Why your ldl and cholesterol may temporarily go up on LC/HF

CholesterolWhen starting the LC/HF WOE (low carbohydrate/high fat way of eating), there is a possibility that you will experience an increase in LDL. Do not despair if this happens for there are 2 different kinds; LDL and VLDL-A which is large-buoyant and is produced by fat intake, as the name suggests, they are large and float in the bloodstream unable to form plaque on the walls. The other kind of LDL is VLDL-B, small-dense which is caused by carbohydrates, these are the kinds that fall under the blood-cells and form plaque. It is difficult for simple blood-tests to show the difference, so the medical industry lumps them all together (its better for selling you cholesterol meds). If your triglycerides are  low that is a good indicator your LDL is mostly the good kind. High triglycerides are the indicator for the bad kind.

Another factor is weight loss. Weight loss can cause a temporary increase in your serum cholesterol levels during the weight loss process, according to “The American Journal of Clinical Nutrition.” AJCN notes a study in 1991 during which six obese women, their cholesterol levels and body composition are all taken into consideration. The study shows an initial decline in cholesterol levels, followed by a rise during continued weight loss. Levels declined again once study participants entered weight maintenance. AJCN offers an explanation for the temporary increase in serum, blood, cholesterol levels with weight loss. Your body has adipose fat stores. The adipose stores begin mobilizing as you lose weight, moving into the blood. This is a possible cause for a late rise in serum cholesterol levels with major weight loss, explains AJCN. As your weight loss stops, so too does the rise in cholesterol levels.

Here are six things that we need to know about cholesterol:

i)    It is virtually impossible to explain how vital cholesterol is to the human body. If you had no cholesterol in your body you would be dead. No cells, no bone structure, no muscles, no hormones, no sex, no reproductive system, no digestion, no brain function, no memory, no nerve endings, no movement, no human life – nothing without cholesterol. It is utterly vital and we die instantly without it.

ii)    Cholesterol is so vital to the body that our bodies make it. The body cannot risk leaving it to chance that we would get it externally from food or some other external factor – that’s how critical it is.

iii) There is no such thing as good cholesterol and bad cholesterol. Cholesterol is cholesterol. The chemical formula for cholesterol is C27H46O. There is no good version or bad version of this formula.HDL is not even cholesterol, let alone good. LDL is not even cholesterol, let alone bad. HDL stands for High Density Lipoprotein. LDL stands for Low Density Lipoprotein. (There are three other lipoproteins, by the way, chylomicrons, VLDL and IDL).

Fat and cholesterol are not water soluble so they need to be carried around the body in something to do their vital work. The carriers of such substances are called lipoproteins. We can think of lipoproteins as tiny ‘taxi cabs’ travelling round the blood stream acting as transporters. So, lipoproteins are carriers of cholesterol – oh – and triglyceride and phospholipids and protein. All lipoproteins carry all of these substances – just in different proportions. LDL would more accurately be called the carrier of fresh cholesterol and HDL would more accurately be called the carrier of recycled cholesterol.

iv)    The standard blood cholesterol test does not measure LDL  – it estimates it. The fasting blood cholesterol test can only measure total cholesterol and HDL. There are two other unknowns in a four variable equation – LDL and VLDL. The estimation is refined further using the Friedewald equation (named after William Friedewald, who developed it).

Total cholesterol = LDL + HDL + VLDL/5 (Ref 8)

As any mathematician will tell you, one equation, with four variables, only two of which can be measured, is a fat lot of good. We need at least one more equation or known variable, to avoid circular references. This also means that:
–    All other things being equal, LDL will rise if a) total cholesterol rises and/or b) if HDL falls and/or if c) VLDL falls.
–    All other things being equal, LDL will fall if a) total cholesterol falls and/or b) if HDL rises and/or if c) VLDL rises.

No wonder an inverse association is observed between LDL and HDL – it is by definition. More surprising is that a fall in VLDL (triglycerides), which would be welcomed by doctors, would be accompanied by an automatic increase in LDL, all other things being equal, which would not be welcomed by doctors. And you thought that this was scientific.

v)    Statins stop the body from producing the cholesterol that it is designed to produce. They literally stop one of our fundamental body processes from being able to function. The intelligent view on statins is that in the very limited arena where they appear to have some ‘benefit’ (men over 50 who have already had a heart attack), they ‘work’ by having anti-inflammatory properties and that the fact that they lower cholesterol (by stopping the body from being able to produce this vital substance) is a very unfortunate side effect. (Drug companies should work on developing something that has the anti-inflammatory benefit without this huge and damaging side effect – it’s called aspirin).

One in 500 people have familial hypercholesterolemia and may have a problem clearing cholesterol in their body (rather like type 1 diabetics who can’t return their blood glucose levels to normal). For anyone else to be actively trying to lower their vital and life affirming cholesterol levels is deeply troubling.

vi)    “Cholesterol in food has no impact on cholesterol in the blood and we’ve known that all along.” Ancel Keys.

Ancel Keys, the same man who did the brilliant Minnesota starvation experiment, spent the 1950’s trying to show that cholesterol in food was associated with cholesterol in the blood. He concluded unequivocally that there was not even an association, let alone a causation. He never deviated from this view.

