Saturated (SFA) and mono/poli unsaturated (MUFA - PUFA) fatty acids

The mainstream idea is that reducing the intake of saturated fat will reduce the coronary heart diseases (CHD). According to the latest researches, it is more important to limit refined carbs and to reduce excess adiposity.

There is a famous research done by Ancel Keys on Japanese men migrating from Japan to Hawaii or California, related to the increased percentage of CHD risk if the calories from SFA increase. If the SFA intake increases, the CHD risk dramatically increase. But the results are still treated as inconclusive, as there are too many variables involved.

The idea behind this is that when the SFA intake increases through dietary intervention, the serum lipids values increase (mostly LDL, but also HDL in a smaller proportion), and the CHD risk prediction also increase.

Few useful conclusions from other researches:

Vegetable oils (poliunsaturated fatty acids - PUFA) replacing SFA from dairy and meat will lower the CHD risk.

Reducing SFA and increasing refined carbs make no change to the CHD risk.

SFA raises LDL (causal factor for CHD and atherosclerosis), replacing SFA with MUFA/PUFA lower LDL levels.

Replacing SFA with PUFA prevents and regresses atherosclerosis in non human primates.



Sources of SFA - dairy foods (butter, cream, cheese, milk), fatty meat, processed meat, salami, sausages, chicken skin, cured meat, palm oil, cooking margarine, coconut oil and milk, fatty snack foods, deep fried, cakes, biscuits, pastries.

Sources of PUFA - Omega3/Omega6 healthy fats - soy bean oil, corn oil, sunflower oil, walnuts, tofu, canola, sunflower and flax seeds, fish (salmon, tuna, trout, herring, mackerel).

Sources of MUFA - nuts, avocado, canola oil, olive oil, peanut oil, sesame oil, peanut butter.

One interesting study about fat and health correlations

As we keep talking about the role of fat in our health, here it is one very important study.

If the study seems to much for your actual level of knowledge you can see some important parts of it here. Or here.

My favorite quote from the text:
"Stupidity is what's killing us, not sugar or saturated fat."

Dietary cholesterol

Low-density Lipids (LDL) are sensitive to changes in dietary fat composition. The amount of cholesterol, trans fatty acids, unsaturated fatty acids in daily diet can change the level of lipoproteins in blood. But, for the majority of the people, the blood cholesterol levels are rather insensitive to the dietary cholesterol intake. Dietary cholesterol contributions are only 33% the total cholesterol content in the body. Also, the changes are influenced differently for every individual, and just for 25-33% of the population a raise in dietary cholesterol will trigger a raise in the cholesterol blood levels. The relation between dietary and blood cholesterol is determined genetically via fractional cholesterol absorption - the proportion of the cholesterol absorbed in intestines can vary between 30-80% at humans.

Dietary guidelines of the past suggested 300 mg daily, but today the researchers said that the cholesterol is much less of a concern. Anyway, the high intake can lead to cardiovascular disease to some segments of the population, such as people with diabetes type 2.

What is the long term strategy?

Avoid cholesterol rich foods like eggs, organ meats, shellfish. Increase the intake of fibers - pectins, psyllium, betaglucans and inulin. Plant sterols and stanols decrease the cholesterol absorption (and they are today added to yogurt, milk and spreads to create functional foods with lower cholesterol).

Different people react different to dietary changes, and the fiber pill relation to the cholesterol levels is not a one size fill all strategy. The latest approach is called personalized nutrition - the possibility to adjust nutritional advice in relation with the person response to dietary changes.

Are you a runner?

What do you know about the ideal running temperature? What about nutrition, race course turns and hills? Pacing formation? Conservative drafting? Nike or Adidas?

Check this link and enjoy the results!

Good luck!

Cardiovascular diseases, atherosclerosis and eicosanoids (good fat vs bad fat)

A cardiovascular disease (CVD) involves heart and blood vessels problems. The most common is the coronary heart disease (CHD), when the coronary arteries become narrow and rigid restricting the blood flow towards the heart. It is also called Ischemic heart disease.

Another common disease is stroke, when the arteries supplying blood to the brain become blocked, reducing the blood flow.

Most of the CVD are related to the atherosclerosis (the build-up of the plaque on the wall of the arteries, gradually obstructing the blood flow due to the narrowing of the arteries). We can also mention here the not-so-common diseases such as heart failure, cardiomyopathy (heart muscle disease), heart valve problems and arrhythmia.

Regarding the cardiovascular diseases, the leading cause of death in the high income countries is CHD, while in the low income countries the infections are the major cause of death. Highest rates of death by CHD are found in Eastern Europe, while the lowest rate is in France and Japan. The substantial increase in Coronary heart disease in Eastern Europe has been linked to tobacco use, dietary behaviors, alcohol use and poor medical care.

Let's talk about atherosclerosis, which is the gradual narrowing of the arteries due to the build of plaque. It is asymptomatic, developing slowly and insidiously. When the oxygen supply cannot meet the demands, because the blood flow is impaired, the problems start to manifest (if it is happening in the heart is ischemia, in the brain is stroke, outside of those two areas is peripheral vascular disease).

