HDL means "High-Density Lipoprotein", meaning "high density lipoprotein".
Technically, HDLs do not consist of "pure cholesterol" and also contain specific proteins that serve to transport fats in the blood.
There are various types of lipoproteins. HDLs are beneficial and are therefore called " good cholesterol "; others are considered potentially harmful and are therefore called "bad cholesterol".
HDLs are measured by analyzing the relative concentration in blood serum.
There are different types of HDL, which vary in shape, size and chemical composition. The most effective in "cleaning" the arteries are those most active in the exchange of lipids with cells and other lipoproteins.
HDL and LDL lipoproteins are indicators of cardiovascular risk; in fact, the reduction of HDL and the increase in LDL always have a negative effect.
It is possible to increase HDL by correcting the diet and increasing the level of exercise. Nutrition, as well as physical activity and certain supplements, make it possible to significantly modify the lipid profile and the consequent cardiovascular risk.
What is HDL cholesterol?
In common parlance, HDLs are called "good cholesterol" because they exert a protective effect on atherosclerotic diseases . From a clinical point of view, HDL (High-Density Lipoprotein) is classified as high-density lipoprotein.
Lipoproteins are particles containing specific apolipoproteic units, necessary for the exchange and transport of fats (cholesterol, phospholipids, triglycerides, etc.).
There are various types of apolipoproteins; both the number and the type of apolipoprotein characterize the various lipoproteins. The apolipoprotein typical of HDL is Apo A1 .
Lipoproteins have a hydrophilic surface (akin to water) and are used to convey lipids into the blood plasma (aqueous matrix). This function is very important, since the fats do not normally dissolve in water and tend to aggregate forming "oily bubbles" (as is done by putting oil in water or in broth).
There are 5 different types of lipoproteins, all with different functions and characteristics:
- Chylomicrons: transport fats from the intestine (which absorbs them with digestion) to muscle cells and adipose tissue
- VLDL: they mainly carry triglycerides from the liver to adipose tissue
- IDL: they are intermediate between VLDL and LDL (not detectable in the healthy subject)
- LDL: transport cholesterol from the liver to peripheral cells
- HDL: they transport cholesterol from peripheral cells to the liver to steroidogenic organs (deputies to the synthesis of steroid hormones, such as cortisol and sex hormones).
HDL metabolism is closely correlated with that of LDL, also in the VLDL form.
Each HDL is made up of 80-100 specific proteins, which make it capable of conveying even several hundred fatty molecules at a time.
The "replenishment" and the "unloading at destination" of fats take place by interaction of HDL with cells and other lipoproteins.
We have specified that HDL are not pure cholesterol, but rather "means of transport" of plasma lipids. However, we have not yet clarified what cholesterol is.
It is a steroid lipid that the body is able to produce independently and take through food.
Its function in the organism is multiple:
- Structural and vehicle in cell membranes
- Precursor of steroid hormones
- Precursor of vitamin D
- Ingredient of bile juices, important for digestion.
Cholesterol circulates inside the blood stream in a form linked to lipoproteins; if it were free, it would aggregate forming potentially harmful or lethal thrombi.
Excess cholesterol in the blood (due to genetic or environmental causes) can be harmful, due to the tendency to deposit in the arteries; this is the first step towards the formation of an atherosclerotic plaque.
It should be remembered, however, that the tendency to settle varies according to the lipoprotein that carries it: LDLs are harmful ones (they bring cholesterol to the peripheries), while HDL are beneficial ones (they bring cholesterol to the organs that metabolize it).
Features and Differences
In healthy individuals, about 30% of blood cholesterol is transported by HDL; the rest is part of VLDL and LDL.
LDL and VLDL (Low- and Very Low-Density Lipoprotein) are larger and have a lower density than HDL; they move lipids (triglycerides and cholesterol) from the liver to the tissues.
HDLs are initially very small and carry fats from the peripheries to the organs. They increase in size and decrease in density with the incorporation of fats.
Each lipoprotein contains:
- A completely different number and type of Apo Protein
- An equally different quantity and variety of lipids.
HDLs mainly contain ApoA1. Compared to LDL and VLDL, they are distinguished by:
- Highest percentage of protein
- Lower percentage of cholesterol
- Lower percentage of triglycerides
- Higher percentage of phospholipids.
All these features help determine the higher density of HDLs.
Why do they do well?
The increase in HDL is associated with a reduction in atherosclerotic accumulation in vascular walls.
Atherosclerosis is a disease that induces potentially lethal complications such as, for example, myocardial infarction and stroke.
