A high-fat low-carbohydrate (HFLC) ketogenic diet is effective for weight loss, is not onerous to adhere to (luxurious even), and has benefits for the body and the brain that go well beyond weight-management. With HFLC, about 70-80% of energy needs should be supplied by fat (animal fat and cold-pressed oils). Most people believe that dietary fat, particularly saturated fat, is bad for our health. So, how can a HFLC diet be good for us?
The widely-disseminated opinion that dietary saturated fat increases the risk of cardiovascular disease (CVD) is not supported by large-scale randomised clinical trials. This is at odds with the US Department of Agriculture (USDA)’s highly influential Dietary Guidelines for Americans that recommend minimising dietary fat (especially saturated fat) to reduce the risk of CVD.
The USDA is sticking to its guns despite now-definitive scientific evidence refuting their hypothesis. It is time to put the USDA’s fat-fallacy to rest, and move on.
What happens to blood fats on a HFLC diet?
HFLC reduces circulating saturated fatty acids and blood triglycerides (TG). With HFLC eating, fats become the primary fuel source and the most readily-available fats are those in the circulation. So they get consumed for energy, and levels of circulating fats (including saturated fatty acids) are reduced.
What about cholesterol?
Cholesterol (which is not water-soluble) is carried around the blood by lipoproteins, as are TGs (fats) and some proteins. There are a number of lipoprotein types, however (rather simplistically) only 3 usually arise in dietary discussions: high-density lipoprotein (HDL), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL). There are sub-classes within each of these, in particular the LDL can range from large and ‘buoyant’ through to small and dense (sdLDL). All of these lipoproteins carry different quantities of cholesterol/TG/proteins. When cholesterol content is being referred to, the nomenclature HDL-C, LDL-C etc is usually used. For simplicity, I will use HDL, LDL etc to refer to the lipoprotein as well as its cholesterol.
So, what does all this mean for HFLC?
Effect on HDL
HFLC usually increases HDL, commonly known as ‘good’ cholesterol (which might contribute to any total cholesterol increase). The combination of a reduction in TG with an increase in HDL results in a reduction in the ratio of TG to HDL. This ratio is considered to be a marker for CVD risk (a lower value is better, which HFLC achieves).
Effect on LDL
While TG, fatty acids and HDL are nearly always improved for people on a HFLC diet, the effect on LDL (commonly known as the ‘bad’ cholesterol) is more variable. On average, HFLC has a negligible effect on LDL, however, it might go up or down for individuals. Not all LDL is the same though, and most concern surrounds sdLDL. These lipoproteins arise as the large buoyant LDL steadily unload their cholesterol cargo by various mechanisms and become smaller and denser. The sdLDL are small enough to penetrate and embed in the arterial wall. There, they can be oxidised or glycated. Glycation is an equally-damaging process (to oxidation) in which excess glucose randomly attaches itself to the lipoprotein and causes it to dysfunction (a good reason to keep blood glucose low, which is difficult with a USDA diet). The oxidised/glycated sdLDL is inflammatory. It is the inflammation that is thought to lead to atherosclerosis.
A HFLC diet reduces sdLDL, whereas a USDA diet can increase it. The ratio of large-buoyant LDL to sdLDL is another biomarker for CVD risk. A HFLC diet improves this ratio also.
More recently, it has been suggested that sdLDL are not alone, and that total small particle count (of any kind) is a better marker for atherosclerosis. This might explain why sdLDL seems to be implicated but, even so, often disassociated, with atherosclerosis.
How is LDL measured in blood tests?
The equation is known as the Friedewald equation. It starts out as:
TC = HDL + LDL + VLDL
It then assumes that VLDL (which is also not measured in blood tests) can be estimated from TG (the triglycerides), and is constantly about equal to TG/5.
Hence we get, with some re-arrangement:
LDL = TC – (HDL + TG/5)
This equation has its conveniences and its weaknesses. In particular, the assumption that VLDL = TG/5 breaks down when TG is too high or too low. Of particular relevance to HFLC is that the equation over-estimates LDL when TG levels are low (remembering that HFLC can lower TG). This means that an elevated LDL, in the context of a HFLC diet, may be an overestimate of actual LDL.
The small-dense and large-buoyant sub-fractions of LDL cannot be measured in routine blood tests and require specialised laboratories. However, TG/HDL (or even TG alone) can be used as an indicator of sdLDL (because TG is involved in the processes of forming sdLDL). Both TG/HDL and TG improve with HFLC, further indicating a reduction in sdLDL.
Do these measures change over time?
Yes. A rise in cholesterol seems to be more associated with the early phases (few months) of the diet. It is thought that cholesterol may increase because it is mobilised from fat stores during the weight-loss phase. During the course of the weight-maintenance phase, the body metabolises this excess cholesterol and homeostasis returns. So, it matters when cholesterol is measured.
Is there anything good about cholesterol?
Yes, cholesterol is a natural part of our metabolism – the body makes all that it needs (up to 3g) daily. Eating cholesterol just means the body doesn’t have to make so much. Cholesterol is used by the liver to produce bile. It is an essential structural component of cell membranes (strengthening them while enabling cell walls to change shape, in distinction to plant cells). Cholesterol is essential for brain function. It is needed for the production of vitamin D by sunlight. All the steroid hormones (testosterone, oestrogen, progesterone, aldosterone) are made from cholesterol. Cholesterol is anti-inflammatory – it might even be sent to deal with atherosclerotic inflammation and stand accused by association.
HFLC results in a favourable shift in many measures of blood lipids and in their relative ratios. The expected increase in HDL (by ~10-15%) is greater than that achievable by any drug or lifestyle change (including stopping smoking), and the reduction in TG (~50% on average) is striking. A potential rise in total cholesterol or LDL has to be balanced against these and other benefits (e.g. for the brain). HFLC may require a new ‘normal’ for some parameters.
Finally, blood lipids (including cholesterol) are only a small part of a bigger picture. Inflammation is implicated in most diseases of our times, including heart disease. HFLC can dramatically improve biomarkers of inflammation and up-regulate the production of anti-oxidants. Insulin and glucose have central roles in type 2 diabetes, and abnormal glucose metabolism is implicated in many cancers. HFLC reduces both insulin and glucose, and improves insulin sensitivity. The benefits of HFLC for brain function has a separate post.
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