Infectious obesity

I posted on AD36, the fat virus, a while ago.

The below quotes are from an article from the NY Times entitled “Fat Factors“. To read the NY times article, you have to register. Try the username/pw bugmenot/bugmenot if you’d rather avoid that.

Here are some excerpts:

One of Atkinson’s most memorable patients was Janet S., a bright, funny 25-year-old who weighed 348 pounds when she finally made her way to U.C.L.A. in 1975. In exchange for agreeing to be hospitalized for three months so scientists could study them, Janet and the other obese research subjects (30 in all) each received a free intestinal bypass. During the three months of presurgical study, the dietitian on the research team calculated how many calories it should take for a 5-foot-6-inch woman like Janet to maintain a weight of 348. They fed her exactly that many calories — no more, no less. She dutifully ate what she was told, and she gained 12 pounds in two weeks — almost a pound a day.

“I don’t think I’d ever gained that much weight that quickly,” recalled Janet, who asked me not to use her full name because she didn’t want people to know how fat she had once been. The doctors accused her of sneaking snacks into the hospital. “But I told them, ‘I’m gaining weight because you’re feeding me a tremendous amount of food!’ ”

[...]

One year ago, the idea that microbes might cause obesity gained a foothold when the Pennington Biomedical Research Center in Louisiana created the nation’s first department of viruses and obesity. It is headed by Nikhil Dhurandhar, a physician who invented the term “infectobesity” to describe the emerging field. Dhurandhar’s particular interest is in the relationship between obesity and a common virus, the adenovirus. Other scientists, led by a group of microbiologists at Washington University in St. Louis, are looking at the actions of the trillions of microbes that live in everyone’s gut, to see whether certain intestinal microbes may be making their hosts fat.

[...]

Gordon first began studying the connection between the microflora and obesity when he saw what happened to mice without any microbes at all. These germ-free mice, reared in sterile isolators in Gordon’s lab, had 60 percent less fat than ordinary mice. Although they ate voraciously, usually about 30 percent more food than the others, they stayed lean. Without gut microbes, they were unable to extract calories from some of the types of food they ate, which passed through their bodies without being either used or converted to fat.

When Gordon’s postdoctoral researcher Fredrik Bäckhed transplanted gut microbes from normal mice into the germ-free mice, the germ-free mice started metabolizing their food better, extracting calories efficiently and laying down fat to store for later use. Within two weeks, they were just as fat as ordinary mice. Bäckhed and Gordon found at least one mechanism that helps explain this observation. As they reported in the Proceedings of the National Academy of Sciences in 2004, some common gut bacteria, including B. theta, suppress the protein FIAF, which ordinarily prevents the body from storing fat. By suppressing FIAF, B. theta allows fat deposition to increase. A different gut microbe, M. smithii, was later found to interact with B. theta in a way that extracts additional calories from polysaccharides in the diet, further increasing the amount of fat available to be deposited after the mouse eats a meal. Mice whose guts were colonized with both B. theta and M. smithii — as usually happens in humans in the real world — were found to have about 13 percent more body fat than mice colonized by just one or the other.

Gordon likes to explain his hypothesis of what gut microbes do by talking about Cheerios. The cereal box says that a one-cup serving contains 110 calories. But it may be that not everyone will extract 110 calories from a cup of Cheerios. Some may extract more, some less, depending on the particular combination of microbes in their guts. “A diet has a certain amount of absolute energy,” he said. “But the amount that can be extracted from that diet may vary between individuals — not in a huge way, but if the energy balance is affected by just a few calories a day, over time that can make a big difference in body weight.”

In another line of research, Gordon and his postdoctoral researcher Ruth Ley compared the microflora in two kinds of mice: normal-weight mice and mice with a genetic mutation that made them fat. Like humans, the mice had microflora consisting almost exclusively of two divisions of bacteria, the Bacteroidetes and the Firmicutes. But the proportions differed depending on whether the host was thin or fat. The normal-weight mice had more Bacteroidetes than Firmicutes in their gut microflora. The genetically obese mice had the opposite proportions: 50 percent fewer Bacteroidetes, 50 percent more Firmicutes.

[...]