It should however be specified that the correlation between HDL and cardiovascular risk is not linear; in practice, it is not possible to proportionally reduce the risk of illness by increasing them above the normal threshold.
HDLs are called "good cholesterol" because they are able to:
- Remove cholesterol from artery walls
- Reducing the accumulation of macrophages in the intimate part of the arteries, whose presence is an integral part of the atherosclerotic process
- Prevent (sometimes regress) atherosclerosis already started.
It is not to be excluded that there are also ways of disposing of HDL-independent cholesterol. In fact, recent studies * have shown that mice lacking HDL lipoproteins are however able to transport cholesterol to the liver to use it in bile (elimination pathway).
HDLs are the smallest and most dense lipoproteins; they contain more protein and less fat than others. The composition of HDL is characterized by the presence of: Apo A 1, Apo A 2 and phospholipids.
Let's briefly summarize the HDL working mechanism:
- HDL is synthesized in the liver and intestines, to be poured into the circulatory stream. Initially they are disc-shaped (since lipid discharges).
- Once in the suburbs, HDLs take free (non-esterified) cholesterol thanks to a specific cell transporter
- Once taken, the free cholesterol is esterified by an enzyme and moved to the nucleus of the molecule. Filling up, HDLs take on an increasingly "round" appearance
- During the circulation, the HDL particles incorporate even more lipids from the cells and other lipoproteins, progressively increasing in size.
Direct and Indirect transportation
HDLs carry cholesterol to the liver and to steroidogenic organs, such as adrenal glands, ovaries and testes. This takes place directly (catchment) and indirectly (exchange).
- Direct way: the HDLs are picked up by the circle thanks to some receptors placed on the cells of the organs, which manage the selective absorption
- Indirect way: probably the most relevant system. It is mediated by the cholesterol ester transfer protein. This protein exchanges VLDL triglycerides with HDL cholesterol esters. Ultimately, the VLDL becomes LDL (then removed from the specific receptor) and the swollen HDLs are degraded by the lipases of the liver to return immediately into circulation.
Cholesterol deposited in the liver is excreted with the bile in the intestine.
In the adrenal glands, in the ovaries and in the testicles, cholesterol is used for the synthesis of steroid hormones.
HDL AND ATEROSCLEROSIS
The HDL metabolism also participates in the removal of cholesterol absorbed by macrophages in atherosclerotic plaques. This pathway (from arteries to the liver) has been called "reverse cholesterol transport" and is considered protective against atherosclerosis.
NB . Once the plaque becomes fibrous or calcified, the HDLs are no longer able to intervene positively in its dissolution.
On the other hand, in addition to cholesterol, HDLs carry various types of lipids and biologically active proteins. Some of these molecules help inhibit oxidation, inflammation, endothelial activation, coagulation and platelet aggregation.
All of these properties can contribute to the anti-atherogenic capacity of HDL, but it is still not clear what the most important factors are.
HDL AND PARASITES
A small sub-fraction of HDL protects the organism from the protozoan parasite Trypanosoma brucei brucei . This specific group is endowed with the so-called lithic factor trypanosoma (TLF) which contains specialized proteins for the fight against protozoa.
HDL AND AMILOID A
HDLs are also responsible for the transport of serum A amyloid to damaged tissues (in response to inflammatory cytokines). This phenomenon, which occurs in acute phase inflammatory reactions, serves to attract and activate leukocytes. In chronic phases, on the other hand, its deposition in tissues is pathological and is called amyloidosis .
DIMENSION OF HDL AND HEALTH
It is shown that, compared to the total quantity, the percentage of large and spherical HDL is a very protective element. The ratio of large and total HDL varies considerably and can only be measured by electrophoresis or innovative spectroscopy methods.
Five sub-fractions of HDL were identified; from the largest to the smallest they are: 2a, 2b, 3a, 3b and 3c.
HDL AND HYPERCOAGULABILITY
Recent studies confirm that, in type 2 diabetic patients, HDL:
- They play a buffer role towards the effects of hypercoagulability
- The risk of complications decreases.
There is a negative correlation between HDL and " thromboplastin partial activation time ", which is a parameter for evaluating hypercoagulability.
HDL AND MEMORY
The level of fasting lipaemia is associated with short-term verbal memory capacity. In middle-aged subjects, low HDL cholesterol levels are accompanied by poor memory and a tendency to worsen.
It is possible that this is an indirect correlation, linked to diet, sedentariness and the absence of motor activity.
Values and Cardiovascular Risk
HDL measurement is performed with blood tests.
For the high cost of direct detection of HDL and LDL cholesterol, the analysis is usually performed by looking for the indirect value of HDL-C (cholesterol associated with ApoA-1 / HDL).
