Do dietary lectins cause disease?

I’m lifting this wholesale from the NCBI site because it’s one of the more reliable articles on lectins and as it dates back to 1999, it seems to be mostly off the radar. My emphasis added.

In 1988 a hospital launched a “healthy eating day” in its staff canteen at lunchtime. One dish contained red kidney beans, and 31 portions were served. At 3 pm one of the customers, a surgical registrar, vomited in theatre. Over the next four hours 10 more customers suffered profuse vomiting, some with diarrhoea. All had recovered by next day. No pathogens were isolated from the food, but the beans contained an abnormally high concentration of the lectin phytohaemagglutinin. Lectins are carbohydrate binding proteins present in most plants, especially seeds and tubers like cereals, potatoes, and beans. Until recently their main use was as histology and blood transfusion reagents, but in the past two decades we have realised that many lectins are (a) toxic, inflammatory, or both; (b) resistant to cooking and digestive enzymes; and (c) present in much of our food. It is thus no surprise that they sometimes cause “food poisoning.” But the really disturbing finding came with the discovery in 1989 that some food lectins get past the gut wall and deposit themselves in distant organs. So do they cause real life diseases?This is no academic question because diet is one part of the environment that is manipulable and because lectins have excellent antidotes, at least in vitro. Because of their precise carbohydrate specificities, lectins can be blocked by simple sugars and oligosaccharides. Wheat lectin, for example, is blocked by the sugar N-acetyl glucosamine and its polymers. These natural compounds are potentially exploitable as drugs should lectin induced diseases be identified.

Wheat gliadin, which causes coeliac disease, contains a lectin like substance that binds to human intestinal mucosa, and this has been debated as the “coeliac disease toxin” for over 20 years. But coeliac disease is already managed by gluten avoidance, so nothing would change were the lectin hypothesis proved. On the other hand, wheat lectin also binds to glomerular capillary walls, mesangial cells, and tubules of human kidney and (in rodents) binds IgA and induces IgA mesangial deposits. This suggests that in humans IgA nephropathy might be caused or aggravated by wheat lectin; indeed a trial of gluten avoidance in children with this disease reported reduced proteinuria and immune complex levels.

Of particular interest is the implication for autoimmune diseases. Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells. The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetyl lactosamine, which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together—a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice. Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.

Another suspect lectin disease is rheumatoid arthritis. The normal human IgG molecule possesses carbohydrate side chains, which terminate with galactose. In rheumatoid arthritis much of the galactose is missing, so that the subterminal sugar—N-acetyl glucosamine—is exposed instead. These deficient IgG molecules feature strongly in the circulating immune complexes that cause fever and symptoms. In diet responsive rheumatoid arthritis one of the commonest trigger foods is wheat, and wheat lectin is specific for N-acetyl glucosamine—the sugar that is normally hidden but exposed in rheumatoid arthritis. This suggests that N-acetyl glucosamine oligomers such as chitotetraose (derived from the chitin that forms crustacean shells) might be an effective treatment for diet associated rheumatoid arthritis. Interestingly, the health food trade has already siezed on N-acetyl glucosamine as an antiarthritic supplement.

Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa. Lectins also cause discharge of histamine from gastric mast cells, which stimulates acid secretion. So the three main pathogenic factors for peptic ulcer—acid stimulation, failure of the mucous defence layer, and abnormal bacterial proliferation (Helicobacter pylori) are all theoretically linked to lectins. If true, blocking these effects by oligosaccharides would represent an attractive and more physiological treatment for peptic ulcer than suppressing stomach acid. The mucus stripping effect of lectins also offers an explanation for the anecdotal finding of many allergists that a “stone age diet,” which eliminates most starchy foods and therefore most lectins, protects against common upper respiratory viral infections: without lectins in the throat the nasopharyngeal mucus lining would be more effective as a barrier to viruses.

But if we all eat lectins, why don’t we all get insulin dependent diabetes, rheumatoid arthritis, IgA nephropathy, and peptic ulcers? Partly because of biological variation in the glycoconjugates that coat our cells and partly because these are protected behind a fine screen of sialic acid molecules, attached to the glycoprotein tips. We should be safe. But the sialic acid molecules can be stripped off by the enzyme neuraminidase, present in several micro-organisms such as influenzaviruses and streptococci. This may explain why diabetes and rheumatoid arthritis tend to occur as sequelae of infections. This facilitation of lectins by micro-organisms throws a new light on post-infectious diseases and makes the folklore cure of fasting during a fever seem sensible.