The idea of infectobesity dates to 1988, when Nikhil Dhurandhar was a young physician studying for his doctorate in biochemistry at the University of Bombay. He was having tea with his father, also a physician and the head of an obesity clinic, and an old family friend, S. M. Ajinkya, a pathologist at Bombay Veterinary College. Ajinkya was describing a plague that was killing thousands of chickens throughout India, caused by a new poultry virus that he had discovered and named with his own and a colleague’s initials, SMAM-1. On autopsy, the vet said, chickens infected with SMAM-1 revealed pale and enlarged livers and kidneys, an atrophied thymus and excess fat in the abdomen.

The finding of abdominal fat intrigued Dhurandhar. “If a chicken died of infection, having wasted away, it should be less fat, not more,” he remembered thinking at the time. He asked permission to conduct a small experiment at the vet school.

Working with about 20 chickens, Dhurandhar, then 28, infected half of them with SMAM-1. He fed them all the same amount of food, but only the infected chickens became obese. Strangely, despite their excess fat, the infected obese chickens had low levels of cholesterol and triglycerides in their blood — just the opposite of what was thought to happen in humans, whose cholesterol and triglyceride levels generally increase as their weight increases. After his pilot study in 1988, Dhurandhar conducted a larger one with 100 chickens. It confirmed his finding that SMAM-1 caused obesity in chickens.

But what about humans? With a built-in patient population from his clinic, Dhurandhar collected blood samples from 52 overweight patients. Ten of them, nearly 20 percent, showed antibody evidence of prior exposure to the SMAM-1 virus, which was a chicken virus not previously thought to have infected humans. Moreover, the once-infected patients weighed an average of 33 pounds more than those who were never infected and, most surprisingly, had lower cholesterol and triglyceride levels — the same paradoxical finding as in the chickens.

[...]

One month before his self-imposed deadline in 1994, Dhurandhar received a job offer from Richard Atkinson, who was then at the University of Wisconsin, Madison. Atkinson, always on the lookout for new biological explanations of obesity, wanted to collaborate with Dhurandhar on SMAM-1. But the virus existed only in India, and the U.S. government would not allow it to be imported. So the scientists decided to work with a closely related virus, a human adenovirus. They opened the catalogue of a laboratory-supply company to see which one of the 50 human adenoviruses they should order.

“I’d like to say we chose the virus out of some wisdom, out of some belief that it was similar in important ways to SMAM-1,” Dhurandhar said. But really, he admitted, it was dumb luck that the adenovirus they started with, Ad-36, turned out to be so fattening.

By this time, several pathogens had already been shown to cause obesity in laboratory animals. With Ad-36, Dhurandhar and Atkinson began by squirting the virus up the nostrils of a series of lab animals — chickens, rats, marmosets — and in every species the infected animals got fat.

“The marmosets were most dramatic,” Atkinson recalled. By seven months after infection, he said, 100 percent of them became obese. Subsequently, Atkinson’s group and another in England conducted similar research using other strains of human adenovirus. The British group found that one strain, Ad-5, caused obesity in mice; the Wisconsin group found the same thing with Ad-37 and chickens. Two other strains, Ad-2 and Ad-31, failed to cause obesity.

In 2004, Atkinson and Dhurandhar were ready to move to humans. All of the 50 strains of human adenoviruses cause infections that are usually mild and transient, the kind that people pass off as a cold, a stomach bug or pink eye. The symptoms are so minor that people who have been infected often don’t remember ever having been sick. Even with such an innocuous virus, it would be unethical, of course, for a scientist to infect a human deliberately just to see if the person gets fat. Human studies are, therefore, always retrospective, a hunt for antibodies that would signal the presence of an infectious agent at some point in the past. To carry out this research, Atkinson developed — and patented — a screening test to look for the presence of Ad-36 antibodies in the blood.

The scientists found 502 volunteers from Wisconsin, Florida and New York willing to be screened for antibodies, 360 of them obese and 142 of them of not obese. Of the leaner subjects, 11 percent had antibodies to Ad-36, indicating an infection at some point in the past. (Ad-36 was identified relatively recently, in 1978.) Among the obese subjects, 30 percent had antibodies— a difference large enough to suggest it was not just chance. In addition, subjects who were antibody-positive weighed significantly more than subjects who were uninfected. Those who were antibody-positive also had cholesterol and triglyceride readings that were significantly lower than people who were antibody-negative — just as in the infected chickens — a finding that held true whether or not they were obese. Fat Factors

A calorie is not a calorie: anyone who says otherwise is ignoring the second law of thermodynamics.