In the blood serum, after subtracting the HDL-C, the remaining cholesterol is LDL and VLDL. The relative concentration, known as non-HDL-C (potentially atherogenic), appears to be a better (and more easily calculated) indicator of cardiovascular risk.
The atherosclerotic risk increases if:
- HDLs are lower than normal
- The non-HDL-C is above the norm.
People with higher HDL levels tend to have less chance of getting atherosclerosis.
Those showing HDL levels below 40mg / dl have a higher incidence of heart disease.
In contrast, those with higher levels of HDL "native" (see last chapter) show a higher cardiovascular health.
In the table below you can find the values recommended by the guidelines.
|Level mg / dl||Level mmol / l||Interpretation|
|<40 for men and <50 for women||<1.03||Low HDL cholesterol, high risk of heart disease|
|40-59||1.03 - 1.55||Average HDL level|
|> 60||> 1.55||High level of HDL, optimal condition considered protective against heart disease|
Compared to fertile women, men tend to have significantly lower HDL levels, with smaller molecules containing less cholesterol.
Men also have a higher incidence of atherosclerotic heart disease.
Conversely, after menopause, women tend to lose this metabolic trait.
Epidemiological studies have shown that high HDL concentrations (> 60 mg / dl) have a protective value against cardiovascular diseases such as ischemic stroke and myocardial infarction.
Logically, low concentrations of HDL (<40 mg / dl for men and <50 mg / dl for women) increase the risk of atherosclerotic diseases.
The " Framingham Heart Study " shows that, for a given level of LDL and with variable HDL, the risk of heart disease increases up to 10 times. On the contrary, for a fixed variable HDL and LDL level, the risk increases only 3 times.
NB . Even subjects with very low LDL, if they show an insufficient amount of HDL, are predisposed to cardiovascular diseases.
Diet is one of the most important factors in improving the blood lipid profile.
There are protective nutrients and harmful molecules.
The distinction between which are able to increase HDL, reduce LDL and decrease total cholesterol is not always clear. Some studies tend to contradict each other.
Nutrients and Foods
However, it is possible to affirm that the following foods / nutrients are able to improve the cholesterolemic profile:
- Essential polyunsaturated fatty acids: they are from the omega 3 group (EPA *, DHA * and ALA *) and omega 6 (LA). They always have a positive effect on cholesterolemia and triglyceridemia.
Omega 3 is found in the form of EPA and DHA in oily fish (anchovies, sardines, mackerel, bonito, tuna, etc.), in cold-sea fish, algae and krill. ALA, on the other hand, is found in some oily seeds (eg linseed, kiwi, etc.) and in the related extraction oils.
The omega 6 (especially LA *) are typical of oilseeds (walnuts, pecans, macadamia, etc.) and their relative extraction oils. Many foods contain both omega 3 and omega 6 (generally more abundant).
- Monounsaturated fatty acids: of which the major exponent is omega 9 (OA *), they play a role similar to that of essential polyunsaturated fats. They are abundant in olives, in oil seeds (eg hazelnuts, argan, etc.) and in the related extraction oils.
* EPA = eicosapentaenoic acid, DHA = docosahexaenoic acid, ALA = alpha linolenic acid, LA = linoleic acid, OA = oleic acid.
- Lecithins: these are large hydrophilic and lipophilic molecules (amphipathic), contained both in foods of vegetable origin (eg in soya and other legumes), and in those of animal origin (egg yolk). These exert a direct cholesterol-lowering action (moderating intestinal absorption) and metabolic action.
- Phytoestrogens: they are steroid molecules contained only in plants. Isoflavones, cumestans and lignans are part of this category. In addition to improving cholesterol, they are also antioxidants. They are found in soy and other legumes, in red clover, in various oil seeds (for example sunflower), in sprouts etc.
- Other phenolic antioxidants: they are contained in all vegetables and fruits. It is impossible to summarize even just the main categories in a few lines. A rather well-known example is that of resveratrol, a typical antioxidant of black grapes and the wine made from them.
- Soluble food fibers: they are contained in foods of vegetable origin (vegetables, fruits, algae, oilseeds, legumes and cereals). In contact with the water they dilute and gel, reducing the absorption of dietary fat and digestive bile salts.
- Exogenous cholesterol: it is typical of foods of animal origin; it is very abundant in egg yolk, in offal (eg liver and brain) and in fat cheeses (pecorino, mascarpone, etc.).