Alternative medicine popularisers are already publishing articles about dietary lectins, often with more enthusiasm than caution, so patients are starting to ask about them and doctors need to be armed with facts. The same comment applies to entrepreneurs at the opposite end of the commercial spectrum. Many lectins are powerful allergens, and prohevein, the principal allergen of rubber latex, is one. It has been engineered into transgenic tomatoes for its fungistatic properties, so we can expect an outbreak of tomato allergy in the near future among latex sensitive individuals. Dr Arpad Pusztai lost his job for publicising concerns of this type (20 February, p 483).


Alzheimer’s and Living Low Carb

The Washington Post reports on the correlation between “pre-diabetes” (high blood sugar levels not yet in the diabetic range) and alzheimer’s:

People with elevated blood sugar levels may have an increased risk of developing Alzheimer’s disease, researchers reported yesterday at an international conference. Scientists already have linked Type 2 diabetes with Alzheimer’s, which afflicts 4.5 million Americans.

Full Article

So what can you do to protect yourself? Go low carb of course… well at least according to Dr. Larry McCleary, the author of  The Brain Trust who describes ketones as “the brain’s preferred fuel.”
Via Living La Vida Low Carb 

Glowing Mice Light the Way

Mice are helping scientists to understand insulin resistance, a precursor to type 2 diabetes. To recap, insulin resistance is a failure of the body to deal with blood glucose normally:

The problem starts during gluconeogenesis–a process by which blood sugar is produced in the liver, explains Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology, who led the study. During fasting, gluconeogenesis maintains blood sugar levels by increasing glucose production. After a meal, the hormone insulin normally turns down gluconeogenesis ensuring that blood sugar levels don’t rise too high. “But in people with insulin resistance, blood sugar levels are elevated because gluconeogenesis continues when it shouldn’t, increasing the risk of developing type II diabetes,” Montminy says.

In order the understand the inner workings of the liver in the process. Scientists spliced the glowing fire-fly genes into mice in such a way that it could only be turned on in the liver by the [gluconeogenesis] switch. Well that’s cool.

Besides just being incredibly awesome, these glowing mice will be useful in research on the effectiveness of future diabetes drugs. The goal being to find a drug that can turn off the light. More.

Indians have Fatter Fat

Indian Killer Belly is a strange and scary phenomenon. Asian Indians have a much higher incidence of diabetes and heart disease that other races even when other risk factors have been factored in.

Indian men, no matter where they live, have one of the highest rates of heart disease in the world, even if they have low levels of traditional risk factors such as cholesterol. In fact, even non-smoking vegetarians under 40 who exercise regularly may be at high risk.

While 60 percent of heart attacks amongst Americans occur after age 55, nearly half of all heart attacks among Indian men strike under the age of 55 and 25 percent under the age of 40. Indian women share these high rates of heart disease. Thousands of Indian American men in their 40s and 50s succumb to a first, fatal heart attack every year.

More. Via.

A new study may shed some light on this problem. It seems that Indians’ fat is fatter. Or more precisely, their fat cells are considerably larger than those of caucasians and this is inversely correlated with ability to cope with blood glucose (ie insulin resistance):

Compared to Caucasians, in spite of similar BMI, South Asians had higher total body fat (22±6 and 15±4% of body weight; p-value<0.0001), higher subcutaneous abdominal (SA) fat (3.5±1.9 and 2.2±1.3 kg, respectively; p-value = 0.004), but no differences in intraperitoneal (IP) fat (1.0±0.5 and 1.0±0.7 kg, respectively; p-value = 0.4). SA adipocyte cell size was significantly higher in South Asians (3491±1393 and 1648±864 µm2; p-value = 0.0001) and was inversely correlated with both glucose disposal rate (r-value = −0.57; p-value = 0.0008) and plasma adiponectin concentrations (r-value = −0.71; p-value<0.0001). Adipocyte size differences persisted even when SA was matched between South Asians and Caucasians.