Zero Carb Daily

I’ve been reading Rob’s Zero Carb Daily blog. He’s one of the carnivores. He has a few interesting things to say. For example, this quote from The Bear (the carnivore’s guru), which I have to reproduce because it greatly amused me:

Green leafy vegetables have little or no nutritive value, and are eaten as “eye food”. In fact some, like celery and lettuce have less caloric value than it takes to process them through your system, like sand. Some, like spinach, contain a toxic blood poison, oxalic acid. This dangerous chemical is so high in rhubarb that the green leaves are capable of causing death. Why eat this rubbish?

I agree that there is only maybe 20 percent of the weight of “leafy greens” which is carbs, but why eat something so toxic and rough? Would you intentionally put a pinch of sand in the crankcase of your car? Older people suffer from malnutrition in spite of “excellent diets” due to the scar tissue in their intestines from a lifetime of exposure to roughage in their food. In the short term it causes the intestines to coat themselves with mucus, which also interferes with absorption of nutrients.

All plants have toxins, chemical defenses against herbivores are much older than the mechanical ones like the spines of cacti. People have struggled for hundreds of years to breed out most of these defenses, which is why you cannot grow them without pesticides.

If you doubt me, eat a cupful of wild lettuce (a very common weed), and see how long you can remain awake. It contains a glucoside, letucin, called “lettuce opium”, which was bred out of the cultivated plant. Zero Carb Daily (Atkins and the Good Carb myth)

Lettuce is one of the very few plants that human beings eat raw, the implication being that it has to be one of the few truly Paleolithic vegetables. But it turns out to be a Neolithic food we’ve cultivated the poisons out of? I’ve maintained for at least a year now the stance that lettuce is pointless. It doesn’t add nutrition or calories. It just adds roughage and poisons. It tastes bad, it has an unpleasant mouth feel, and my life was about 10% better when I gave up forcing myself to eat it.

Rob also has an interesting post about fibre. Now, I have an instinctive aversion to fibre because of what it does to my guts, which is not pleasant. I’ve also had some pretty good nutritional reasons for avoiding it since I read Barry Groves’ Fibre and Colon Cancer article a couple of years ago.

It turns out that the mechanism by which fibre keeps you regular is deeply unpleasant:

If you ever wondered just how a high-fiber diet helps keep you, well, “regular,” scientists may have the answer.

Their results suggest that as these bulky foods make their way down the gastrointestinal tract, they run into cells, tearing them and freeing lubricating mucus within.

More mucus is good, says Dr. Paul L. McNeil, cell biologist at the Medical College of Georgia and corresponding author on the study published online Aug. 21 and scheduled for the September print issue of PloS Biology. “When you eat high-fiber foods, they bang up against the cells lining the gastrointestinal tract, rupturing their outer covering. What we are saying is this banging and tearing increases the level of lubricating mucus. It’s a good thing.” Scientists learn more about how roughage keeps you “regular”

It’s a good thing? Does that mean that the resultant colon cancer caused by all the cell damage is also “a good thing”?

The scientists aren’t certain how many times cells can take a hit, but they suspect turnover is so high because of the constant injury. Potentially caustic substances, such as alcohol and aspirin, can produce so much damage that natural recovery mechanisms can’t keep up. But they doubt a roughage overdose is possible.

This caught my eye. Though intestinal problems including malabsorption syndromes are common amongst the food chemical intolerant, I hadn’t investigated how salicylates (aspirin) might cause this. It seems salicylates simply cause so much cell damage to the colon that the body can’t repair itself fast enough.

Food for thought?

This post is for a couple of friends of mine who are big fish eaters.

Mercury released by coal-fired power plants contaminates waterways and accumulates in fish. Many thousands of the pregnant women in America who eat fish consume enough mercury to potentially harm their children’s neurological development. Some states warn that children should not eat more than a can of tuna per week; based on EPA guidelines, a twenty-pound child may exceed a level considered safe for the most sensitive populations with just 1.3 ounces.