- Saturated fatty acids: typically animals, they are abundant especially in cheeses and in certain cuts of meat (land animals). There is also no lack of frying oils of poor quality, such as, for example, palm kernel oil or all bifractionated ones.
- Hydrogenated fatty acids: these are vegetable fats modified by the food industry. They have the same physical properties and the same metabolic impact as saturated but, in some cases, they are even worse. In fact, during their production, a part of the fatty acids turns into conformation -trans (much more harmful).
Foods that contain hydrogenated fats are margarines and packaged foods: sweets, snacks, etc.
- Excess carbohydrates, especially from refined foods: in association with obesity, they tend to cause hyperglycemia and type 2 diabetes mellitus. Hyperglycemia compromises the molecular structure of lipoproteins reducing their metabolic effect. It is therefore necessary to reduce the load of high glycemic index foods such as: discretionary sugar, sweets, sweet drinks, white bread, large portions of pasta and pizza, snacks, etc.
- Poor foods of all the preventive molecules we have listed above and rich in harmful molecules; especially junk food.
Alcohol consumption tends to increase HDL levels and, if MODERATE, is associated with a low risk of mortality1.
Smoking appears to have a negative effect on HDL cholesterol. However, it appears that the use of cannabis has a positive effect2.
1 Types of alcoholic beverages and blood lipids in a French population - Ruidavets JB, Ducimetière P, Arveiler D, Amouyel P, Bingham A, Wagner A, Cottel D, Perret B, Ferrières J (Jan 2002) - Journal of Epidemiology and Community Health 56 (1): 24–8.
2 The impact of marijuana use on glucose, insulin, and insulin resistance among US adults - Penner EA, Buettner H, Mittleman MA (Jul 2013) - The American Journal of Medicine 126 (7): 583–9.
Physical activity is able to increase HDL, while keeping LDL constant. As a result, total cholesterol undergoes an increase. This phenomenon, which at first sight might appear counter-productive, is instead particularly desirable.
The most effective sports in increasing HDL are those that activate aerobic metabolism. It has been shown that, in sedentary patients, starting an aerobic activity protocol induces an increase of HDL equal to 3-9%.
Moreover, aerobic sporting activity promotes weight loss. Especially in the case of visceral obesity, the weight loss imposed by physical activity and diet leads to an increase in HDL of 0.35mg / dl per kilogram lost.
The sports protocol for increasing HDL must have the following requirements:
- 5 workouts divided into 5 days a week
- Moderate intensity
- Duration 30-40 '.
- 3 workouts divided into 3 days a week
- High intensity
- Duration 20-30 '.
In total, it would be better to reach around 150 'weekly with medium intensity.
Tips for Increasing HDL
In practical terms, to increase the HDL and lower the LDL it is necessary to follow these indications:
- If overweight, lose weight
- Stop smoking
- Practicing physical activity that includes aerobic exercise
- Decrease saturated or hydrogenated fats
- Decrease food cholesterol
- In the case of chronic hyperglycemia, decrease carbohydrates
- Decrease the fraction of simple added carbohydrates and all those with a high glycemic index; replace them with whole foods, unprocessed and with a low glycemic index
- Increase fiber in the diet, especially of the soluble type; in addition to lowering the glycemic index, they reduce the absorption of fat and the reabsorption of bile salts
- Promote the consumption of unsaturated fatty acids in conformation -cis (all vegetable ones of unrefined oils; preferably cold pressed)
- Proportionally increase the consumption of essential fats (omega 3, omega 6) and omega 9, preferring omega 3
- Take magnesium and vitamin PP supplements (niacin); some insights reveal a correlation between these two nutrients and the increase in HDL. For more information, see the next chapter.
Are there any useful drugs?
As for food supplements, there is a positive correlation between the intake of magnesium and niacin (vitamin PP or B3) and the increase in HDL.
Niacin (1 to 3g / day supplementation) increases HDL by selectively inhibiting the hepatic enzyme diacylglycerol acyltransferase 2, reducing the synthesis of triglycerides (carried by VLDL) and its secretion. The margin of improvement is between 10 and 30%, which makes vitamin PP the most effective molecule ever in the increase of HDL.
The most commonly used drugs for reducing cholesterol are statins. Most of these molecules exert a cholesterol-lowering effect on LDL. Statins are also naturally found in food; for example, in fermented red rice.
Note : No drug designed to increase HDL has been shown to consistently improve health by reducing cardiovascular risk.
In other words, the high levels of HDL correlate with an improvement in the state of health ONLY when this increase is of a metabolic type (HDL native).
It is not to be excluded that this facet interests, in addition to the quantity, the type of specific HDL. Or that other factors are involved that we do not currently know exist.