The bottom line is that big fat cells and high levels of subcutaneous fat (but not visceral fat) were found to be risk factors for insulin resistance and heart disease. More.

Health warning: the innocence of visceral fat is not supported by other studies. Also, this study only included a total of 29 south Asians and 19 Caucasians. More research is needed.

Paracetamol may impair Bone Growth

 A much abused substance may have a negative impact on bone growth:

In Medicine, paracetamol is used to soothe every kind of pain, from simple molar pain to pain produced by bone fractures. This medicine is one of the most used nowadays. However, [researchers] showed that taking paracetamol slows down bone growth, as has been proved by ‘in vitro’ studies.

This research is very theoretic ie it has been carried out in a petri dish and the assumption is that the same process takes place in the body. It may be a stretch. However given the role of bones in the regulation of insulin, this may be a factor to consider for those trying to improve their insulin sensitivity.

What is Metabolic Syndrome?

More from the European Society of Cardiology

The metabolic syndrome (MS) is a cluster of metabolic abnormalities with abdominal obesity (increased waist circumference) at its centre. Although all forms of obesity have a negative impact on human health, metabolic syndrome describes a set of particularly adverse biochemical changes accompanying (abdominal) obesity.

MS is most often identified by having three or more out of five possible abnormalities (components) which form the metabolic syndrome cluster. These five abnormalities in the cluster are:

  1. increased waist circumference (abdominal obesity),
  2. elevated triglycerides (a fat component in the blood),
  3. low HDL-cholesterol (“good” cholesterol),
  4. a slightly increased blood glucose level (impaired fasting glycemia: the blood sugar level is not as high as in diabetes but is elevated above normal), and
  5. high blood pressure.

Our research (…) indicates that in (young) middle-aged subjects (35-55 year old) MS is frequently present (9-16% of subjects depending on the definition used) and that its presence coincides with a wide range of adverse cardiovascular changes.

More specifically we found a strong association between presence of MS and inflammation (a well documented marker of risk for future heart attacks and stroke), thickening and stiffening of the heart (potentially predisposing to heart failure) and more pronounced atherosclerosis (calcification and narrowing of the arteries). Importantly these effects were graded, every additional MS component present translated into a gradually higher likelihood of finding cardiovascular damage.

Efforts should be focused on awareness of abdominal obesity as a risk factor for developing heart disease, and on wide ranging preventive strategies to avert its (potentially epidemic) consequences.

The condition is known by a number of different names including syndrome X and insulin resistance amongst others.

People with the metabolic syndrome are at increased risk of coronary heart disease and other diseases related to plaque buildups in artery walls (e.g., stroke and peripheral vascular disease) and type 2 diabetes. – American Heart Association

While most factors leading to metabolic syndrome are under your control (diet, excercise, smoking, etc.) there appears to be at least one that isn’t: your place in the pecking order:

It is well documented that individuals with higher social status have lower risk of coronary heart disease (CHD). This is generally not explained by differences in lifestyle factors such as smoking and lack of exercise.

and your level of education:

When combining the factors in the metabolic syndrome, individuals with the highest level of education had 68% lower risk of having the metabolic syndrome than individuals with the lowest educational level. Surprisingly, this difference was not explained by differences in lifestyle or psychosocial factors: when taking these factors into account individuals with highest level of education still had 60% lower risk of having the metabolic syndrome. This is equal to a 2.5 higher risk of metabolic syndrome in the lowest socio-economic position compared to the highest.

Your Fat Cells May Be Sick

The Journal of Lipid Research, reports on research which indicates that in obese individuals, fat cells are bloated and inflamed because they receive too many nutrients, including lipids. In these cells, various components cannot work properly anymore and, instead, they activate new proteins to cope with the situation.

Researchers show that when a fat cell receives too many nutrients, the ER is overwhelmed and triggers a process called the unfolded protein response (UPR). This process is one of many cellular responses that activate proteins that increase inflammation and can even result in the death of the cell. UPR also causes insulin resistance, a condition in which the production and function of insulin – a hormone produced by the pancreas – is impaired and blood sugar is too high.

In English: too many calories heading to your fat cells leads to inflammation and insulin resistance.