Lakes fish contaminated with PCBs showed lowered IQs and shortened attention spans. And these effects on intelligence and behavior have been shown to persist throughout childhood. A Dutch study confirmed that increased maternal levels of PCBs can impair cognition in infants. Young monkeys exposed to PCBs at low levels show learning disabilities and hyperactivity. ADHD leaflet from childenvironment.org

If you are a pescatarian or a regular fish eater (i.e. you eat fish more than once a week), I advise you to visit gotmercury.org immediately and calculate your mercury exposure, because you’ll probably never eat tuna or other oily fish again.

I’ve calculated mine. One 6 oz serving of cod (comparatively low in mercury), gives me around 40% of the maximum weekly exposure of mercury. One 6 oz serving of tuna gives me between 140% and 270% of my maximum weekly exposure.

Eat fish every day? You’re in deep trouble.

Chocolate addicts take note!

Who needs crack when chocolate is freely available?

I’ve mentioned before how I’ve come to realise I have unpleasant reactions to chocolate, and how other failsafers have also reported extreme reactions, including wild bouts of paranoia. I’ve always been a chocolate addict, and even on a strict low-carb diet, a meal didn’t feel “complete” without a small piece of very strong dark chocolate at the end. I always blamed this on carbohydrate cravings, but I realised when I tried to replace chocolate with other foods – like dates – that I would still crave chocolate when the sweet cravings were satisfied. The problem was the chemistry of chocolate, which is high in a raft of amines and other neurotransmitters like endorphins.

Amines are something in particular that I associate with being put in what I can only describe as a “black mood”, like a seething thundercloud. I hate everyone and everything, I’m disgusted by the selfishness and idiocy of humanity (normally the selfishness and idiocy of humanity does not bother me particularly, LOL), and I want to be as far away from all other human beings as possible.

Chocolate in particular, not only puts me in a “black mood”, it also makes me fairly paranoid. Some people experience the feeling that they are being victimised. I don’t (I already know they’re out to get me, LOL), instead I’m paranoid about things like dying in car accidents or leaving the gas on. Chocolate is particularly high in dopamine, and I’m aware that too much dopamine in the limbic system and not enough in the cortex creates an imbalance that produces suspicion, paranoia and inhibits social interaction. Something else I tend to get with chocolate consumption and amines (and I have this in common with side effects experienced by Seroxat/Paxil and Prozac users, so is possibly serotonin related) is that I’ll flash on violent scenarios or morbid fantasies in which I die. Fortunately I’m a very level-headed person and have trained myself to put such images straight out of my mind.

In real life I’ve heard many tales of women who have chocolate addictions who get such powerful chocolate cravings that they have to drop everything that they are doing and go out (or more often, their boyfriend is hassled into going out) to buy chocolate from the local newsagent. One friend of mine swears she cannot go a single day without a bar of chocolate. She’s a Muslim and observes fasting during Ramadan – every day she would count down the seconds until the sunset fell and would rush to the office snack machine to buy a big Mars bar.

This is from the latest failsafe newsletter:

The biggest shock for me however, was when I recently discovered I was a food reactor!! I was a junk food addict and would eat about 5kg of chocolate a week. I can’t believe now I had so many symptoms, and I never even put them together as symptoms, let alone found the source of the problem! I was getting migraines, I constantly had a headache behind my eyes, I felt very faint and disoriented, had stomach pains that felt like needles – usually after eating lollies, and I was always bloated – something which really upset me.

The weirdest thing to attribute to food however was my extreme ‘fear of the dark’ as I called it. I would be terribly scared of the dark, I would think that my mind thought it could see little people and things out of the corner of my eye, even though I knew they weren’t there, I would open my eyes every 10 seconds while trying to get to sleep, just to check if there were monsters or robbers there, and every time I closed my eyes all I could picture in my head was horrible things that would scare me. I was a bit worried I was starting to go crazy, then I stopped eating chocolate and didn’t even notice all these symptoms disappeared.

It wasn’t until I splurged on a whole chocolate cake over two nights that I discovered what had caused these problems. After eating the cake I was completely on edge. I couldn’t sit down for ten seconds without turning around to make sure there were no monsters or robbers behind me. Eventually I had to sit with my back to the wall so I wouldn’t think there were things behind me. That was the last time I ate chocolate, and the thought of ever eating it again scares me! – by email. [447] ‘Fear of the dark’ really a food reaction (August 2006)

Wow. Five kilograms of chocolate a week. That’s quite an achievement. In this case, a food chemical addiction was the primary problem, and the calorie consumption was a secondary, inevitable aspect. I don’t believe people naturally overconsume food, I believe they do it when what they are eating is giving them cravings.