The normal artery contains three layers. The inner layer - the endothelium - is in direct contact with the blood. The middle layer contains smooth muscle cells that expands and contracts the blood vessels. The outer layer is composed mostly form connective tissue. The experts believe that the plaque begins to form due to the damaged endothelium, highly supported by an elevated lipids level in the blood, high blood pressure and smoking. Because of the damage, we have white cells sticking to the endothelium, as this layer starts to produce sticky molecules called adhesion molecules, with role in the capture of the white cells. After adhesion, the white cells can move even further into the wall of the arteries. (including t-cells and macrophages). In the vessel wall, the macrophages can take up lipid droplets, becoming foam cells and the wall gradually thicken as it fills up with lipids. When the process advances, the smooth muscles move up to the inner layer and start to produce collagen, giving a connective tissue appearance to the inner wall. As the atherosclerotic process advances even more, cells die and the cell debris and lipids accumulates in the central region of the plaque (called lipid core or necrotic core). Lipids from the atherosclerotic plaque primarily originate from LDL cholesterol, which is interacting with the macrophages creating foam cells, which in turn produce molecules that aggravate the inflammation.

The lipid hypothesis says that lipids, especially LDL cholesterol are deposited in the atherosclerotic lesions and it is a 60 years old supposition. But the idea that elevated lipid levels contribute casually to atherosclerosis is still faced with skepticism. The other mainstream hypothesis is the inflammatory one, stating that inflammation and the immune system got a role in the apparition of the atherosclerosis. It is not proved yet that anti-inflammatory therapy reduces the myocardial infarctions (heart attack).

What we know is that the atherosclerosis lesions are quite stable most of the time, as the lipid core is covered in a thick layer of materials creating the fibrous cap. When inflamed, the white cells produce molecules that gradually break the fibrous cap. The plaque is thinning out and break, then rupture of the plaque leads to thrombosis, triggering the blood clotting. The blood clot can occlude the blood vessel partially or completely at the site of rupture. The blood clot stays there or it is dislodged and block the blood vessel elsewhere. Thrombosis is the formation of a thrombus (blood clot) inside of a blood vessel, impairing the blood flow. Blood clots are formed via coagulation (a process characterized by activation, adhesion and aggregation of the platelets). When someone suffer from heart attack, receiving rapid treatment with thrombolytic drugs (blood clot dissolvants) can save them.

The interesting part is that the blood coagulation is controlled by certain eicosanoids (as we know the eicosanoids are made from unsaturated fatty acids). A way to deal with this is to use not-steroidal anti-inflammatory drugs to inhibit the synthesis if the eicosanoids, blocking the cyclooxigenase enzyme, as primary and secondary prevention (for people who already had a heart attack). Because the eicosanoids are made mostly from essential fatty acids, the types of poli-unsaturated fatty acids present in our diet can influence the production of eicosanoids or just to put it in another way, the fatty acids that we eat may influence the blood clotting, in a good or a bad way. 

And another thing for you to know, the atherosclerosis process can be reversed and reduced using a right diet. We will talk about this another time. 

Eicosanoids, atherosclerosis and cardiovascular diseases

In my next post i will try to delve even further in the role played by the eicosanoids in the prevention of the cardiovascular diseases.

I am working currently at a careful wording, in order to not use to many scientific terms. I try.

Talk to you soon.

The eicosanoids and their relation with the essential fatty acids

This is a bit complicated, but please read slowly and check the connections with the previous posts.

Not very well known, the eicosanoids have roles in virtually every process in the body. Mainly they are binding to receptors on the surface and inside the cells. They can be categorized in prostaglandins (prostacyclins, thromboxanes) and leukotrienes (lipoxins).

The main substrate for eicosanoids synthesis is the arachidonic acid, resulted from the linoleic acid, one of the essential fatty oils. The prostaglandins synthesis from arachidonic acid, catalyzed by cyclo-oxigenase, can be inhibited by certain non-steroidal anti-inflammatory (Aspirine).

The other essential fatty acid - the linolenic acid - is transformed in EPA - a precursor for other eicosanoids synthesis - types that have more anti-inflammatory properties. We can mention Resolvins - which are made only from EPA.

In US and Norway, the main source for linolenic acid is soybean oil and its derivatives (tofu and other soybean-based products). EPA and DHA are obtained from krill and algae, but the real source is the algae producing the EPA/DHA, which is consumed by the krill, which in turn is eaten by the fishes. (30% of the fatty acids are in DHA form). In the infant formula all over the globe, the DHA  is coming from algae.

As you can see, i mentioned the essential fatty acids, the linoleic (part of the n-6 fatty acids family) and the linolenic acid (part of the n-3 fatty acids family). Those fatty acids need to be provided in diet, the lack of it can lead to poor growth and even death. They are essential because mammals cannot introduce double bonds beyond Carbon10 (counting from the carboxyl (end of the fatty acid). We cannot introduce Delta12 and Delta15, but we can make arachidonic acid (C20:4, N-6) from linoleic acid (C18:2:N-6) and EPA (C20:5,N-3) from linolenic acid ( C18:3, N-3).

The linoleic acid is a precursor for the arachidonic acid, source for various eicosanoids (functions in the body, pain management, immune function, blood pressure regulation and blood clotting). The linolenic acid is a precursor for EPA (eicosapentoic acid) and DHA (docosahexapentoic acid), serving to certains prostaglandins, such as the phospholipids in the brain and retina (from DHA). EPA and DHA can be found only in fatty fish and are sometimes reffered as fish oil fatty acids. A vegan or vegetarian diet will never have any EPA/DHA, so you will need to compensate by choosing good sources for linoleic and linolenic acids.