Archive for August 2006
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.
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.
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.  ‘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.
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.
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.
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?