That saturated fat meal that's bad for your arteries

I’ve seen a couple of critiques of the latest tiresome anti-saturated-fat scare-story put out in the media a few weeks ago, that “just one meal high in saturated fat can harm your arteries!“

Here’s Anthony Colpo’s critique, which points out what a teeny tiny differences the massive relative percentages really are.

Here’s Chris Masterjohn’s critique, which examines vitamin E content as an alternative hypothesis.

Something I’d like to point out that seems really obvious to me, but is probably quite specialist knowledge – too specialist even for the researchers who designed the study – is that:

Safflower oil is extremely low in phenolic chemicals including salicylates.

Coconut oil is extremely high in phenolic chemicals including salicylates.

Unlike fat, salicylates are vasoactive. The study measures the dilation of the arteries after eating identical meals, one containing virgin safflower oil, the other containing virgin coconut oil. Of course they will be different.

Personally, I believe that all the study is doing is measuring the effects of phenols on arterial dilation and forms of inflammation.

A funny kind of diet

Most people don’t even hit 50% of RDA on a lot of vitamins and minerals without help from fortified products or multivitamins, whether they eat nothing but wholefoods or not. However, you can meet or exceed your RDA in every vitamin and mineral by eating the following extremely limited diet:

1 tbsp butter
2 medium eggs
1.5 pints whole milk
3 oz wheat germ
10 brussels sprouts
8 oz beef steak

This diet meets the RDAs of all vitamins and minerals, hits 200% RDA for most, and goes up to 400-600% for some micronutrients. These foods are very carefully chosen. Carbohydrate is less than 70 grams per day, which is still a quantity classified as low in carbohydrate. There’s room for several hundred spare calories depending on your size. And it’s failsafe, if you tolerate milk and wheat.

Crap nutritionists strike again

GP Wendy Denning and nutritionist Vicki Edgson, stars of Channel Five’s The Diet Doctors Inside And Out, have exclusively teamed up with Now to answer your diet and health questions.

Q I started drinking about a litre of fruit juice a day and eating grapes, pineapples, melons and oranges. But I got painful red cracks on the edge of my mouth. Could this be due to too much citrus fruit in my diet?

Vicki says I’m surprised you haven’t also had extreme bloating and wind! In fact, the only fruit you’re eating that strictly falls under the citrus category is oranges, but the others are highly acidic. Also, a litre of fruit juice every day will cause disruption to your blood sugar levels, causing highs and lows of energy.

May I suggest that you cut back your consumption of fruit to two to three portions a day and don’t have grapes on the same day as melon, as these are both very high in fruit sugars? Don’t get me wrong – fruit’s great, but vegetables should also be making up your five a day. You may also like to include the humble apple, pear and banana in your fruit diet, all of which contain pectin, which helps to remove toxins from the digestive tract, as well as providing fibre. – Now magazine, 23 Aug 2006

Did it not at all strike Vicki Edgson that “painful red cracks on the edge of my mouth” sounds exactly like riboflavin deficiency? Especially in the context of consuming huge amounts of fruit-sugar carbohydrates which are deficient in B vitamins?

True, occasionally the same symptoms can be caused by B6 deficiency (which in this case may be caused by the vast quantities of pyridoxine glycosides this girl must be consuming), or even iron deficiency anaemia, which wouldn’t be surprising as this sounds like it may well be a fruitarian diet.

These symptoms could well be caused by salicylates and polyphenols, but I doubt the great intellects that are Wendy and Vicki have ever heard of salicylate intolerance.

But surely not even considering riboflavin deficiency in the context of “cracks at corners of mouth” is tantamount to negligence?

And the moral of the story is…

I cannot count on both hands the number of people I know in real life, and have met online, who I would like to send these extracts from Sue Dengate’s “Fed Up with ADHD”.

One new friend kept telling me about her nephew who was on a diet low in salicylates. I had never heard of salicylates. In retrospect I can see she was observing my child’s behaviour and trying to get the message across. I was totally unreceptive. When my friend told me that most fruits contain salicylates I was horrified. Life without fruit was unimaginable. “I’m glad we don’t have to worry about that,” I told her. P17

[...]

