About a month ago, a new study warning about the dangers of “super-sticky cholesterol” made a bit of a splash in the media. I ignored it at the time, but thought about it today when I received an email from a Fat Head viewer who’s raising a diabetic child. We’ll come back to that in a minute.
The study, in case you missed it, produced headlines like this:
Super-Sticky ‘Ultra-Bad’ Cholesterol Revealed in People at High Risk of Heart Disease
When I was in journalism school, we were taught that many people don’t read much more than the headline and the first few paragraphs of a news story. That’s why student journalists are taught to write in reverse-pyramid style: get the important ideas in those first few paragraphs, then expand on the details. Here are the first few paragraphs of a Science Daily article about the study:
Scientists from the University of Warwick have discovered why a newly found form of cholesterol seems to be ‘ultra-bad’, leading to increased risk of heart disease. The discovery could lead to new treatments to prevent heart disease particularly in people with type 2 diabetes and the elderly.
The research, funded by the British Heart Foundation (BHF), found that ‘ultra-bad’ cholesterol, called MGmin-low-density lipoprotein (LDL), which is more common in people with type 2 diabetes and the elderly, appears to be ‘stickier’ than normal LDL. This makes it more likely to attach to the walls of arteries. When LDL attaches to artery walls it helps form the dangerous ‘fatty’ plaques’ that cause coronary heart disease (CHD).
CHD is the condition behind heart attacks, claiming 88,000 lives in the UK every year (1).
If you stop there, the takeaway message is that evil ol’ cholesterol also comes in an especially evil form that’s even more likely to cause heart disease. Yikes! Better go on a low-fat diet and get your cholesterol down, maybe even take a statin just to be safe. You have to read further to spot the true villain:
The researchers made the discovery by creating human MGmin-LDL in the laboratory, then studying its characteristics and interactions with other important molecules in the body.
They found that MGmin-LDL is created by the addition of sugar groups to ‘normal’ LDL — a process called glycation — making LDL smaller and denser. By changing its shape, the sugar groups expose new regions on the surface of the LDL. These exposed regions are more likely to stick to artery walls, helping to build fatty plaques. As fatty plaques grow they narrow arteries — reducing blood flow — and they can eventually rupture, triggering a blood clot that causes a heart attack or stroke.
What turns cholesterol into “sticky” cholesterol? Sugar.
In 1976 a prominent researcher named Peter Cleave told the McGovern committee that if anything in our diets causes heart disease, it’s probably sugar. McGovern sided with the researchers who blamed dietary fat, perhaps because he couldn’t imagine how sugar could produce fatty streaks in our arteries. This study describes a plausible (and likely, in my opinion) mechanism: high blood sugar produces small, dense LDL through glycation.
Glycation is what happens when sugars bind to proteins. I’ve heard various descriptions, but the one that stuck with me (pun intended) is that glycation “caramelizes” your tissues. The Wikipedia entry on glycation gives a good description of why you want to avoid being caramelized:
Endogenous (inside the body) glycations occur mainly in the bloodstream to a small proportion of the absorbed simple sugars: glucose, fructose, and galactose. It appears that fructose and galactose have approximately ten times the glycation activity of glucose, the primary body fuel. Glycation is the first step in the evolution of these molecules through a complex series of very slow reactions in the body … all lead to advanced glycation endproducts (AGEs).
Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as: cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer’s disease (amyloid proteins are side-products of the reactions progressing to AGEs), cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination).
Quite a horror show, eh? As the article in Science Daily notes, pharmaceutical companies may use this information to develop drugs that help prevent heart disease by reducing glucose levels.
Yes, yes, I know … you’re probably sitting there, dangerously close to banging your head on your desk, wondering why doctors don’t just tell people to stop jacking up their blood sugar with too many carbohydrates. Well, heck, they can’t do that because everybody just knows we need those carbohydrates –- which brings me back to the email I received today:
Our son was diagnosed with type 1 diabetes a year ago this August. Doctors told us that we should feed him whatever he wanted, even after I pushed to speak with their staff nutritionist and nailed her about their suggested carb intake. Their response to our concerns was, “He needs to grow healthier and stronger and the only way to do this is to feed him more carbs and give him more insulin injections.”
This would be to any Fat Head unsatisfactory as best. Three months after beginning our son’s insulin regimen, we noticed he began to show signs of symptoms he had never had before. The doctors again explained that he was fine in their opinion and his symptoms (while major and included loss of sight, balance, headaches, ear aches, and loss of cognitive function) were nothing more then simple effects of his disease and we would have to manage by continuing with their recommended treatment plan: injections and carb counting.
We did some research — as good Fat Head parents tend to — and found that the insulin prescribed for our two year old son was only approved by the FDA for children age six and over. We stopped use and contacted his doctor’s office. After two days all our son’s symptoms vanished and he began to function normally again. When we confronted the doctor about this issue they claimed that this drug is being used world-wide among the same age group as our son and it wasn’t uncommon or irregular.
Then about two weeks ago we found Fat Head. I have been doing research to that (fat) end for months, but I was missing the key component that Fat Head was able to deliver: Fat. In all the information I’ve pored over, it is always the same story. Stay away from sugar, carbs, processed foods, etc. But no one said anything about adding animal fat.
Just as a kind of experimental joke my husband and I took the information in Fat Head literally and began to cut out two-thirds of the carbs from our family diet. In only two days our son’s sugar levels went from spiking randomly at 480-600 and fell to 140-160. Our daughter also began to show signs of improved health — which for us meant more trips to the time-out chair. Having more energy evidently means more Fat Head mischief. You might want to make that a disclaimer for unsuspecting parents *wink* … just a thought.
Most doctors still believe high-fat diets cause heart disease, and diabetics are three times more likely to eventually develop heart disease. Put those together, and you get the standard advice for diabetics: go on a low-fat diet with plenty of complex carbohydrates, then take insulin to control your blood sugar. Following that advice, this poor kid was getting glucose spikes of 600. That’s major glycation territory.
Ignoring the standard advice, the same kid dropped his glucose to almost-normal levels. Given more time on a low-carb / high-fat diet, he may even reach normal levels. I certainly hope so.
Cholesterol isn’t the villain; “super-sticky cholesterol” resulting from too many carbohydrates is. And by recommending low-fat / high-carbohydrate diets, doctors are putting diabetics and other people prone to heart disease in a sticky situation indeed.