Growth and bone health status were suboptimal as were serum 25-OHD concentrations and dietary intake of calcium and vitamin D." Like, Duh!

Everybody knows.........Part 2

.........that ketogenic diets like the Atkins diet destroy your kidneys and rot your bones, right? Wrong!
.........that the Atkins diet causes ketoacidosis which is a very dangerous condition requiring urgent hospital treatment, right? Wrong!

There's a lot of nonsense spoken about ketogenic diets by people who really should know better. I suspect that they have been taught wrongly at uni or med school as per the quote in Everybody knows.........Part 1.

Benign Dietary Ketosis is NOT Ketoacidosis.

Consider the following four cases:- Note: Figures are from "Introduction to Nutrition and Metabolism" By David A Bender (Senior Lecturer in Biochemistry, UCL)

1) Healthy human, fed state: Glycogen stores are replete. Serum glucose = ~5.5mmol/L. Serum fatty acids = ~0.3mmol/L. Serum ketones = 0mmol/L. No gluconeogenesis is taking place. Amino acid pool is replete. Cortisol level is normal so there is no loss of muscle mass.

2) Healthy human, fasting for 7 days: Glycogen stores are depleted. Serum glucose falls to ~3.5mmol/L. Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is depleted. Cortisol level is high, causing slow loss of muscle mass. This is bad ketosis.

3) Healthy human, low-carbohydrate diet: Glycogen stores are depleted. Serum glucose falls to ~5mmol/L.
Serum fatty acids rise to ~1.2mmol/L. Serum ketones (mainly D-3-hydroxybutyrate) rise to ~4.5mmol/L (not high enough to cause acidosis). Gluconeogenesis is occurring. Amino acid pool is replete (due to protein intake). Cortisol level is normal so there is no loss of muscle mass. This is good ketosis.

4) Human with untreated type 1 diabetes: Glycogen stores are depleted. Due to lack of insulin, the Glu-T4 transporters in cells cannot move to the surface so glucose cannot enter cells. Serum glucose = >20mmol/L. This causes major damage to kidneys, arteries, eyes, nerves etc by cross-linking with proteins (glycation) resulting in major disability and eventual death. As the body is forced to run on fatty acids & ketones, metabolic processes are out of control and ketones rise to much higher levels than in 2) or 3) (I don't know how high exactly) resulting in acidosis and eventual death. This is ketoacidosis.

Conclusion: Low-carbohydrate, very-low-carbohydrate & ketogenic dieting is similar to fasting in that serum glucose levels are lower than normal and glycogen stores are depleted. The body is encouraged to burn less glucose and more fatty acids & ketones, but the metabolic processes are all under control. The big difference between low-carbohydrate dieting and fasting is in the amino acid pool and cortisol levels.

Everyone is Different.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Continued on We are not all the same.

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

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

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

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

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

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

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

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

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

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

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

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

Cheers, Nige.