During this holiday we began a blitz on saying “please” and “thank you”. It would take us about three years of persistent effort to get Rebecca to say these reliably. Arran learned in about three weeks. This summarises for me the size of the problem we were up against. Expecting Rebecca to acquire common social skills through observation was unrealistic, including basic skills such as washing of hands and waiting in turn. I estimated that if I needed to remind Arran about something several hundred times, for Rebecca it would take several thousand times. This represented a drastic increase in parenting workload which could have been avoided. She learned eventually, but why bother? It would have been easier to change what she ate. P21

[...]

I thought if my children were affected by food additives, I would notice an obvious reaction, but the truth is, parents usually don’t. The effects just seemed to be part of their normal behaviour. When I removed food colours and some preservatives from Arran’s diet he started sleeping through the night straight away, although he still had diarrhoea.

From The Medical Journals
‘The younger children had constant crying, tantrums, irritability, restlessness and severe sleep disturbance, and were described as “disruptive”, “easily distracted and excited”, “high as a kite” and “out of control”. Their parents were exhausted through lack of sleep and the constant demands of their children, who were unable to be comforted or controlled. THe older children were described as “irritable”, “aimlessly active”, “lacking self-control”, “whiney and unhappy”, and “like a bear with a sore head”.’
Rowe KS and Rowe KJ, “Synthetic food coloring and behavior”, J Pediatrics 1994;125:691-698

In retrospect, I wish the dietitian had explained more to me about the effects of food intolerance and how to use the RPAH elimination diet, in case avoiding additives wasn’t enough. Unlike the other health professionals I saw, she had all the information I needed. She just didn’t give it to me. It didn’t occur to me that Arran’s health problems and Rebecca’s behaviour problems could have the same cause so I didn’t talk about Rebecca and I don’t think the dietitian realised just how bad our situation was. P27

[...]

One weekend we went to visit some good friends in a nearby city and I noticed that their five-year-old son, whom I normally regarded as rather demanding, was unusually agreeable. For morning tea there was a pink iced bun, which my children were not allowed to eat. I watched their son eat the pink icing and right under my eyes, he became restless and demanding.

“When we came in he was behaving very well, but I’ve noticed he’s changed since we had morning tea. Do you think he could have the same problem was Rebecca?” I asked his mother.

My friend was remarkably receptive. “I’ve been wondering about that,” she admitted, and described how the preschool teacher had referred him to the school nurse for an assessment. The nurse had commented, “He doesn’t concentrate very well, does he?” It was true. He wasn’t concentrating, and couldn’t finish the test, despite excellent concentration at home.

By the end of our visit my friend had bought a copy of Dr Feingold’s classic book, which is still a good read despite the outdated diet. Her son was already on the diet although he was not a hyperactive child. In many ways he was the opposite of Rebecca – a sendentary, good sleeper who was reading fluently before he entered preschool. But his messy handwriting, poor social skills, intermittent concentration problems and inappropriate temper outbursts improved on the diet. “He seems to be most affected by salicylates, just as the book says,” his mother commented.

“Thank goodness that’s not a problem for us,” I answered. “I’d hate to have to cut out fruit, although I have noticed that Rebecca gets aggressive if she eats a lot of almonds, so I suppose that’s salicylates. I think she has a mild intolerance.” How I wish I had paid more attention. Dietary management so far had improved all of Rebecca’s behaviours except sleeping. Here was someone telling me the answer to our problems but I still wasn’t listening.

Like most people, I didn’t want to hear about salicylates. I still thought that if your child was sensitive to certain foods, then you would see an obvious reaction soon after eating. I couldn’t understand that when children eat food chemicals many times a day, as with salicylates, the result is good days and bad days which come and go for no obvious reason. The concept of trying an elimination diet in which all additives and salicylate-containing foods are avoided, then reintroduced one group at a time, was still far beyond me. PP32-33

[...]

Rebecca had so many problems that I decided it was time for us to take diet seriously. The dietitian was not helpful. “I don’t believe the Feingold diet works,” she said, “and it’s not my job to help hyperactive children.” She persuaded me not to try the elimination diet which I had requested. “It’s very difficult, and you’ve done most of it already.” If only I could have talked to a sympathetic dietitian at this stage. I was finally ready to hear what they had to say, and it would have saved us years of anguish. [...]