Cholesterol is only found in animal foods (it is a vital substance for every living creature). Hence the only foods that Keys could add to human diets, to test the impact of cholesterol, were animal foods. Given that he concluded that eating animal foods had no impact on blood cholesterol levels, it follows that animal foods per se have no impact on blood cholesterol levels.

There is no need, whatsoever, to avoid liver, red meat, other meat, fish, eggs, dairy products etc for any cholesterol that they may contain, or for any other reason.

The body makes cholesterol. It will continue to do so regardless of whether we eat cholesterol laden foods or not.

Ref. Zoe Harcombe’s blog on cholesterol.

So how does this apply to the low carbohydrate way of eating?
Question: How do low-carb diets affect cholesterol and triglycerides?
Answer: In general, low-carb diets tend to improve blood lipids. Specifically:


Triglycerides are the form in which the body stores fat (our body fat is mainly made up of triglycerides.) When we talk about someone’s triglyceride level, however, we usually mean the amount of triglycerides that show up in the blood when it is tested. A high triglyceride level is a risk factor for heart disease and stroke.

Numerous studies find that low-carbohydrate diets cause high triglyceride levels to fall; in fact, the results are quite consistent and dramatic. Many physicians now recommend reducing carbohydrate as the first line of defense against high triglyceride levels, and this is often successful.

High Density Lipoprotein Cholesterol (HDL) — “Good Cholesterol”

HDL cholesterol seems to protect against heart disease; it becomes a risk factor for heart disease if it’s low. Scientists think it carries excess cholesterol back to the liver, where is it broken down. There is also evidence that some aspect of HDL is involved in the initial response after injury or acute illness, and that people with higher levels of HDL have improved recovery.Low-carbohydrate diets tend to raise HDL cholesterol levels, so this is a good thing.

Low Density Lipoprotein Cholesterol (LDL) — “Bad Cholesterol”

Although there is some controversy on this point, LDL cholesterol is considered “bad” in terms of heart disease risk. The relationship between low-carb diets and LDL cholesterol is more complex than with triglycerides and HDL cholesterol. There are some studies in which LDL is reduced on a low-carb diet, some in which it doesn’t change, and some in which it goes up. But there is one thing about LDL changes which is consistent with low-carb diets, and that is that it causes a change in cholesterol particle size.

What has particle size got to do with it? Evidence is accumulating that the size of cholesterol particles has a lot to do with risk for heart disease. Basically, the smaller the particles are, the greater the risk — it is thought that perhaps the small particles lodge in the walls of blood vessels more easily.The good news for those of us following a low-carb way of eating is that studies of diet and cholesterol particle size have consistently shown that low-carb diets produce larger-sized cholesterol particles. However, a larger-sized particle weighs more than a smaller one. When LDL does go up on a low-carb diet, it may be due to the larger particles, since weight is what’s being measured. (A total cholesterol of 200, for example, means 200 mg per deciliter.)

On the other hand, high-carb diets seem to produce a greater percentage of smaller cholesterol particles in some people. So the total LDL goes down (particles are smaller, so the total is lighter.) While the reading may be low, it can be deceiving as risk goes up in those cases.

A good way to sort out risk? LDL particle size seems to be strongly correlated with triglyceride level (high triglycerides go with small particle size and vice versa). So if your triglycerides are low, your LDL particles are probably larger.

Another article about a Swedish study on the low carb high fat way of eating:

A recent study confirms the results of prior U.S. studies 

showing that lower carb and higher fat diets improve blood 

sugar status, as well as weight and other markers.

Diabetes is a deadly epidemic, afflicting 11% of adults as well as one in every 400 children in the U.S. Conventional diabetic diets (high in carbohydrates and low in fat) are notoriously unsuccessful. In this Swedish study, insulin levels were reduced by 30% and “good” cholesterol levels improved in the diabetics on the higher fat, lower carb diet compared to those on a conventional low calorie, higher carb diet.

Earlier studies of low-carb, higher-fat (including unlimited saturated fat Atkins-type diets) came to similar conclusions. Quoting from chapter 10 in the Diet Cure: “Other studies have confirmed the superiority of Atkins-type diets’ positive impact on blood pressure and on the lowering of weight, cholesterol, tryglycerides, glucose, insulin, and A1C levels. These last three are diabetes markers. Several studies on diabetes document the benefits of lowering carbs and including fat in the diet. To quote one such study’s author, ‘When we took away the carbohydrates, the patients spontaneously reduced their daily energy consumption by 1,000 calories a day. Although they could have, they did not compensate by eating more protein and fats and they weren’t bored with the food choices. In fact, they loved the diet.The carbohydrates were clearly stimulating their excessive appetites.’”

“Four studies, three on type 2 diabetics and one on mildly obese men and women, used a high-fat and protein, low-carb diet. Their results: all subjects showed improvement in weight, as well as insulin and cholesterol levels. A fifth, Harvard School of Public Health, study ‘found no association between low-carbohydrate diets and increased cardiovascular risk, even when these diets were high in saturated animal fats.’ “

In summary, the low carb/high fat way of eating is good for all aspects of a person’s health.


1 Comment (+add yours?)

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    Apr 26, 2015 @ 21:17:51

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