[After being given advice to increase vegetables and fruit] I thought that I was feeding my children good food but the dietitian could hardly have given me less helpful advice. I had decided we didn’t have to worry about salicylates. I couldn’t have been more wrong. We embarked on a two-year period of even worse sleeping problems than we had already encountered.

Researchers comment that mothers rarely see a correspondence between food and behaviour. It was true. I did not relate Rebecca’s increasing inability to go to sleep at night and worsening problems in other areas to the “healthier” diet we were eating. PP49-50

Reye's syndrome

Reye’s syndrome is the reason that junior aspirin was withdrawn from the market in the UK some years ago now. Take a look at the symptoms:

• Nausea
• Recurrent vomiting
• Listlessness
• Personality changes
• Progressive mental changes
• Irritability
• Combativeness
• Disorientation
• Confusion
• Forgetfulness
• Lethargy
• Agitation
• Disorientation
• Delirium
• Convulsions
• Loss of consciousness
• Coma
• Brain swelling
• Encephalopathy
• Liver dysfunction
• Enlarged liver
• Reye’s Syndrome from WrongDiagnosis.com

If you are food chemical intolerant you will probably recognise most of these symptoms and associate them with salicylates, i.e. aspirin.

Salicylate induced hypoglycaemia

These are extracts from Sue Dengate’s “Fed Up with ADHD”

One morning we all arranged to go on a long bushwalk. After a short distance Rebecca stopped. “I’m too tired,” she said and lay down on the track.

“Nonsense. A child of that age should be able to walk this distance,” said our friend. She clearly thought we were being too easy on Rebecca. I had noticed food would get her moving and I gave her some dried fruit. After another ten minutes she was up again but quite white-faced and shaky. Howard helped her back to camp.

Episodes like this were to occur sporadically, usually associated with exercise. A friend suggested hypoglycemia and the symptoms did seem to fit. I talked to our doctor, who described hypoglycemia as an American fad and reassured me that Rebecca did not have diabetes. We adopted the principles of the diet anyway, feeding Rebecca every couple of hours, especially on waking and before going to sleep and avoiding refined foods and sugar. This seemed to help and so we embarked on what turned out to be the wrong track for the next six years. PP36-37

[...]

Suddenly Rebecca said “I’m tired” and lay down. She was panicky and uncoordinated and we had to almost carry her down the steep, slippery path. When we reached the tent she lay unmoving, refusing to eat. I forced her to drink some juice and soon she got up and started playing as if nothing had happened.

Episodes like this always seemed to happen when we were staying in a cabin and I remember over the week Rebecca had been eating a lot of bread and marmalade. When she suddenly said “I’m tired” I decided to see if she would sleep it off. I left her lying on her bed in the twilight.

About an hour later, expecting her to be asleep, I found her crouched under a bench in the now dark room. She did not seem to recognise me, was incapable of speech and appeared terrified. I led her gently to the kitchen and stuck a spoonful of sugar in her mouth. In a few minutes she was back to normal.

I tried to find out how to prevent these alarming episodes. The doctor I talked to said, “She’s probably got hypoglycemia, but she’s too young to have a glucose tolerance test.” He also suggested that her night waking with panic may be due to hypoglycemia and that we might have to wake Rebecca and feed her in the middle of the night.

We took his advice on feeding her before sleeping. If she spent several hours trying to fall asleep, as usual, then she ate some more supper. This did reduce the night panic and if she woke eating helped her to get back to sleep.

I thought I could see a pattern. The episodes usually occurred when we were out of our regular routine and they seemed to be associated with exercise. If Rebecca ever mentioned she was hungry I learned to feed her immediately, as the feeling quickly passed. This lack of self-awareness characterised both Howard and Rebecca.

Arran frequently complained “I’m hungry”, but food could be delayed without any ill effects. Rebecca rarely complained of hunger. I was more likely to observe, “You are getting grumpy. I think you need to eat.” She would often deny this and have to be cajoled into eating, but improved quickly after eating. If Rebecca actually said she was hungry I regarded this as a red alert situation and fed her immediately. Five minutes delay was too long. The feeling would have passed, soon becoming “I’m tired”, refusal to eat, and lying down. Sometimes there was another stage, “I want some sugar,” before the tiredness.

Many years later I would find the explanation. Salicylates can impair production of glucose in the body while increasing glucose utilisation. This causes an imbalance, resulting in salicylate-induced hypoglycemia. Rebecca’s problems while on holidays or bushwalking were related to our higher consumption of salicylate-containing foods such as dried fruit. The effect was worsened by exercise, which increases the body’s need for glucose. PP56-57

[...]

We were still worried about Rebecca’s lack of energy during exercise. When I explained the symptoms in detail to our pediatrician, he agreed to have her tested for hypoglycemia and booked her into hospital.

Rebecca spent twenty-four hours in hospital on a water-only diet, having regular blood tests to see if her blood sugar level changed. It didn’t. The hospital doctor was contemptuous. She thought that ADHD was overdiagnosed, that Rebecca’s problems were due to poor parenting and that food intolerance was “clutching at straws” but we noticed a remarkable change.

From a rude and angry start, Rebecca progressively became more polite and cooperative, sweet-natured and clear-thinking. That evening she was fun to be with and played the best game of checkers ever. We thought she was lovely. “That is how I want my daughter,” I joked to our pediatrician on our follow-up visit. “We’ve discovered the right diet for her. Water only!”

I was surprised to find he took me seriously. Hadn’t he ever believed me before?

“Perhaps the hypoglycemic symptoms are being triggered by a food sensitivity,” he suggested. The upshot was that he arranged a case conference with a new dietitian. PP107-108

[...]

For nearly six years we had been convinced that Rebecca reacted to sugar and had avoided it in our diet. Refined white sugar is permitted on the elimination diet – as part of a balanced diet – and the children were now eating sugar to compensate for the restrictions on fruit sugar.

I had to admit Rebecca did not seem to be affected, but when she had a big reaction five hours after eating a lemonade icy pole, I blamed sugar. To confirm this, we did a challenge with ten sugar cubes. No reaction. Still unconvinced, we tried again with twenty sugar cubes. Still no reaction. I had to accept that Rebecca did not react to sugar and that I had been wrong for all those years. Lemonade icy-poles contain small amounts of salicylates. I had finally seen for myself that Rebecca’s hypoglycemic symptoms had been related to salicylates not sugar.

In the years that followed, I came to understand salicylate-induced hypoglycemia. When Rebecca avoids salicylates, she can eat sugar with no problems. If Rebecca eats too many salicylates, especially while exercising, under stress or skipping some meals, she suffers a hypoglycemic episode and improves instantly with a spoonful of sugar. I would prefer my daughter to be able to eat fruit rather than sugar. But that’s not the way it is. PP114-115

I regained my carbohydrate tolerance after going on failsafe for a few weeks. I was curious because I knew that I definitely experienced reactions to carbohydrate before going on the diet. I mentioned at the time that I came across numerous studies in Medline/Pubmed (too many to list!) confirming that salicylates induce hypoglycaemia by stimulating insulin release.

When I was worst affected, at a time in my life when I was eating additives and salicylates, and before I had started low-carbing, my symptoms could be equally as bad as those listed above. I could not skip meals without very unpleasant consequences. I was regularly shaky, snappy, and even violent, and several times came close to fainting when food was not available.

In my case I managed to control my hypoglycaemic symptoms with a very strict carbohydrate-controlled diet. Friends and family could be intolerant and dismissive of my need for this (comments ranged from “yeah, yeah”, to “I think if you try to do any diet when you go out you are going to fail,” to “can’t you just try to fit in for tonight?” to all kinds of mocking and dismissive comments about what a “dangerous” diet Atkins is). Unfortunately I did not allow myself to become hypoglycaemic often enough to prove the reaction to them.

It is such a relief to know that salicylates are the cause of the hypoglycaemia I was experiencing. I had been afraid that I was damaged in some way, perhaps for the rest of my life. Ironically, though Atkins relieved my symptoms, the huge emphasis on eating “wonderful, healthy” vegetables on the Atkins diet also kept me sick.

FYI, I still keep my carbs between 40-70 grams per day, because I’ve no desire to get fat in a hurry. It’s just that I eat more milk, biscuits and bread these days.

…At this point several people will write to me to tell me “you are damaged if you can’t eat fruit and vegetables” – and I will be forced to look up the quote from the study where 60% of ordinary children experienced behavioural improvements after beginning a partial elimination diet.